Management of Neck Pain Disorders: a

Research-Informed Approach

Gwendolen Jull, PhD, MPhty, GradDipManipTher,

DipPhty, FACP
Emeritus Professor, Physiotherapy, School of Health and Rehabilitation Sciences, The
University of Queensland, Australia

Deborah Falla, PhD, BPhty

Professor; Chair in Rehabilitation Science and Physiotherapy, School of Sport, Exercise
and Rehabilitation Sciences, The University of Birmingham, UK

Julia Treleaven, PhD, BPhty

Senior Research Officer in Physiotherapy, School of Health and Rehabilitation Sciences,
The University of Queensland, Australia

Shaun O’Leary, PhD, MPhty, BPhty, FACP

Senior Research Fellow in Physiotherapy, School of Health and Rehabilitation Sciences,
The University of Queensland, Australia
Foreword by

Jeremy S Lewis, PhD, FCSP

Consultant Physiotherapist, MSK Sonographer, Independent Prescriber, Professor of
Musculoskeletal Research, Department of Allied Health Professions and Midwifery,
School of Health and Social Work, University of Hertfordshire, UK

Edinburgh London New York Oxford Philadelphia St Louis Sydney 2019

Table of Contents
Cover image
Title Page
Copyright
Foreword
References

Preface

Section 1 Introduction
Introduction
1 Neck Pain Disorders
Basic tenets of neck pain
Contemporary issues
Conclusion
References

Section 2 Clinical Sciences

Introduction
2 Nociception and Pain Perception
Introduction
The nociceptive pathway: from noxious stimuli to pain perception
Nociceptive pain
Neuropathic pain
Inflammatory pain
Peripheral and central sensitization
The influence of psychological factors
Conclusion
References

3 Movement and Posture in Neck Pain Disorders

Cervical posture
Movement of the cervical spine
Relationships to adjacent regions
 Cervical posture and neck pain disorders
Conclusion
References

4 Neural Tissue in Neck Pain Disorders

Nerve injury and neck pain disorders
Pathophysiological mechanisms of nerve injury—the basis for clinical presentation and examination
procedures
Cervical spine-related nerve conditions
Conclusion
References

5 Neuromuscular Disturbances in Neck Pain Disorders

Anatomical considerations
Changes in motor output in people with neck pain
Changes in the coordination between muscles
Subtle variations in the distribution of activity within muscles
Changes in the temporal characteristics of neck muscle activity
Individual variability in motor adaptations to pain
Changes in peripheral properties of neck muscles
Time course for development of neuromuscular dysfunction
Implications for management
Conclusion
References

6 Sensorimotor Control Disturbances in Neck Pain Disorders

Cervical mechanoreceptors
Mechanisms underlying disturbances in sensorimotor control
Symptoms of altered cervical sensorimotor control
Signs of altered cervical sensorimotor control
Onset of disturbances in sensorimotor control
Relationships between sensorimotor measures
Conclusion
References

7 Psychological and Social Considerations in Neck Pain Disorders

Psychological features
Social features–the work environment
Conclusion
References

Section 3 Clinical Assessment

Introduction
8 Clinical Assessment
 Elements of the patient interview
Outcomes of the patient interview
Treatment goals and outcome measures
Conclusion
References

9 Clinical Assessment
Analysis of provocative movement or posture
Analysis of posture
Analysis of cervical motion
Assessment of cardinal planes of motion
Sensory testing and pain mechanisms
Examination of the nervous system
Manual examination
Assessment of the neuromuscular system
Assessment of disturbances in sensorimotor control
Conclusion
References

10 The Differential Diagnosis of Symptoms and Signs of Sensorimotor Control

Disturbances
Differential diagnosis of dizziness
Differential diagnosis of other symptoms
Clinical examination
Conclusion
References

11 Headache
Neck pain and headache
What defines cervical musculoskeletal dysfunction?
Cervical musculoskeletal dysfunction in headache: clinical decisions
Conclusion
References

Section 4 Clinical Management

Introduction
12 Principles of Management
Selection of management strategies
Selection of interventions
Conclusion
References

13 Communication, Education and Self-Management

Communication
 References

14 Management of Joint and Movement Dysfunction

Manipulative therapy
Active exercise
Self-management
Conclusion
References

15 Management of Neuromuscular Dysfunction

Exercise adherence
The home program
Neuromuscular training
Posture training
Training the activation and endurance of the deep cervical and axioscapular muscles
Training muscle control and coordination in movement and postural tasks
Training muscle endurance and strength
Dosage and intervention timelines
Maintenance program
Conclusion
References

16 Management of Sensorimotor Control Disturbances

Approaches to management
Principles for tailored sensorimotor control exercises
Exercises to train sensorimotor control
Self-management
Conclusion
References

17 Management of Nerve Tissue

Neurophysiological mechanisms underpinning nerve tissue management
Matching management to the nature of the nerve-related condition
Conclusion
References

18 Case Presentations
Case 1: Directionally biased persistent neck pain (Fig. 18.1)
Case 2: Headache—differentiating the role of the neck (Fig. 18.2)
CASE 3: (1) Learning from past treatment response; (2) Importance of differential diagnosis to guide
management of complex patients after a whiplash injury (Fig. 18.3)
Case 4: Clinical reasoning in the physical examination guides treatment decisions (Fig. 18.4)
Case 5: Neck pain associated with neuropathy (Fig. 18.5)
Conclusion

19 Concluding Remarks
 Prevention
Conclusion
References

Index
Copyright

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Foreword
It remains an on-going challenge to keep up to date with advances in science and changes
in clinical practice to provide the best care for people experiencing neck pain disorders.
The amount of new knowledge available is bewildering not only for patients, but also for
clinicians. This is due to the rate at which new ideas, philosophies and research are
published and disseminated across a vast range of communication systems, traditional and
new. Gwen Jull, Deborah Falla, Julia Treleaven and Shaun O’Leary have, in a unique and
uncompromised manner, brought together, between the covers of this wonderful text book,
the knowledge and understanding any clinician from any discipline, and from any level of
experience and knowledge, would require to confidently guide and support the
management of a person experiencing neck pain. The breadth and depth of information
contained within these pages is unparalleled, and this text would make an invaluable
resource to any personal or public library.
The Global Burden of Disease Study has ranked neck pain, along with low-back pain,
as the main health conditions associated with the longest number of years lived with
disability (1). For some, musculoskeletal pain is associated with a reduction in the
subjective quality of life that is comparable to complicated diabetes mellitus, chronic liver
disease requiring transplantation, and those diagnosed with terminal cancer (2).
Knowledge of this should encourage and inspire all clinicians entrusted with the
unassailable privilege of caring for a member of their society to learn more, know more
and do better. Through its 19 chapters, presented in 4 sections, Management of Neck Pain
Disorders supports clinicians to realise these important goals taking them through a truly
biopsychosocial journey of discovery that synthesises the research evidence and clinical
knowledge that has taken many, many decades to acquire.
Section 2 of Management of Neck Pain Disorders covers the Clinical Sciences and the
text synthesises modern pain science in the context of pain experienced in the region of
the neck and explores in-depth the psychosocial factors that may influence the perception
of pain. Uncertainties surrounding the relationship between cervical posture and
symptoms are explored. The anatomy and biomechanics of the region, as well as adjacent
regions, are expertly presented, as are injuries and pathology of the neural tissues and their
impact locally and more distally. Currently, there is no better synthesis of the research
evidence available for clinicians with detailed information exploring changes in motor
output, muscular co-ordination and activity, temporal characteristics of neck muscle
activity, and pathological changes within muscle tissue and disturbances in sensorimotor
control, for those that experience neck pain.
Section 3 skilfully guides the clinician through every stage of the clinical-assessment
process, from interview though the physical examination, and comprehensively supports
the clinician’s ability to clinically reason and conduct a state-of-the-art examination.
Pertinent issues such as the patient–clinician relationship, language, outcome measures,
psychosocial factors, lifestyle factors and sleep, and red-flag recognition are presented.
The physical examination includes provocative movement testing, comprehensive
movement assessment procedures, neurological and vascular testing methods, all-inclusive
muscle testing in multiple positions, ligament tests, balance, and a battery of methods of
assessing a wide range of sensorimotor disturbances including oculomotor assessment.
The importance of differential diagnosis is emphasised throughout the text and includes
sections on headache, and the differential diagnosis of dizziness, including minor brain
injury, benign paroxysmal positional vertigo, peripheral vestibular lesions, tinnitus and
visual disturbances, and much, much more.
Section 4 provides the reader with the most comprehensive system of care imaginable,
and is uncompromising in its patient-centred approach to management. It includes sections
on communication, education, and work and life-style advice. Guidance on selection of
interventions, together with comprehensive exercise strategies, including sensorimotor
exercise and virtual-reality exercises, balanced and wide-ranging manual-therapy
procedures, the management of nerve tissue, home-based rehabilitation, and a detailed
section on self-management, will prove invaluable for all clinicians caring for people with
neck pain disorders. The penultimate chapter presents the reader with a series of five
comprehensive case studies aiming to support clinical reasoning and clinical decision-
making strategies. The final chapter discusses the role of prevention in neck pain
disorders.
For Management of Neck Pain Disorders to achieve its intended purpose, as an essential
clinical resource, it should not remain in the unspoiled condition in which it was delivered.
In order for this text to support clinical practice and to provide the best possible care to the
most important person in healthcare, the patient, the pages in this textbook should quickly
become well thumbed, reflected upon, annotated with reference tabs, discussed with
colleagues, and its information compared to new and emerging research. Providing care
for people with musculoskeletal conditions, including neck pain disorders, is not only a
privilege but also comes with a responsibility. It demands that you conduct your practice
with understanding, empathy and knowledge, translated from the best possible resources.
Management of Neck Pain Disorders will assist you in achieving these goals, and should
quickly become the go-to resource for every clinician, newly qualified or experienced.
Currently, there is no better resource for the management of neck pain disorders and all
will find value within its pages.
Jeremy Lewis

2018

References
1. Global Burden Disease 2015 Disease and Injury Incidence and Prevalence
Collaborators. Global, regional, and national incidence, prevalence, and years
 lived with disability for 310 diseases and injuries, 1990-2015: a systematic
analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388:1545–
1602.
2. Taylor W. Musculoskeletal pain in the adult New Zealand population: prevalence
and impact. N Z Med J. 2015;118:U1629.
Preface
It is certainly not enjoyable to have neck pain. It is a common and recurrent disorder
characterized by episodes over many years, if not a lifetime. For some persons, it is of
nuisance value but for many others it affects their work and leisure activities and for a few,
especially in association with trauma from a motor vehicle crash, its onset may
substantively change their quality of life and work well into the future. Our clinical and
research interests over the past 15 to 20 years have been in neck pain where we have
worked in a “laboratory to bedside” framework to better understand the pathophysiology
of neck pain disorders, the person with neck pain and the interrelationships of these
features in the context of the biopsychosocial model. The overarching aim of our work has
been to improve the outcomes for people with neck pain disorders by utilising and
developing best practice, research informed assessment and management strategies. The
aim of this text is to inform clinicians and assist them to provide optimal management for
their patients presenting with neck pain disorder.
We previously presented our work in the text, Whiplash, Headache and Neck Pain,
published by Elsevier in 2008. This current book is, in part, a second edition reflecting the
advances in research and clinical practices in the last 10 years, but it has been completely
rewritten. Its new title reflects a new structure and emphasis, and it presents a more
comprehensive coverage of the features we contend need to be considered in the
assessment and management of patients with neck pain disorders. We discuss some
contemporary issues in patient presentation, assessment and management across a range of
cervical disorders and hope to stimulate clinicians’ and researchers’ thinking about current
and future practices in both research and patient management.
In particular, we stress the importance of regarding each patient as an individual with
each person’s management guided by a clinically reasoned and comprehensive patient-
centred assessment. We stress the importance of regarding neck pain as a recurrent
disorder for many, if not most, individuals. Patient management should not focus only on
relieving the presenting episode of pain (although this an important aspect): rather,
management must also be concerned with rehabilitation of movement, neuromuscular and
sensorimotor function. The aim of management should be to try to prevent or lessen the
frequency of recurrent episodes and, as with degenerative joint disease in other regions of
the body, try to slow disease progression. It is critical to provide the patient with the
knowledge, understanding and tools to empower them to self-manage their necks. This
might sound an idealistic approach and certainly more expensive than administration of a
generic programme of exercise or advice. However, thinking about the cost of one episode
of care is narrow thinking because the costs are not in a single episode. The real costs and
burden of neck pain are in its recurrent nature with the costs of repeated occasions of care,
reduced work productivity, reduced quality of life and the cost of harms (e.g., the
significant harms of prolonged use of nonsteroidal antiinflammatory drugs). Prevention at
primary, secondary and tertiary levels must be the focus of research and practice into the
future.
Research is a collaborative venture. In writing this text, we acknowledge the assistance
we have received from our numerous multidisciplinary research and clinical collaborators,
who are too many to name, as well as the work and stimulation provided by our many
doctoral students and postdoctoral fellows. These collaborations have not only ensured
quality and productive work, but have cemented friendships all over the world. We also
wish to thank Susan Davies and Dominic Truong who modelled for the photographs in the
text and Helen Leng and Poppy Garraway of Elsevier for their support in bringing the text
to publication.
GJ, DF, JT, SO’L
SECTION 1

Introduction
OUTLINE

Introduction
1 Neck Pain Disorders
Introduction
1 NECK PAIN DISORDERS 3

This chapter introduces the topic of neck pain disorders and, as background to the text,
presents some of the contemporary issues that are impacting on decisions for assessment
and management of persons with neck pain disorders. From the outset, clinicians are
challenged to change their thinking from a focus on relieving a presenting episode of neck
pain, to a focus on the real challenge in management which is lessening or preventing the
potential years of recurrent episodes of neck pain.
1

Neck Pain Disorders

Neck pain is common. In the main it is not a catastrophic condition, but it can have a
significant impact on a person’s work, recreation and quality of life. Neck pain spares no
age group, gender or culture.1 Following a first episode of neck pain, there is a high
chance of repeated episodes, which may extend over a lifetime.2 Recovery from an acute
episode is frequently incomplete.3 Neck pain is a condition characterized by recurrence, or
in some cases, persistent pain. Recent findings of the Global Burden of Disease Study
indicated that neck pain along with low-back pain, ranked as number one of 310 chronic
medical conditions in terms of years lived with a disability. Neck pain is a problem
worldwide, it ranked as number one in the majority of the 195 countries surveyed.1 The
burden of neck pain for the individual manifests not only in the symptoms and physical
complaints, but in its impact on their work and social participation and the related
financial, family and emotional consequences.4
Neck pain disorders are heterogeneous in presentation.5 Symptom intensities range from
“nuisance value” to disabling pain, as evident in some cases of whiplash-associated
disorder and cervical radiculopathy. In tandem, the impact on function is variable, ranging
from a negligible impact, to a particular activity or action being difficult, to activity
restriction to such an extent that it limits a person’s participation in activities of daily
living and work. Not all people with neck pain seek treatment and many self-manage
either relying on time, over-the-counter medication or self-management strategies
commonly gleaned from the internet. When treatment is sought from a health practitioner,
conservative management is the first line of management. Recurrence is common whether
the neck disorder begins as a minor or significant pain.6 Clinicians and researchers across
public health, medical and rehabilitation fields must assume the responsibility to further
develop and deploy effective preventative and management strategies to assist and
empower people to reduce the incidence, recurrence and consequent burden of neck pain
globally.

Basic tenets of neck pain

Neck pain is a symptom of various origins. Musculoskeletal causes are by far the most
common, but neck pain can also be a symptom of non-musculoskeletal sources such as
infection, neoplasm, vascular disorders (carotid or vertebral arterial dissection), metabolic
bone disease, inflammatory, neurological and visceral diseases, causes for which a
clinician must always remain vigilant. From a musculoskeletal perspective, all structures
of the cervical spine are innervated so all may be a source of peripheral nociception
contributing to a primary neck pain disorder. Pain from a cervical musculoskeletal
disorder is typically felt in the posterior neck. Depending on the segmental source and
structure, it may spread to the head, shoulder, upper thoracic region or down the arm.7
Although cervical musculoskeletal dysfunction usually underlies neck pain, there are other
presentations. Neck pain and dysfunction may be secondary or comorbid features of pain
syndromes in the craniomandibular complex, the shoulder or upper limb. Alternately, the
neck itself may be a site of referred pain, rather than a pain source, as encountered in
disorders such as migraine,8 cardiac disease9 or cervical arterial dissections.10 Such
presentations emphasize the necessity for a skilled physical examination. Clinicians need
to be able to identify the presence or absence of a cervical musculoskeletal source to neck
pain and, when present, if it is a primary cause, a secondary cause or comorbid problem.
Neck pain of musculoskeletal origin initially arises from a nociceptive source such as a
local injury or mechanical stress or strain, from inflammation, or from injury or irritation
of nerve structures, i.e., a neuropathic pain. Very simply, signals from the periphery travel
to the central nervous system and are processed and modulated in various regions of the
spinal cord and brain. There is much contemporary interest in sensitization and
neuroplasticity at all levels of the nervous system and their possible role in persistent
pain.11 It is well recognized that pain is not merely a sensory event but a multidimensional
experience with emotional reactions or psychological moderators, which all input into the
plastic nervous system. Likewise, there can be social drivers and moderators in work and
lifestyle that can impact on the pain experience and the neck pain disorder. The necessity
for a skilled and comprehensive clinical examination is again evident to ensure a broad
consideration of the patient and their neck pain disorder to inform a best practice
management program.
Pain is an important consideration and patients usually seek pain relief as a primary
goal of treatment. As important as pain relief may be, it is but one consideration. Pain and
injury to any region of the musculoskeletal system have profound effects on the
neuromuscular system. The cervical region is no exception where changes in both muscle
behaviour and structure have been clearly demonstrated.12 There is no evidence that
neuromuscular function will always automatically return to normal when an episode of
neck pain resolves. Indeed, there is evidence to the contrary.13–16 The burden of neck pain
to many individuals is in its recurrent or persistent nature, with numerous years lived with
pain and disability. Recurrent neck pain impacts on physical health related quality of life.17
Although pain relief is an important outcome, best practice management must also focus
on decreasing the recurrence rate. Rehabilitation to restore neuromuscular function is a
logical component of the management program.
Pain is not the only symptom of neck disorders. Other symptoms may include feelings
of light headedness and unsteadiness, visual disturbances and cognitive difficulties such as
problems concentrating.18 The cervical spine is an important proprioceptive sensory organ.
Together with input from the vestibular and ocular systems and somatosensory input from
the rest of body, proprioceptive input from the neck muscles plays an important role in the
control of posture, locomotion and oculomotor control. When cervical afferentation is
disturbed, the mismatch in information processed in the central nervous system from all
component systems is reasoned to underlie symptoms. Together with symptoms, deficits
in cervical joint position and movement sense, balance, eye movement control and eye-
head, trunk-head coordination are variously present. Symptoms of light headedness and
unsteadiness, visual disturbances and cognitive difficulties can be functionally
debilitating. Management must also focus on addressing these symptoms and sensorimotor
deficits when present. There are many treatments that may help symptoms, but again,
decreasing symptoms does not automatically mean the somatosensory impairment has
resolved.19 Best practice management should include specific rehabilitation of the
impairments if sights are on decreasing recurrence rates as well as alleviating symptoms.

The biopsychosocial model

Neck pain disorders are multidimensional. Some 30 years ago, Waddell20 adapted
Engel’s21 biopsychosocial model for the field of psychiatry to apply it to low-back pain.
Consideration of biological features in the traditional medical approach could not alone
explain the disability associated with low-back pain and it was not logical to separate the
person from their condition. Subsequently, the biopsychosocial model was adopted for
neck pain and other musculoskeletal disorders. The biopsychosocial model, as its names
implies, encourages simultaneous consideration of all potential biological, psychological
and social determinants of a patient’s neck pain presentation. The model accords with
other frameworks such as the International Classification of Functioning, Disability and
Health (ICF). It promotes consideration and assessment not only of multiple domains, but
also of the potential moderating and mediating characteristics of features within and
between the different domains. The model has limitations. It does not indicate which
features should be evaluated in any domain and consequently cannot inform or guide
selection of interventions. It is not an interventional model.22
The biopsychosocial model is often depicted as three symmetrical circles suggesting
“equal” contributions of biological, psychological and social domains to every person’s
neck pain disorder. This is an inaccurate picture. The contribution of each domain varies
between patients (Fig. 1.1). Even within a patient, the contribution of each domain is
likely to change throughout the course of their disorder. The model provides a philosophy
underpinning a comprehensive consideration of a patient’s neck pain disorder in
assessment and management. Lack of appreciation of the variable contribution of each
domain in the individual patient, and relative importance of each domain at initial and
subsequent time points will negate or compromise patient-centred management. It leads to
the erroneous belief of a “one size fits all” treatment.
 FIG. 1.1 The three domains of the biopsychosocial model are fluid and will vary in
their contribution between different patients and in different stages of a patient’s neck
pain disorder. Three examples of relative contributions of domains are presented in
order of their probable frequency based on contemporary evidence.

Contemporary issues
No approach whether medical, physiotherapeutic, chiropractic, psychological, educational
or any alternate or complementary therapy has as yet met the idealist challenge of
successful primary and secondary prevention of neck pain. Controversies continue around
the management of neck pain disorders. Although conservative physical therapies are not
proving the answer for all with a neck pain disorder, there are positives. The majority of
individual patients gain some if not considerable relief from physical therapies. The
challenges are in selecting appropriate interventions and identifying likely responders and
non-responders so that inappropriate treatment is not delivered. Although not a pure
science, progress is being made to meet these challenges. This text will overview and
explore neck pain disorders from the basic and applied clinical sciences in a
biopsychosocial context. It will overview our and others research, which is increasing the
understanding of neck pain disorders and which is informing patient assessment,
management and prognosis. A research informed, comprehensive management and
rehabilitation approach will be presented, which will emphasize the indications for and
application of individualized multimodal management and, as relevant, multidisciplinary
management. However, in the first instance, some of the issues and debates in the field of
neck pain disorders will be presented to stimulate thought as the reader progresses through
the text.

Classification of neck pain

Classification is a popular topic in physiotherapy research and clinical practice. It is well
recognized that neck pain disorders as with most musculoskeletal disorders, have great
variety in their presentations. Classification aims to group similar individuals. Its main
purposes are to define diseases, to help direct management or to allocate resources to
provide care. There are many criteria on which neck pain has been and may be defined. It
would be ideal to have one classification system that could define neck pain disorders and
direct appropriate management. Towards such an ideal, it is relevant to briefly overview
some of the current criteria on which neck pain disorders are defined and explore whether
or not they should be retained or discarded in a classification system.

Defining the neck pain disorder by mechanism of onset

Historically, neck pain disorders have been grouped or classified into one of three major
domains: mechanical (or idiopathic or non-specific) neck pain; traumatic onset neck pain
(e.g., whiplash associated disorders, sporting injuries, falls, blunt trauma to the head or
neck); and degenerative (spondylosis) disorders, which can range from minor disc
narrowing to acquired stenosis (lateral canal stenosis—cervical radiculopathy; central
canal stenosis—cervical myelopathy). Two domains relate to mechanism of onset and the
third to pathoanatomy, (which is discussed in the next section). Traumatic onset neck pain
is self-explanatory. Mechanical neck pain is a descriptor term, predominantly of exclusion,
for pain not arising from an incident of trauma, an inflammatory disease process or any
other identifiable intrinsic or extrinsic pathology. The catchment for the term mechanical
neck pain is large and variously includes pain induced by an unaccustomed movement or
activity, postural strain or accumulated adverse strains from repetitive, static or high-load
activity.
It would be easy to dismiss this onset-based classification as too unrefined, but there are
differences between the groupings. In the first instance, the sites and nature of pathology
could be expected to differ. Trauma from a motor vehicle crash or blunt trauma can result
in lesions of several cervical structures of a greater variety and to a greater range with
attendant bleeding and inflammation than may occur with accumulated postural or activity
strain.23 There are many similarities in the presentation of insidious onset mechanical neck
pain and traumatic onset neck pain from the musculoskeletal impairment perspective. Yet
there are differences. Taking comparative population averages, patients with whiplash-
associated disorders, on average, present with higher pain and disability than patients with
mechanical neck pain.24 Furthermore, cohorts of patients with whiplash-associated
disorders are more likely to exhibit central nervous system sensitization,25 have greater
physical impairments,26,27 exhibit distinctive changes in cervical muscle morphology28–30
and have impaired somatosensory function of greater magnitude than insidious onset neck
pain.31 Emotional responses are also often more pronounced in whiplash-associated
disorders. As will be illustrated in this text, such differences have implication for designs
and components of patient-centred, management programmes. Hence this first basic
classification, mechanism of onset, contributes to patient characterisation and makes a
contribution to patient assessment and management planning. It should not be discarded.

Defining the neck pain disorder by pathoanatomy

The terms mechanical or non-specific neck pain and whiplash-associated disorders have
been adopted in place of nominating a particular lesion, pathoanatomy or pathological
process in the cervical musculoskeletal system. Even today, imaging methods such as
standard x-rays or magnetic resonance imaging (MRI) are often not sensitive enough to
identify relevant lesions.32,33 Often there is little relationship between x-ray findings and
pain.34 This insensitivity has led to advice against routine imaging of the cervical spine as
a first assessment in neck pain presentations. Guidelines (Canadian Cervical Spine Rule;
National Emergency X-Radiography Utilization Study [NEXUS] Low-Risk Criteria) have
been developed to designate specific indications for imaging especially in the case of
traumatic onset neck pain to avoid unnecessary x-rays.35 The absence of a lesion on x-ray
does not necessarily mean there is no lesion. It could mean that the imaging method or the
time it was used, was unable to detect a relevant lesion.23,32 Care is needed when
conveying information to patients regarding radiological findings. Although patients
should be reassured that a lack of radiological findings does not question or discredit their
report of symptoms, at the other extreme, patients should also be reassured that the
presence of marked radiological findings does not necessitate marked levels of pain and
disability. Poor communication of radiological findings can compromise patient clinician
relationships. Explanation and qualification of x-ray findings should always be provided.
Recent decades have seen a move away from attempting to define a precise lesion,
reflecting the challenges of identifying the lesion and differentiating it from age changes.34
Furthermore, x-ray findings provide limited direction in management of the majority of
persons with neck pain disorders. The previous emphasis on “biology” was a main driver
for the adoption of the biopsychosocial model. Knowing that a patient has C2–3
osteoarthritis on x-ray, does not inform on pain mechanisms, reactions in the
neuromuscular or somatosensory systems or emotional responses to the disorder which
could direct treatment. Yet should attempts to make a pathoanatomic diagnosis be
abandoned entirely? Surgeons operate on pathoanatomy, so for them a pathoanatomic
diagnosis cannot be abandoned. Likewise, it might be premature to discard changes seen
on x-rays as not relevant. Recent MRI research in low-back pain suggests that the
presence of three or more changes in lumbar structures (as opposed to a single sign), is
associated with a higher risk of future recurrence of low-back pain.36,37 These findings
encourage continued consideration of pathoanatomy. A similar line of research is
warranted for cervical disorders because neck pain too is a recurrent disorder. Having a
way to identify, quantitatively, those at high risk of recurrence would be a major advance
in management planning. It would be unwise to dismiss identifying pathoanatomy in
future research and practice, thus it cannot be discarded.
Identifying or nominating the precise lesion in a cervical structure may be difficult, but
a symptomatic cervical segment can be identified with considerable accuracy in a clinical
examination of patients with neck pain. Manual examination is not without its
controversies, but there is now a considerable body of evidence indicating that manual
examination is an accurate clinical method to locate a symptomatic cervical segment.38–42
This should not be surprising because even at a very basic level, palpating for tender areas
is a fundamental medical examination technique and is a minimum expectation of patients.
Identifying the symptomatic cervical segment(s) is important to define the disorder and
cannot be discarded.

Defining the neck pain disorder by time

It is common to define pain on the basis of time into acute, subacute and chronic. The
criteria for chronic pain in these terms is pain which persists past the normal time of tissue
healing which is customarily, greater than 12 weeks. This definition based on tissue
healing is well recognized as flawed.43 Healing may occur well within or well outside this
timeframe or it may never occur (e.g., as in osteoarthritis, or spinal stenosis). Neck pain is
recognized as an episodic disorder with pain free periods of months or even years between
episodes—periods where tissues had apparently healed. Is recurrent neck pain over years
the same as chronic neck pain? Using time alone to classify chronic pain tends to portray a
“sameness” across all pain states lasting greater than 12 weeks, which is far from reality.
What is chronic pain? Chronic pain may involve, in any combination, physical
disorders both peripheral and central, biochemical disturbances in various body systems,
local disease processes, psychological responses or unhelpful personal beliefs. The
International Association for the Study of Pain43 discourages the use of the term chronic
pain syndrome because it usually implies persisting pain, which is driven by behavioural
changes induced by psychological and social problems. They contend that the term helps
clinicians evade the requirement for all patients to have accurate physical and
psychological diagnoses, and that the term is often used disparagingly. Until there is better
taxonomy for chronic pain, it behoves researchers and clinicians alike to clearly define the
physical and psychological characteristics of the chronic pain presentation of the patient or
patient group under discussion to facilitate accurate communication and importantly,
management prescription. Time-based classification certainly contributes to defining the
disorder. It should not be discarded, but its substantial limitations must be appreciated.

Defining the neck pain disorder by mechanisms

A diagnostic label is limited in the extent to which it can help direct management. The
mechanisms underpinning symptoms and other functional limitations on the other hand,
can direct management.
There is great interest in the mechanisms underlying various clinical pain presentations,
the plasticity of the nervous system and how it can be modulated by both endogenous and
external features. Knowledge is growing and constantly developing. Treatments can be
guided by several features, such as whether pain is nociceptive, inflammatory or
neuropathic in origin, if local or widespread mechanical or thermal hyperalgesia are
present suggesting peripheral or central nervous system sensitization and by the extent to
which emotional or psychological features might be moderating symptoms. Several
studies have shown that patients cluster into groups on the basis of outcomes of
quantitative sensory testing, which might indicate different pain mechanisms.5,44,45
Understanding pain mechanisms can guide assessment protocols and treatments towards
all levels of the nervous system.
Knowledge of the neurophysiological mechanisms underpinning symptoms of cervical
dizziness such as light-headedness and visual disturbances is growing rapidly as is
knowledge of the manifestations of impaired proprioception (position, movement and
force sense), balance and eye, head and trunk coordination.46,47 Understanding
mechanisms of cervical somatosensory dysfunction helps define the condition and can
guide assessment and management approaches.
Functional impairments such as poor control of posture, poor patterns and control of
movements and inabilities to perform or sustain performance of an activity reflect deficits
in the neuromuscular system. There is now a wealth of knowledge about the changes in
the neuromuscular system with neck pain and injury in the acute, recurrent and persistent
pain states. Understanding these changes defines the condition in neuromuscular terms
and guides assessment and management approaches.
Defining the condition in terms of mechanisms clearly and precisely directs patient
assessment and management planning and cannot be discarded.

Defining the neck pain disorder by predictors

Knowledge is increasing about predictors of neck pain as well as predictors of recovery
and future neck pain in the general, occupationally induced neck pain and whiplash
populations.48–53 More studies are needed to explore predictors of neck pain of
occupational, sporting, traumatic and insidious origins, so that certainty for a feature can
be established by a critical number of studies.52 Likewise, more studies need to consider
all domains within the biopsychosocial context simultaneously, rather than focus on one
domain. This provides a clearer picture of the relative predictive roles of features within
and across all domains.
Knowledge of predictors for the development of, or recovery from neck pain informs
our understanding of a patient’s neck pain disorder. How useful it is to use predictors to
direct management is yet to be explored in any detail.54 Many predictors of persisting or
recurrent episodes of neck pain cannot be modified, for example, age, gender or previous
episodes of neck pain. However other features are possibly modifiable, for instance social
features at work such as job control or physical features such as reduced neck muscle
endurance.50,51,53 Initial high-pain intensity and disability are strong risk factors for
persistent pain following a whiplash injury.52 Knowing this fact is important. Nevertheless,
not all patients with initial high-pain intensity have a poor prognosis. For some, their
condition resolves in a straight forward way. Likewise at this time, no treatment approach
(physical, medical or psychological) has been successful in reducing the risk of transition
to persistent pain for this small but difficult group of patients. At this point, there is little
evidence or research to inform whether targeting risk factors for persistent neck pain
improves outcomes. Yet risk factors help define neck pain and should not be discarded at
this time.

Defining the neck pain disorder by clinical prediction rules

There has been interest over the past decade in developing clinical prediction rules (CPRs)
to identify the characteristics of patients who may respond to a certain treatment technique
or approach. CPRs have been developed to indicate the use of cervical or cervicothoracic
manipulation for neck pain and for shoulder pain, for the use of cervical traction as well as
the use of neurodynamic techniques in the management of arm pain and carpal tunnel
syndrome.55–59 However, most CPRs to direct treatment have remained in the first stage of
development. CPRs that have been tested in validation studies to date have failed to gain
support.60–62 The use and indeed the future of CPRs to direct a particular treatment regime
is uncertain. At this time their clinical use is not supported.63

Defining the neck pain disorder by subgrouping

The heterogeneity in presentation of neck pain disorders is recognized. There is
widespread acknowledgement that a one size fits all treatment approach is ineffective.
Subgrouping is a means to address the issue by grouping patients with similar clinical
characteristics with the aim to better tailor treatments. Subgrouping has been explored for
neck pain, but to a far lesser extent than for low-back pain. There are perhaps only two
specific subgrouping systems for neck pain at this time. One is based on the overall goal
of treatment.64 Patients are allocated to one of five groups depending on whether the
treatment intent is to increase mobility, to centralize pain, to condition the patient and
increase exercise tolerance, to assist pain control or to reduce headache. There has been
some preliminary research supporting the potential benefit of this classification system65,66
but more research is required to determine whether this subgrouping method clearly
improves treatment outcomes overall. A similar classification system has been
incorporated in the Clinical Practice Guidelines for neck pain presented by the
Orthopaedic Division of the American Physical Therapy Association.67,68 The groups here
are: neck pain with mobility deficits; neck pain with headaches; neck pain with movement
coordination impairments; neck pain with radiating pain. The other system, Mechanical
Diagnosis and Therapy, which was originally devised for the low back, has been applied
to the neck.69,70 Depending on the response to repeated movement, patients can be
classified into four basic syndromes: posture, dysfunction, reducible derangement,
irreducible derangement or “other” category. At the current time, this subgrouping has not
proved to have resulted in any superior treatment effects.71 Although subgrouping may
have promise, it is considered that research and achievements in this field (whether neck
or low-back pain) are far from optimal. Evidence does not as yet support their widespread
adoption in clinical practice.72
This brief overview illustrates the breadth of factors that need to come under
consideration to define or classify neck pain to direct management. Few can be dismissed.
At this current time, and especially in research and clinical trials, the most common
grouping is by mechanism of onset, that is, insidious onset (mechanical neck pain),
traumatic onset (e.g., whiplash) and degenerative onset (including radiculopathies),
reflecting some recognisable differences in these disorders within and between
biopsychosocial domains. Perhaps this is the best starting point in developing a
hierarchical classification algorithm to guide management. Nevertheless, the algorithm
should incorporate all defining features of neck pain disorders, including stepped rankings
of their importance, influence and dominance, and the potential interdependence or
independence of the various features. In other words, it should reflect the high-level
clinical reasoning processes that will define the patient’s particular neck pain disorder and
direct appropriate management.

Management of neck pain disorders

A considerable portion of the text will be devoted to describing conservative management
options for patients with neck pain disorders. Many issues will be discussed in relation to
best practice in the model of evidence-based practice. In this first instance, three issues are
highlighted to stimulate thought before they receive fuller attention in the text.

Effectiveness and ineffectiveness; responders and non-

responders
Recent updates of systematic reviews by the Bone and Joint Decade Task Force on
interventions for neck pain and whiplash-associated disorders found evidence of benefit
for manual/manipulative therapy, exercise, multimodal management, with some evidence
of cost-effectiveness of conservative management.73–76 Evidence points to the use of
education as an adjunct but not a sole therapy.77 There was neither evidence for or against
the use of psychological interventions for neck pain disorders.78 This evidence for
conservative physical therapies is encouraging, but effect sizes are often at best moderate
if not small.79,80
Small effect sizes have been associated with the heterogeneity of mechanical neck pain,
which is often not considered in participant selection in randomized controlled trials
(RCTs). This challenge has fuelled the move to have better classification or subgrouping
of neck pain disorders. A part of the complex process of optimizing classification to guide
management is to recognize the characteristics of patients who are likely and who are not
likely to respond to conventional physical therapies or conventional physical therapies
alone. Understanding the characteristics of patients who do not respond is equally
important as identifying responders. These patients need to be identified as early as
possible so that alternate management strategies can be explored both in research and
clinical practice in a multiprofessional manner.

Single or multimodal interventions

Often single treatment modalities are tested in RCTs and evaluated in systematic reviews.
There is scientific merit in trying to discover the effects of a particular intervention.
However, it is an unrealistic expectation that one modality/intervention will be a “cure all”
for all abnormal, impaired or maladaptive features within and between each domain of the
biopsychosocial model. There are criticism of practitioners of any discipline who focus
predominantly on biological domains, resulting in many “hands on, hands off” debates.81,82
Even within a biological focus, it is a flawed expectation that relieving pain will resolve
automatically, any motor or proprioceptive impairment.13–16 Equally, it is quite illogical to
expect that interventions focussing on behavioural or central nervous system processes
alone will automatically “fix” all abnormal, impaired or maladaptive features within each
biopsychosocial domain. Outcome measures must be chosen to represent each impaired
feature within each domain, so that clear knowledge is built about the effects of an
intervention on each and every impairment. Such knowledge will further inform
multimodal management approaches. This is the challenge in both clinical and research
environments.

Neck pain—an episodic or a recurrent disorder

Neck pain is a recurrent disorder, the episode of pain returns again and again over the
following months or years.2,3 Neck pain (along with low-back pain) results in more years
lived with a disability than any other chronic condition.1 A review of RCTs of acute neck
pain quickly reveals that pain is the primary outcome. The aim is to relieve that single
episode of neck pain. There is no apparent interest in whether or not the neck pain recurs.
Cost effectiveness is almost a mandatory feature of current RCTs. There seems to be a
trend, not only to judge cost effectiveness, but to find the cheapest intervention. Yet it can
be argued that the cost of neck pain is not in a single episode. Rather the financial, social
and personal burdens are in repeated episodes of pain, repeated episodes of care, lost work
productivity and costs of harm (e.g., side effects of nonsteroidal antiinflammatory drugs).
Relief of pain is an important clinical outcome and certainly patient centred. Yet this
focus on pain seems to have dulled or eliminated a focus on rehabilitation to reduce
recurrences. A major divide has developed between rehabilitation of a neck pain disorder
and rehabilitation of an extremity disorder. A rehabilitation program for a knee or ankle
disorder is usually inclusive of a comprehensive exercise program to train neuromuscular,
proprioceptive and functional deficits to a normal functional level. Patients with neck pain
are given exercises and numerous RCTs have tested exercise regimes for neck pain
disorders. Yet the primary outcome is their effect on pain. Attention is usually not given to
the neuromuscular impairment for which the exercise program was prescribed and
whether or not that neuromuscular impairment was trained successfully. If a primary aim
is to decrease the burden of neck pain, there needs to be a focus not only on pain relief but
on the return of physical function towards decreasing recurrence rate. Restoration of
normal neuromuscular function and proprioception, especially in the early stages of the
disorder should contribute to this aim. Indeed, primary, secondary and tertiary
preventative rehabilitation programs deserve equal attention to pain relief.

Conclusion
The statistic that neck pain along with low-back pain is the world’s leading cause of years
lived with a disability sends a major challenge to clinicians and researchers alike.
Research has progressed knowledge at a remarkable pace particularly over the last 2
decades and this research is informing assessment and management. This text will
synthesize knowledge relevant to the clinical sciences underpinning neck pain disorders
and present a comprehensive approach to patient assessment and management, as well as
commentary on key issues for defining neck pain disorders and primary, secondary and
tertiary prevention. The approach is informed by our and others research and clinical
expertise and patient experiences. Clinical relevance and application are key themes.

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SECTION 2

Clinical Sciences
OUTLINE

Introduction
2 Nociception and Pain Perception
3 Movement and Posture in Neck Pain Disorders
4 Neural Tissue in Neck Pain Disorders
5 Neuromuscular Disturbances in Neck Pain Disorders
6 Sensorimotor Control Disturbances in Neck Pain Disorders
7 Psychological and Social Considerations in Neck Pain Disorders
Introduction
2 NOCICEPTION AND PAIN PERCEPTION 17
3 MOVEMENT AND POSTURE IN NECK PAIN DISORDERS 29
4 NEURAL TISSUE IN NECK PAIN DISORDERS 41
5 NEUROMUSCULAR DISTURBANCES IN NECK PAIN DISORDERS 51
6 SENSORIMOTOR CONTROL DISTURBANCES IN NECK PAIN
DISORDERS 71
7 PSYCHOLOGICAL AND SOCIAL CONSIDERATIONS IN NECK PAIN
DISORDERS 87

The chapters in this section present key clinical sciences in biopsychosocial domains
that underpin musculoskeletal practice to manage patients with neck pain disorders. The
neurosciences and clinical sciences that underlie symptoms commonly reported by
patients with neck pain disorders are discussed, as is the pathophysiology of the sensory,
articular, nervous, neuromuscular and sensorimotor systems. The basic and clinical
sciences provide the foundation for clinical practice. They provide the basis on which
clinicians can undertake informed clinical reasoning in the clinical assessment, diagnosis
and management of patients who will present with the infinite variety of neck pain
disorders.
2

Nociception and Pain Perception

Introduction
Pain, as currently defined by the International Association for the Study of Pain (IASP), is
“an unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described [by the patient] in terms of such damage”.1 This definition carries
within it several important points for the clinician. Firstly, pain is not always associated
with tissue injury or damage. As such, it should be realized that pain is distinct from
nociception; a physiological term, defined as “the neural process of encoding noxious
stimuli”.2 Nociception is commonly associated with pain, yet it is neither necessary nor
sufficient for the perception of pain. The second important point to be gained from the
definition is that pain is not a sensation that simply reflects the state of peripheral tissues.
Pain is, by definition, a multidimensional sensory and emotional experience; its unpleasant
nature always bringing with it negative affect, notably distress.3,4 This multidimensionality
is also the route through which psychological factors, stress and immune responses may
modulate and intensify a painful experience.
There are additional definitions that categorize pain by location (space), and some that
do so by chronology (time). Cervical spinal pain is defined by the IASP as “arising from
anywhere within the region bounded superiorly by the superior nuchal line, inferiorly by
an imaginary transverse line through the tip of the first thoracic spinous process, and
laterally by sagittal planes tangential to the lateral borders of the neck”.1 Cervical spinal
pain can be further categorized into upper versus lower cervical pain by subdividing the
region caudocephalically into two equal halves.1 In addition, pain perceived between the
superior nuchal line and an imaginary transverse line through the spinous process of the
second cervical vertebra is defined as suboccipital pain.1
Chronic pain is considered that which “persists beyond normal tissue healing time”;1 3
to 6 months is generally accepted as the period within which “normal tissue healing”
should have occurred and has therefore been used to define chronic pain,5 accepting its
limitations. Pain has an adaptive (useful), protective role in that it can alert an organism to
threatening circumstances, which could lead to real bodily harm if ignored. However,
when pain persists beyond such threatening circumstances for some people it may no
longer be adaptive or protective, instead becoming a source of poor quality of life, low
mood, reduced function and even shortened life.6,7
This chapter will briefly review the different mechanisms that can lead to a perception
of pain:8,9 nociceptive, neuropathic, inflammatory and central hypersensitivity. These
distinct pain mechanisms are clinically important for neck pain because they have
implications for management.

The nociceptive pathway: from noxious stimuli to pain

perception
The nociceptive pathway consists of four main processes: transduction, encoding,
conduction and transmission.10 Transduction is the process where a damaging or
potentially damaging noxious stimulus (mechanical, thermal, chemical or electrical) is
converted into electrical signals within specialized receptors of nerve endings that are
embedded in the stimulated tissues. Encoding is the process of signal formation that
contains information relevant to the nature and intensity of the stimulus. Consequences of
encoding may be autonomic (e.g., elevated blood pressure) or behavioural (motor
withdrawal reflex), however pain perception is not necessarily implied.1 Transmission is
the process whereby this encoded information is passed on from one nociceptive neuron to
another, via synapses, toward higher brain centres. Perception is the conscious experience
that follows the decoding of nociceptive information by higher brain centres.10 At every
stage along this nociceptive pathway, it is possible to interrupt, reduce or amplify the
passage of encoded information; this is known as modulation, and is exploited by many
therapeutic interventions.10
The high-threshold sensory neurons that respond to noxious stimuli are called
nociceptors. They encode and transmit sensory information from the periphery to the
central nervous system (CNS). Nociceptors include small-diameter, slow conducting,
predominantly unmyelinated neurons known as C fibres and thinly myelinated neurons
known as Aδ fibres.10,11 They terminate as free, unencapsulated peripheral nerve endings in
most tissues of the body including skin, muscles, joints and viscera and respond to various
different stimuli. When stimulated, C fibres act almost like a gland, releasing a range of
proinflammatory substances, such as prostaglandins, cytokines, bradykinin, from their
peripheral terminals into the surrounding tissues.10 These substances directly stimulate
nearby nociceptors, proliferating the effect.12 Simultaneously, nociceptor thresholds of
activation reduce, in a process known as peripheral sensitization, so that less stimulation
is needed to further activate the nociceptor receptors.13
The synaptic transmission of encoded signals is complex. The primary neurotransmitter
of nociceptors appears to be glutamate, but multiple other chemicals are also released.14
Nociceptors terminate in the dorsal horn of the spinal cord, predominantly within spinal
lamina I and outer lamina II.10,14 They pass their encoded signal on to relay nociceptive
neurons, and local interneurons that are important for signal modulation.14 This contrasts
to low-threshold Aβ fibres, which transmit innocuous touch signals and synapse onto
neurons primarily in lamina III.15 A loss of this separation is intrinsic to the phenomenon
of allodynia, in which pain is evoked as a result of innocuous stimuli such as light touch.16
The encoded signal can be modified within the dorsal horn. Local inhibitory and
excitatory interneurons, in addition to descending pathways, can modulate the
transmission of nociceptive signals.14 These might, for example, facilitate the prioritization
of pain perception over other competing demands, or block such perception if chances of
survival are increased by doing so.14 Second order neurons then transmit nociceptive
signals through ascending pathways in the spinal cord, to higher centres in the brain.10,13
The spinothalamic tract (also known as anterolateral system) transmits nociceptive signals
to nuclei within the thalamus where third order neurones then ascend to terminate in the
primary somatosensory cortex as well as other regions such as the cingulate cortex.10 This
pathway is particularly relevant for the localization of painful stimuli.10,13 In contrast, the
spinoreticular pathway is involved in the emotional aspects of pain.10,13 Here fibres reach
the brainstem reticular formation, before projecting to the thalamus and hypothalamus
with further projections then to the cortex. The spinomesencephalic tract terminates
primarily in the superior colliculus and the periaqueductal grey and is likely to be involved
in multisensory integration and in behavioural reactions and orientating to painful
stimuli.13
There are a number of brain regions activated during the experience of acute pain. They
are collectively referred to as the pain matrix, which includes the primary and secondary
somatosensory cortex, insular cortex, anterior cingulate cortex, prefrontal cortex and the
thalamus.10,13 This distributed cerebral activation likely reflects the multifaceted nature of
pain involving discriminative, affective, autonomic and motor components.13 The
perception of pain is then subjective and can be modified or affected by numerous
influences including distraction/attention and beliefs/attitudes.10,17
The brain is able to modulate nociceptive processing via descending pathways and
descending inhibitory connections project back to the spinal cord to decrease the activity
of nociceptive neurons thereby providing pain relief.18 The descending pain control system
includes the dorsolateral prefrontal cortex, periaqueductal grey, locus coeruleus of the
pons and the nucleus raphe magnus of the medulla oblongata. Studies have revealed a
correlation between the amount of pain relief reported and the extent of both activation
and functional connectivity between these regions.18–20 Descending pain inhibition is
largely facilitated through endogenous opioids;20,21 however, other neurotransmitters such
as cannabinoids and dopamine can contribute.12,18,19,22,23

Nociceptive pain
Damage or threatened damage to non-neural tissue, which results in activation of
nociceptors can lead to nociceptive pain.1 Many structures within the cervical region are
innervated by nociceptors and can therefore provide nociceptive input, including muscles,
zygapophysial joint capsules, intervertebral discs and ligaments.24 All too often a
“pathoanatomic” lesion cannot be demonstrated with imaging for people with neck pain,25
and it is often not possible to make a definitive pathoanatomic diagnosis, but that does not
negate the existence of a physical cause. Several cadaveric studies have demonstrated the
presence of subtle pathoanatomic lesions in cervical structures, which have so far evaded
detection by current imaging techniques.26,27 In the case of motor vehicle accidents and
whiplash trauma, there may be subtle lesions in the intervertebral discs and the
zygapophysial joints,25,28 with biomechanical studies confirming that even minor loads can
lead to lesions of the latter.29,30
 Zygapophysial joint capsules contain low-threshold mechanoreceptors, mechanically
sensitive nociceptors and silent nociceptors31,32 confirming them as a potential source of
ongoing nociceptive pain. Various studies have described the area of experienced pain
following noxious stimulation of individual cervical structures33–35 (Fig. 2.1). Notably, the
distribution of pain may become even larger when already symptomatic structures (e.g.,
zygapophysial joints) are stimulated.33
 (A) The patterns of referred pain reported in healthy volunteers following
stimulation of cervical zygapophysial joints by distending the joint capsule
with injections of contrast medium. (From Dwyer A, Aprill C, Bogduk N. Cervical
zygapophysial joint pain patterns I: a study in normal volunteers. Spine 1990;15:453–
457.)

(B) Representative examples of pain referral maps generated for the C5–
6 and C6–7 disc levels from patients undergoing cervical discography.
(From Slipman CW, Plastaras C, Patel R, et al. Provocative cervical discography symptom
mapping. Spine J 2005;5:381–388.)

FIG. 2.1

Controlled diagnostic blocks of the medial branches of cervical posterior primary rami
can be used to determine the prevalence of cervical zygapophysial joint pain in a given
population.36 Typically, a positive test is awarded when at least one-half of the pain is
reduced soon after the medial branch block. In one study,33 of 194 patients with chronic
neck pain lasting more than 6 months (with a total of 347 diagnostic blocks performed),
134 patients (69%) presented with at least one symptomatic level. A recent review
determined that the prevalence of zygapophysial joint pain varies from 36% to 67% with
C5/C6 the most common joint affected.37 In those involved in high-speed motor vehicle
accidents, the prevalence may be as high as 74%.38
Recent studies have also demonstrated that radio​frequency denervation, a technique that
reduces peripheral nociception from a zygapophysial joint by removing the sensory
innervation of the joint, leads to enhanced neck range of motion, decreased psychological
distress and reduced signs of central hyperexcitability in people with whiplash-associated
disorders,39,40 thus supporting the opinion that the zygapophysial joint is a continuing
source of neck pain for many with chronic neck pain.

Neuropathic pain
The IASP defines neuropathic pain as “pain caused by a lesion or disease of the
somatosensory nervous system”.1 Neuropathic pain can be further divided into central or
peripheral components. Central neuropathic pain is that “caused by a lesion or disease of
the central somatosensory nervous system” whereas peripheral neuropathic pain is
“caused by a lesion or disease of the peripheral somatosensory nervous system”.1 Nerve
compression, nerve trauma, infection and diabetes are all examples of conditions that may
lead to neuropathic pain, typically described by patients as burning, shooting and/or
pricking and prickling in nature.41,42 Neuropathic pain is attributed to an imbalance of
activity in pathways resulting from actual loss or a disturbance to the physiological inputs
caused by lesions in neurons.41 More specifically, disparities between excitatory and
inhibitory signalling, changes in ion channels and modification to the modulation of
nociception are mechanisms associated with neuropathic pain.41
Neuropathic pain may be associated with dysesthesia (defined as unpleasant abnormal
sensations), allodynia (which is the sensation of pain to non-noxious stimulation such as
light touch) and hyperalgesia (which is an increased response to a normal noxious
stimulus).42,43 Cold hyperalgesia in particular is a common feature of neuropathic pain
attributed to peripheral nerve injury.44,45 Aberrant temporal summation of pain and pain
continuing after stimulation has ceased are other regular features observed in people with
neuropathic pain.42
A neuropathic pain mechanism is commonly implied in cervical radiculopathy, although
it is likely that these patients present with a combination of both nociceptive and
neuropathic pain; that is, a mixed pain syndrome.46,47 Signs of neuropathic pain may be
present in some people following a whiplash trauma suggesting that there may be nerve
injury as part of their presentation. For instance, cold hyperalgesia has been observed in
people with moderate to severe pain following a whiplash injury and its presence is
associated with poor recovery.48 Moreover, loss of sensitivity or increased detection
thresholds (hypoesthesia) to vibration, electrical and thermal stimuli have been observed
in people following whiplash trauma49 as they are in patients with cervical
radiculopathy.47,50,51 In addition, studies have confirmed neural tissue mechanosensitivity
in patients with whiplash-associated disorders (WAD)52,53 which could be an indication
that nerve injury is a contributor to persistent symptoms seen in this condition. These
findings are supported by cadaveric investigations which have revealed nerve damage
(e.g., nerve roots and dorsal root ganglia) following motor vehicle accidents.27
Certain self-reported questionnaires can be used to help identify neuropathic pain. One
such questionnaire, the Self-Administered Leeds Assessment of Neuropathic Symptoms
and Signs (S-LANSS),54 was completed by people with acute pain following a whiplash
injury; around 20% were identified as having a likely neuropathic component.55 The
painDETECT questionnaire56 can also be used to facilitate the identification of
neuropathic pain, with convergent validity demonstrated with similar neuropathic pain
screening tools56 and to pain severity.57 Although this questionnaire has been commonly
applied to identify a neuropathic pain component in people with low-back and leg pain,58,59
it has been less frequently applied in neck pain populations. One study showed that 30%
of participants with cervical radiculopathy demonstrated the likely presence of
neuropathic pain as identified by the painDETECT questionnaire, whereas neuropathic
pain components were not identified in the enrolled participants with non-specific neck-
arm pain.47 The participants with cervical radiculopathy also displayed significant side-to-
side differences in mechanical and vibration detection in their maximal pain area, the
symptomatic side being less sensitive to the stimuli than the control side, consistent with
observations in patients with peripheral nerve injury.47 Approximately 50% of the
participants also presented with cold hyperalgesia, another common feature following
peripheral nerve injury.

Inflammatory pain
Inflammatory pain is facilitated by an abundance of substances released following tissue
damage in addition to the surge of inflammatory processes which follows. Inflammation
following tissue injury results from plasma extravasation and infiltration of immune cells
into the injured region including macrophages and neutrophils.60 These immune cells, in
addition to resident cells, release numerous inflammatory mediators including
prostaglandins, bradykinin, nerve growth factors, proinflammatory cytokines, interleukin-
1β and proinflammatory chemokines.60,61 Some of these inflammatory mediators will
directly activate and sensitize nociceptors, which changes their response characteristics14
and may activate “sleeping” or “silent” nociceptors, which do not usually respond to
noxious stimulation but can be woken as a result of chemical mediators related with tissue
damage.14,62,63 Inflammation-induced nociceptor hyperactivity can also facilitate the
release of neurotransmitters (e.g., glutamate) and neuromodulators (e.g., substance P)
leading to hyperactivity of postsynaptic nociceptive neurons which contributes to the
process of central sensitization.64,65 Some proinflammatory cytokines, including tumour
necrosis factor alpha (TNF-α) and interleukin-1β, have been implicated in the
development of chronic pathological pain and both proinflammatory cytokines and
chemokines can modulate the activity of both peripheral and central neurons.61
 C-reactive protein (CRP) is an acute-phase reactant released by hepatocytes and the
production of CRP may be regulated by proinflammatory cytokines including TNF-α and
interleukin-1β.66 Levels of CRP are typically elevated following traumatic injury, infection
and autoimmune disease, but have also been observed to increase in some conditions
including acute sciatica67 and whiplash.68,69 CRP typically peaks within 48 hours of injury
but usually falls rapidly, whereas persisting elevated levels of CRP is indicative of
ongoing inflammation.70,71
There has been little investigation of inflammatory biomarkers in people with neck pain
and this will likely become an area of future research. One study by Kivioja et al.69
showed the presence of an immune response within 3 days of a whiplash trauma as
evidenced by elevated TNF-α and interleukin-10-secreting blood mononuclear cells
however, this had resolved by 14 days. This finding suggests an initial but resolving
inflammatory response following whiplash injury. In another study, elevated CRP levels
were identified in people when measured 2 to 3 weeks after a whiplash trauma68
suggestive of ongoing inflammation of injured tissues. Interestingly, when tested 3 months
after the injury, CRP levels had returned to normal in those who considered themselves
recovered or only with mild disability whereas CRP remained elevated in those continuing
to experience moderate to severe pain and disability likely because of unresolved tissue
lesions.68

Peripheral and central sensitization

Sensitization is defined as “increased responsiveness of nociceptive neurons to their
normal input, and/or recruitment of a response to normally subthreshold inputs”;1 a
process that can include a drop in threshold and an increase in suprathreshold response. It
is important for the clinician to note that sensitization processes are physiological and
adaptive, selected via evolutionary processes to confer protection to the organism.
However, like many protective adaptations, sometimes the apparatus and processes
underlying the mechanism can malfunction leading to problems; specifically,
disproportional pain for somatosensory sensitivity.
Sensitization can occur after tissue injury or nerve damage and generally results in a
heightened perception of pain for a given stimulus. When the painful stimulus is noxious,
a heightened response is known as hyperalgesia; when the painful stimulus is innocuous,
the phenomenon is allodynia. Spontaneous discharges and spatial expansion of the
receptive field size also typically result.1 Moreover, these consequences can outlast the
stimulus considerably, almost like a “pain memory”; a process known as long-term
potentiation.10,13 As a result, spontaneous continuous pain, spontaneous intermittent pain
and abnormally evoked pain (e.g., by light touch or movement) may occur.72
Sensitization may develop both through central and peripheral mechanisms. Peripheral
sensitization is attributed to sensitization of the peripheral primary sensory neurons
located within the dorsal root ganglia and trigeminal ganglia and can be caused by a
number of mechanisms including inflammatory mediators (e.g., prostaglandins) and the
release of substances from damaged cells.42 In contrast, central sensitization comprises
increased excitability of central nociceptive neurons in the cortex, brain stem, trigeminal
nucleus and spinal cord.65 A number of mechanisms have been implicated in long-term
central sensitization, including cortical reorganization and maladaptive neuroplasticity,
alterations in neurochemistry, loss of inhibitory neurons, alerted glial activity, dysfunction
of endogenous pain control mechanisms, alterations in grey-matter volume and altered
structural integrity and connectivity of white matter.16,65,73
One of the first studies to demonstrate central sensitization and widespread
hypersensitivity in people with chronic WAD was performed by Koelbaek-Johansen
et al.74 In this study, hypertonic saline was injected into the tibialis anterior muscle of
healthy controls and people with chronic WAD, and the participants were asked to draw
their perceived pain on a body chart. Larger areas of referred pain were identified for the
patient group with both distal and proximal referred pain areas.74 Since then, a number of
studies have applied quantitative sensory testing (QST) to evaluate both peripheral and
central sensitization in people with neck pain disorders. QST involves the assessment of
responses to controlled and quantifiable physical stimuli, typically either pressure or
temperature. The pain threshold is commonly measured and is defined as the minimum
amount of stimulation required to evoke pain. For instance, in the case of the pressure pain
threshold, increasing amounts of pressure is applied at a standardized rate over a point
(e.g., over a muscle belly) using an algometer and the patient is instructed to push a button
as soon as the sensation changes from one of pressure to one of pain. Less commonly
assessed is the pain tolerance, which measures the maximum stimulation a person is
willing to bear. Temporal summation and conditioned pain modulation are also established
ways of quantifying sensitivity, measuring excitability of afferent nociceptive pathways
and evoked descending pain inhibition, respectively.75,76
Mechanical hyperalgesia locally over the neck region is often detected in people with
neck pain regardless of the aetiology of their pain.77–81 However, mechanical hyperalgesia
at remote sites (indicative of central sensitization) has been observed in people with WAD,
especially those with greater pain severity,77–79,82 or in some cases, people with non-
traumatic neck pain of greater severity.83 Thus this feature of widespread sensitivity to
mechanical stimuli is not usually present in people with milder symptoms or those with
neck pain of insidious onset.77,78 Sensitivity to both heat and cold stimuli has also been
seen in people with moderate to severe pain following a whiplash trauma and this has been
found both at local and remote sites48,51,78,84 with cold hyperalgesia having moderate
evidence as a prognostic indicator of poor recovery following a whiplash injury.48,85
Similar sensory disturbances have been shown in people with chronic cervical
radiculopathy presenting with higher pain and disability levels.47,51 However, sensitivity to
thermal stimuli was not demonstrated in people with neck pain of non-traumatic origin47,78
(Fig. 2.2). The nociceptive withdrawal reflex has been used to study the excitability of
spinal cord neurons with evidence that people with chronic WAD have significantly lower
thresholds compared with asymptomatic people, indicative of spinal cord
hyperexcitability.82,86 Recent systematic reviews have confirmed the presence of
sensitization as a common feature in WAD87 whereas it is not a characteristic feature of
chronic idiopathic and non-traumatic neck pain.88
 FIG. 2.2 Temperature pain thresholds measured over the cervical spine, deltoid and
tibialis anterior muscle in people with chronic whiplash associated disorders, chronic
idiopathic neck pain and healthy controls. Note the significant change in temperature
pain thresholds for the whiplash group only. (From Scott D, Jull G, Sterling M. Widespread
sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck
pain. Clin J Pain 2005;21:175–181.)

Studies have also examined hypoesthesia by evaluating detection thresholds for non-
painful stimuli and, consistent with thermal pain threshold testing, sensory hypoesthesia
was detected in people with chronic WAD49,77 whereas it was not a feature of chronic
idiopathic neck pain.77 The widespread and generalized nature of hypoesthesia seen in
people with WAD is again suggestive of central sensitization.

The influence of psychological factors

The pain literature over the last two decades, particularly relating to low-back pain, has
been dominated by the influence of psychological factors. The development of “yellow
flags” for psychological risk factors initially focused around chronicity and disability
related to low-back pain. However, it has gradually become apparent that the same risk
factors act across a wide variety of musculoskeletal pain conditions, including neck pain.
In addition, event-related distress can be a consequence following a whiplash injury.89,90
Psychological factors, such as anxiety and distress create very real, measurable activity
in the CNS. It is within this CNS activity that signals from the peripheral nervous system
converge and interact to produce the effects we see in patients. Indeed, psychological
factors (e.g., depression) that are known to increase the longevity of pain conditions
increase activity of similar brain regions known to be involved in the processing of pain
signals.91,92
Acute stressors activate the adrenomedullary hormonal system (AHS), hypothalamic-
pituitary-adrenocortical (HPA) axis and sympathetic nervous system (SNS), which can
induce transient stress-induced analgesia as part of the flight-or-fight response.93 These
processes also help to remember the stressful event in a process referred to as memory
consolidation.94 It is thought that an exaggerated stress response may actually lead to over
consolidation of memories contributing to the development of posttraumatic stress
disorder.95
There is accumulating evidence suggesting that the stress response may become
maladaptive and can contribute to ongoing pain and progression to chronicity.96,97
Moreover, activation of the stress systems can contribute to hyperalgesia and allodynia
after stressful events98 and in neck pain, in the case of a motor vehicle accident.48,99
Posttraumatic stress disorder has been detected in some people within just weeks of a
whiplash injury which can persist and contribute to greater perceived pain and disability
and poor recovery.85,90 In this case, the initial and ongoing stress response becomes
maladaptive and can facilitate the transition to chronicity.
Some evidence suggests that cortisol secretion may become dysfunctional in people
with chronic pain, and reduced cortisol levels have been observed in chronic WAD100 as
well as other chronic pain conditions such as low-back pain and fibromyalgia.101–104
Studies have also demonstrated altered activations of the HPA axis in response to
experimentally induced pain.97,105
There may be a genetic predisposition to stress-induced pain; genetic variations with the
capacity to influence responses of the stress system could explain the vulnerability of
some people developing ongoing pain following a stressful/traumatic event such as a
whiplash injury.98,106 The catechol O-methyltransferase (COMT) gene is one such example.
The COMT gene provides commands for producing the enzyme called COMT which
degrades catecholamines, including epinephrine, norepinephrine and dopamine.107 Studies
have shown that variants of the COMT gene are linked to greater sensitivity to
experimentally induced pain108,109 and chronic pain.108,110 A recent study evaluated the
association between neck pain intensity and the COMT genotype immediately following a
motor vehicle accident.107 Interestingly, those with a COMT pain vulnerable genotype had
more severe neck pain, headache and dizziness. Moreover, they estimated that a longer
time would be needed for both their physical and emotional recovery. Thus genetic
variations affecting the stress response have the capacity to influence both symptoms and
psychological status following a motor vehicle accident.107 No doubt future studies will
shed more light on these influences.

Psychosocial influences on pain perception

When a person experiences acute pain, it is highly likely that they will have some degree
of psychological distress. Chronic pain, by its very nature, can be associated with ongoing
psychological distress but also with other features including negative beliefs, fear and
depression. Psychological factors can have a powerful influence on pain perception and
can play a key role in the transition from acute to chronic pain for some people. The social
and environmental context, cultural background, socioeconomic status, attitudes,
expectations and beliefs can also have a powerful influence on pain perception and can
amplify peripheral sensations. As an example, when a patient receives a negative
diagnosis and/or prognosis, it can amplify their pain.111 Imaging studies have confirmed
that a negative expectation increases the activity of the prefrontal cortex, anterior cingulate
cortex and insula areas associated with pain processing and emotional regulation.112,113 As
a neck-specific example, poor expectations for recovery following a whiplash injury is
associated with poor recovery even when accounting for potential cofounders such as
initial pain and health status.114–116 Other work has shown that a negative treatment
experience can impede subsequent unrelated treatment effects.117
Anxiety and fear can also accentuate pain.118 People presenting with pain-related
anxiety and fear report greater attention to pain sensations and predict that they will
experience a greater amount of pain during a physical assessment.119 Fear can contribute to
behavioural avoidance, inactivity, disability, and an increased focus on pain avoidance as
described by the fear avoidance model.120 Another relevant feature for some patients is
pain catastrophizing, which is an exaggerated focus on the pain experience in addition to
negatively evaluating the ability to deal with pain.17 Pain catastrophizing has been
identified as a prognostic factor for poor outcome following a whiplash injury121,122 and
people who catastrophize present with greater disability, higher pain medication use and
higher rates of health care usage.17
Depression has been consistently associated with chronic pain92 and is associated with
decreased pain thresholds and pain tolerance levels, reduced activity and passive coping
strategies (e.g., withdrawing from activities).114,123,124 The use of passive versus active
coping strategies (e.g., exercising) is associated with poor recovery following a whiplash
injury especially in those also presenting with depressed mood.123 Depression may also be
associated with larger pain areas. For instance, in a study that examined factors associated
with larger pain extent in people with chronic WAD, we found that when accounting for
age, sex, education, insurance status, financial status and neck pain intensity, pain extent
remained associated with depression and self-efficacy.125 That is, people with depressed
mood presented with more widespread pain. Interestingly, this was not the case in a cohort
with cervical radiculopathy.126
Lower socioeconomic status is associated with greater symptom severity127 and in both
whiplash-induced neck pain as well as cervical radiculopathy, lower socioeconomic status
is associated with larger pain extent.125,126 Social factors including poor social support, low
job control, low skill discretion and job dissatisfaction are all identified risk factors for
higher levels of neck pain.128,129 Moreover, the interactions between job demands, decision
authority and supervisor support are linked to higher perceived pain and disability in
office workers.130 As an example, if an employer remains in regular communication with
employees off work with back pain, then the employees take less time off work and are
more positive about recovering.131 Likely, this would hold true also for neck pain. Support
from family and friends is also highly relevant. For instance, measures of sensitivity as
well as pain intensity scores are lower when taken in the presence of the family and
friends versus when the patient is alone.132 Thus both psychological and social factors can
influence pain perception and can modify both the severity and distribution of pain and
can modify patient behaviour. These factors can be relevant for the transition to chronicity
and maintenance of a chronic pain disorder.

Conclusion
The experience of pain is not a direct representation of the state of peripheral tissues, but
rather is shaped by the context in which it is experienced. People with neck pain will
present with different underlying pain mechanisms, which can be nociceptive,
neuropathic, sensitization and inflammatory, with often multiple mechanisms at play.
Regardless of the mechanisms, the severity and impact of symptoms can be modified by
various psychological and social factors. It is important to understand and, when possible,
identify these processes because they have relevant effects on response to different
interventions and can imply the need for different management approaches.

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3

Movement and Posture in Neck Pain

Disorders
The cervical spine is an intriguing and complex structure. Both sophisticated mobility and
stability are demanded concurrently; mobility to subserve vision and hearing, stability to
support the weight of the head and in large part, the load of the upper limbs. The cervical
spine is also an important sensory organ. It provides knowledge of head position in
relation to the body and makes an important contribution to balance and coordination of
eye and head movement. This chapter overviews posture and movement of the cervical
region, as well as the interactions with adjacent regions in the healthy state. Impairments
in posture and movement in neck pain disorders are then explored to inform clinical
reasoning in patient assessment. Control of posture and movement and impairments in
neuromuscular and sensorimotor control in neck pain disorders are discussed in Chapters
5 and 6.

Cervical posture
A common aim of rehabilitation of people with neck pain is to train patients to function in
an upright neutral posture, based on the premise that neck pain is often associated with
prolonged postures, which expose the cervical spine to excessive mechanical load at or
near end ranges (e.g., a forward head posture). A neutral cervical posture is one where
load is distributed evenly through the anterior (vertebral bodies and discs) and posterior
(articular processes and facet joints) elements of the cervical segments,1,2 the joints are in a
mid-position and there is minimal muscle activity to support the position. The shape of the
“ideal” cervical lordosis permits optimal sharing of loads between anterior and posterior
elements. In contrast, a flattened cervical lordosis increases compressive forces on anterior
vertebral elements and tensile forces on posterior vertebral elements. An increased
lordosis increases compressive forces on the posterior elements and tensile forces on the
anterior vertebral elements.3 Altered load distribution may irritate pain-sensitive
structures. Certain sitting postures (e.g., a slumped posture) place motion segments
towards the limit of their range with potential for adverse load.4
The position of the head and the angle of the cervical lordosis at any moment in time is
largely dependent on the orientation of the cervicothoracic junction and head orientation
for vision. The cervical spine has a strong biomechanical relationship with the thorax and
the lumbopelvic region.5 The sagittal orientation of the cervicothoracic junction largely
dictates the angle of the cervical lordosis.6,7 Because the angle of the thoracic kyphosis
changes with age, the shape of the cervical lordosis changes.8 Thus the orientation of the
thoracic spine, combined with the need to maintain forward vision, potentially dictates the
loading mechanisms of the cervical spine.

Movement of the cervical spine

From a movement perspective, the functional cervical spine extends from the occiput to
the upper thoracic region. There are three functional divisions; the craniocervical (C0–2),
cervical (C2–7) and cervicothoracic regions. C2–3 and C7–T1 are transitional
segments.9,10 The craniocervical and cervical regions have distinct motion characteristics.
Motion of these areas is independent or interdependent depending on the task. There is
also an intimate relationship between cervical movement and function of the thorax, the
upper limbs and the craniomandibular region.

Movements of the craniocervical region

The craniocervical region comprises the atlanto–occipital and atlanto–axial articulations.
The craniocervical segments overall provide approximately one-third of the flexion and
extension excursion of the head and one-half of the axial rotation of the cervical region.11
The shape of the atlanto–occipital (C0–1) articulation permits a generous range of motion
in the sagittal plane, but minimal motion in lateral flexion and axial rotation because of the
steepness of the lateral walls of the atlas sockets and the tension of the joint capsules.12
The atlanto–axial (C1–2) articulation consists of four joints: two biconvex joints laterally
and two joints medially, between the odontoid process and the ring of the atlas and the
transverse ligament. C1–2 can be regarded as a pivot joint. It permits a large excursion of
axial rotation, and some flexion and extension. This freedom of head motion facilitates
great visual excursion. With this mobility, specific craniocervical ligaments, such as the
alar and transverse ligaments as well as the tectorial membrane, enhance the stability of
the region.11,13,14
Movements at the C0–1 and C1–2 segments are coupled, such that rotation is
accompanied by contralateral lateral flexion at each segment.15–17 Any coupled flexion-
extension motion with these movements is negligible.15 Translational movements occur
with the angular movements in the craniocervical joints, but likewise, the excursions are
minimal.11
Functionally, nodding and shaking the head in the act of saying yes and no are
predominantly craniocervical motion. Of clinical interest, C1–2 axial rotation can be
accurately localized from axial rotation of the cervical region by fully flexing the cervical
region before performing head rotation,18 the basis for the flexion-rotation test (Fig. 3.1).19
 FIG. 3.1 The Flexion Rotation Test (C1-2). The test localizes axial rotation to
predominantly the atlanto–axial joints. (A) The patient is asked to lift their head to look
at their feet to assist the clinician to gain full cervical flexion. (B) The head is rotated to
encounter a solid end feel. Cut-off values for the test are less than 30-degrees head
rotation or an asymmetry between sides of more than10 degrees.105

Movements of the cervical region (C2–7)

The movements of the C2–7 segments reflect some of the unique features of the cervical
motion segment. The adult cervical motion segment is characterized by the formation and
presence of uncovertebral joints and the transverse fissure dividing the posterior aspect of
the intervertebral disc.20,21 Fissuring of the disc is a normal response to the formation of
the uncinate processes and the repeated translational and torsional strain imposed by large
excursions of cervical movement. By the age of 40 years, adjacent vertebral bodies are
bound together only by the anterior annulus and the two longitudinal ligaments.20
Movements in the C2–7 cervical segments are guided by the orientation of the facet
joints and uncinate processes. Flexion and extension at each segment consist of an angular
and a translational displacement. The angular excursion is highest in the middle segments
(largest at C5–6) and least at C2–3 and C7–T1. Accompanying translational displacements
are highest at C2–3 and progressively decline down the spine.22 Translational
displacements are small. An in vivo study using kinetic magnetic resonance imaging
(MRI) documented 0.85 ± 1.22 mm translation at C2–3, declining to 0.16 ± 0.86 mm at
C6–7.22 All segments contribute to axial rotation with the middle segments (C3–C6)
making the greatest contribution.16,17 Likewise, all segments contribute to lateral flexion,
with a progressively increasing contribution from C2–3 to C6–7.15 However, rotation and
lateral flexion are separated artificially because in vivo, there is a strong ipsilateral
coupling of these movements.15,16,22 The exception is the transitional C2–3 segment, where
contralateral coupling is frequent.23 When rotation is performed, it is associated with
extension at the C2–5 levels, and flexion at the C5–7 segments.16,17

Movements of the cervicothoracic region (C7-T4)

The cervicothoracic region acts functionally with the cervical spine,24 although it is far
stiffer compared with adjacent cervical segments.10 This reflects the presence of the ribs
and their attachments to the manubrium. Motion in this region, although lesser ranges, has
the same characteristics as cervical segments. Coupling of axial rotation and lateral flexion
is usually ipsilateral.25,26 Upper thoracic motion occurs with head excursions in all
directions in the magnitudes of roughly 10 degrees for each of flexion and extension, 8
degrees for axial rotation and 5 degrees for lateral flexion in each direction.24,27 From a
clinical viewpoint, this means that full head excursions cannot occur without a
contribution from the cervicothoracic region (Fig. 3.2).

FIG. 3.2 Full head rotation is a sum of movement at the craniocervical, cervical and
cervicothoracic regions. In the person depicted, the reduced excursion of motion is
mainly emanating from the lower cervical and cervicothoracic regions.

Integrated segmental motion

An intriguing aspect of coupled axial rotation and lateral flexion in the cervical spine is its
contralateral nature in the craniocervical segments and ipsilateral nature in the cervical
segments. This is a good example of the integrated nature of segmental motion. Opposite
coupling between the two regions allows the head to maintain vertical alignment during
axial rotation.28
Radiological studies have been undertaken to analyze the dynamics (movement
amplitude and timing) of individual cervical motion segments during active cervical
movements in each plane.12 Some basic patterns emerge. Flexion may be initiated and
terminated predominantly in lower cervical segments (C4–7), with middle cervical (C2–4)
and craniocervical (C0–2) segments contributing mostly during the middle phase of
motion. The C0–2 segments tend to move towards extension at end range flexion because
of passive insufficiency of the nuchal ligament. Clinically, this means that the examination
of flexion should be undertaken separately for the craniocervical segments because their
capacity for flexion will not be adequately examined during flexion of the entire neck
(Fig. 3.3 A and B). A similar pattern of motion is observed during extension although C0–
2 reaches its maximum extension during the final phase of movement.29,30 Segmental
contributions can vary through range. Some display greatest motion during a movement
rather than at the end range, emphasizing the flaws of analyzing movement at the end of
range only.29 Likewise, when the segments move depends on the movement task. If the
task is a nodding movement of the head, movement will be initiated and mainly confined
to the craniocervical segments. Protraction/retraction movements result in another pattern.
Protraction places the lower segments near their end range of flexion and the upper levels
in progressively greater extension, replicating the orientation of the neck in a forward head
posture. Retraction positions the lower segments in a mid-extension range with each
superior level demonstrating more flexion, with C0–1 and C1–2 achieving full flexion.31
These variations have underpinned the clinical practice of examining different movement
tasks and movement sequences as in, for example, combined movement examination
protocols32,33 and may in part explain differences in symptomatic responses.

FIG. 3.3 (A) The examination of cervical flexion (cervical and cervicothoracic) is
undertaken with the craniocervical region remaining relaxed. If the craniocervical
region is flexed, insufficiency in the ligamentum nuchae prevents full flexion of the
cervical and cervicothoracic regions. (B) Craniocervical flexion is assessed with the
cervical region in a more neutral position.
Relationships to adjacent regions
The cervical region has functional relationships with the upper limbs and
craniomandibular region in postures and movement.

The cervical spine and upper limb

The shoulder girdle and upper limb have a close relationship to the cervical region via the
axioscapular muscles, which suspend the scapula, clavicle and upper limb. This important
relationship in function and dysfunction is discussed in Chapter 5. Although we often
think in terms of loads transmitted to the cervical spine as a result of upper limb
function,34 here the focus is on spinal movement associated with upper limb function.
The thoracic spine moves during arm elevation.35–38 To achieve full arm elevation
bilaterally requires around 10 degrees of thoracic extension. All thoracic segments move,
although the segmental contribution is more in the mid-lower thoracic region than the
cervicothoracic region (T1–6). There is a strong correlation between the angle of thoracic
kyphosis and arm elevation.37 Not surprisingly, the presence of a slumped posture will
prevent full shoulder elevation.38 Single arm elevation also induces movement in the
thoracic region. Extension again occurs, but in the upper thoracic region (T1–6), the
movement is predominantly rotation, coupled with lateral flexion. The coupling is usually
ipsilateral, but there is variability.39,40 These are important relationships to consider in
assessment and management from both neck and shoulder perspectives (Fig. 3.4).
 FIG. 3.4 Movement in the cervicothoracic region is necessary to achieve full arm
elevation. Arm movement can be used to assess cervicothoracic movement. The
patient performs single arm elevation while the clinician palpates for displacement of
the thoracic spinous processes at each thoracic segment (C7–T1 to T3–4 or T4–5).
This examination technique can be used as a treatment technique. In treatment, the
clinician performs a passive transverse glide through the spinous process of the
hypomobile thoracic segments to augment the rotation occurring as the patient
performs single arm elevation.

The cervical segments also move with arm abduction under light load.41 Although
passive abduction essentially elicits no movement of cervical segments, it has been shown
that the addition of a 2-kg resistance at the 0-degrees position and at each of four
abduction angles between 30 to 120 degrees, induced cervical segmental rotation at each
cervical segment (C1–T1) (Fig. 3.5). Displacement of C6 was greatest and most marked at
the lower angles of right arm abduction, notably ranges where most functional activities
might take place. Rotation of most segments was to the left, which could reflect the angle
of muscle pull. This segmental movement, which is a normal occurrence with load, is a
likely mechanism by which the cervical spine absorbs and distributes the load of upper
limb function.
 FIG. 3.5 The motion induced in each cervical segmental with right shoulder abduction
under a 2-kg load assessed by magnetic resonance imaging. ABD, Abduction. (From
Takasaki H, Hall T, Kaneko S, et al. Cervical segmental motion induced by shoulder abduction assessed by
magnetic resonance imaging. Spine 2009;34:E122–126.)

The cervical spine and the craniomandibular region

The craniomandibular complex is in close anatomical relationship with the cervical spine,
and from a neurophysiological perspective, both regions in common, access the
trigeminocervical nucleus. With these close anatomical and neurophysiological links,
some interdependent relationships can be expected, such as an overlap in pain
distributions. From a movement and posture perspective, the orientation of the mandible
can be influenced by head and neck posture.42 For example, the mandible pursues a more
posterior path of opening in a forward head postural position.42 The neck and the mandible
also exhibit coordinated movement with wide opening and closing of the mouth. These
movements are associated with craniocervical extension and flexion respectively.43,44 Full
extension of the cervical spine is dependent on mouth opening, particularly in the presence
of reduced extensibility of the hyoid muscles. Coexistent osseous changes have been
found in the temporomandibular joint and upper cervical joints. Sonnesen et al.45 contend
that these coexisting changes might either reflect a biomechanical relationship or at least a
shared general disposition between the upper cervical spine and temporomandibular joint
for degenerative osseous changes. In line with this contention, intraarticular interventions
for temporomandibular joint osteoarthritis have been shown to improve neck pain and
range of movement.46
There is a popular belief that head and neck posture is often related to
temporomandibular joint dysfunction and pain, yet the evidence is inconclusive.47
Historically, studies have been at odds in their findings and the situation continues.
Current studies range from finding no relationship between head and neck posture and
temporomandibular pain disorders, to others claiming close links between changes in
craniocervical postures and disc displacement in the temporomandibular joint.48–51 At this
time, clinicians cannot automatically presume or dismiss a relationship. Each patient must
be examined individually to determine the presence or not of any relationship between
cervical posture and their presenting craniomandibular disorder.

Cervical posture and neck pain disorders

There has been a long-standing interest in the relationship between cervical posture and
neck pain. In particular, most interest has been in the forward head posture because it
places joints more towards their end of range.4
The head assumes a more forward posture as a factor of age.52,53 Not surprisingly, and
historically, there have been disparate findings regarding the relationship between the
static forward head posture and the presence or magnitude of neck pain. This is apparent
when the measurements of the cervical lordosis are made either radiographically53–55 or
measured using external landmarks and measurement techniques.56–60 Quite simply,
whereas some studies find that neck pain is associated with a forward head posture, others
do not. This probably reflects large individual variations in spinal and even segmental
curvatures55 as well as age effects, which challenge interpretations of clinical significance.
There is some evidence that the posture of the cervicothoracic region might better predict
neck pain than the forward head position.57 A traditional interpretation that a flattened
cervical curve on x-ray is associated with neck pain is also questionable because a
flattened cervical curve occurs with similar frequency in asymptomatic populations.55,61 It
is possible that the cervical curve on x-ray might need to be kyphotic rather than flattened
to be of any clinical significance.55,61 Once more, clinicians cannot automatically presume
or dismiss a relationship between the static forward head position and neck pain, and any
relationship must be decided on an individual patient basis.
External measurements of posture or the radiological measure of lordosis in the static
upright posture might not be the critical measure. The posture adopted by the patient in
function may be more relevant. This was illustrated in studies showing that measurements
of the static posture at the start of a computer task did not differ between neck pain and
control groups, but persons with neck pain drifted into a more forward head posture as
they worked on the computer.62,63 In addition to changes in posture, increases occur in
cervical flexor and extensor muscle activity in persons with neck pain during such tasks,
which can increase load on cervical structures.64–66 Cervical extensor activity is 40%
higher in the slouched posture.67 The current high use of smartphones and tablets by the
very young to the elderly has escalated the adoption of prolonged head flexion postures.
Note that the mechanical demand on extensor muscles increases 3 to 5 times with the head
flexed using a tablet versus sitting in a neutral posture.68 Thus the functional posture
adopted by the patient during work may be of greatest importance. Importantly, a poor
habitual posture is modifiable by rehabilitation. It is more difficult to change a static
postural shape.

Cervical movement disturbances in neck pain

disorders
Movement disturbances are pathognomonic of cervical musculoskeletal disorders. The
disturbances present in several ways, ranging from changes in the nature and extent of
neck motion at the segmental and regional levels to how movement is performed and
controlled.

Range of motion
Loss of cervical motion is characteristic of both mechanical neck pain and pain of
traumatic origin (e.g., whiplash associated disorders) and distinguishes between healthy
persons and those with cervical disorders.69 Both primary plane movements and associated
conjunct motions are reduced.70,71 In accord, segmental movement is usually reduced.72
Several processes might underlie the loss of cervical motion including; changes in
articular or other soft tissues as a result of injury; the degenerative or ageing process; local
segmental or regional muscle spasm as a response to pain; increased muscle activity as
part of a change in neuromuscular or sensorimotor control associated with a neck pain
disorder; and possibly fear of movement.
It is often difficult to identify an injury or relevant pathology with current imaging
methods and guidelines. Yet lesions and pathological changes do occur in both the cervical
discs and zygapophysial joints and the pathophysiological processes together with
attendant nociception can be responsible for the abnormal motion in the acute or chronic
states.73–79 Structural changes as a result of injury or disease will affect motion but the
nature of abnormal segmental motion may vary depending on the type or stage of the
disorder. For example, capsular and joint changes associated with osteoarthritis of the
zygapophysial joints restrict motion, whereas in early to moderate stages of disc
degeneration, translatory motion increases slightly before it declines in advanced disc
degeneration.80
The craniocervical region has the potential for instability as a result of trauma (e.g.,
whiplash, sports injury), inflammatory arthropathies as rheumatoid arthritis81 or a genetic
disorder such as Down syndrome. Loss of transverse ligament integrity permits anterior
and posterior migration of the atlas from the dens during sagittal plane motion. A loss of
alar ligament integrity influences stability of both C0–1 and C1–2 motion segments in
multiple motion planes, but especially rotary stability.82 The challenge is to identify
ligament injuries. Debate continues about the relevance of MRI signal changes of alar and
transverse ligaments to a whiplash induced lesion and symptoms83,84 and the value of
clinical tests is uncertain.85 Another example of excessive abnormal movement in the
craniocervical complex is manifest in the neck tongue syndrome, which is a relatively rare
presentation, more common in children or adolescents. In this condition, the excessive
movement is associated with a temporary, abnormal subluxation of C1–2 with sudden
turning of the head which impinges the C2 ventral ramus against bone, producing the neck
and tongue symptoms.86 At the other extreme, and again more common in children, is
atlanto–axial rotatory fixation, presenting as an acute wry neck.87
 One of the major causes of restricted segmental and regional motion is muscle spasm as
a reaction to pain or pathology. The muscle spasm may be “regional” as seen in an acute
wry neck or in cases of severe pain. More frequently, the muscle spasm is more
“segmental” and clinicians are very familiar with the “hardness” perceived when palpating
over symptomatic cervical zygapophysial joints. Increased muscle activity as feature of a
change in neuromuscular control associated with a neck pain disorder may also limit
motion. This might occur when there is excessive co-contraction of the cervical flexors
and extensors65 or when muscles display a loss of direction specificity.88

Movement performance
Historically in manipulative therapy practice, interest in movement has been largely
around range of movement and pain response. In recent years, more attention is being
given to what might be called movement performance. These movement or kinematic
disturbances are explored fully in Chapter 6. Poor movement performance is an expression
of altered sensorimotor function.89,90 It is included here to encourage expansion in
observations and interpretation of the movement examination. Poor movement
performance points to the need for other specific tests (e.g., proprioception).
Reduced acceleration and velocity of neck movement are commonly documented in the
presence of neck pain.70,89,91,92 It is proposed that reduced velocity is an impairment of
greater consequence functionally than some loss of range of movement. Picture the rapid
head movement required to check that it is safe to change lanes while driving.
Furthermore, altered neck movement velocity, more so than range of motion, appears to be
a particularly sensitive and specific measure of neck pain.91 Variability in acceleration,
commonly termed reduced smoothness of movement has also been found during cervical
rotation in individuals with neck pain.70,89,91 Other movement disturbances include
unsteady or irregular head movements in prescribed tasks.93–95
Disturbances are also apparent in more general activities, not only in specific neck
movements. For example, abnormal helical axes (instantaneous axes of motion) have been
observed when patients perform functional tasks with their upper limbs.96 It has also been
observed that people with chronic neck pain walk with reduced trunk rotation.97
Consideration of the elements of movement performance is a necessary part of the clinical
examination of the neck pain patient.

Psychological considerations
Range and performance of movement may be restricted by unhelpful beliefs such as fear
of movement,98,99 although there are often many interacting factors.100 It is understandable
that a person in acute pain may be guarding their neck and be reluctant to move because it
hurts. As witnessed in the clinic as well as in clinical trials, this guarding in many cases
resolves as pain subsides and range of movement returns. This is observed in both acute
and chronic pain states.101,102 Nevertheless a fear of movement (kinesiophobia) with the
belief that pain is harmful and threatening is counterproductive to recovery.103 The effect
of psychosocial features is considered further in Chapter 7. However, characteristics such
as kinesiophobia reinforce the need to consider patients in both biological and
psychological contexts so all features contributing to abnormal movement are considered
in developing a multimodal management program.
Nevertheless, presumptions should not be made that kinesiophobia is an automatic
occurrence. A study of factors associated with movement performance and sensorimotor
features in patients with neck pain determined that range and velocity of motion were not
related to fear of motion but rather to visual disturbances, pain and balance.90 In another
recent study which examined factors associated with reduced range of active neck
movements in persons with chronic whiplash associated disorders (n = 216), only age and
measures of perceived pain and disability correlated with range of motion, whereas fear of
movement, pain catastrophizing, anxiety and depression were not related to reduced
motion.104

Conclusion
Posture, especially work postures or postures adopted when using various electronic
devices or during other recreational activities, can overload cervical structures and
contribute or precipitate a pain state. Movement is a critical function of the
multisegmented cervical region. Both the range and how movement is performed and
controlled can be affected by pain, injury, degenerative disease and ageing. Understanding
the complexities of posture and movement from the segmental to the regional level in the
healthy and pain states forms the basis for a relevant examination of the patient with a
cervical disorder to inform diagnosis and management.

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75. Farrell S, Osmotherly P, Cornwall J, et al. Morphology of cervical spine
meniscoids in individuals with chronic whiplash-associated disorder: a case-
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76. Farrell S, Osmotherly P, Cornwall J, et al. Cervical spine meniscoids: an update on
their morphological characteristics and potential clinical significance. Eur Spine
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77. Manchikanti L, Cash K, Pampati V, et al. Two-year follow-up results of
fluoroscopic cervical epidural injections in chronic axial or discogenic neck pain:
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78. Russo V, Duits A, Dhawan R, et al. Joint arthropathy at the cranio-vertebral
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79. Taylor J. The Cervical Spine. An atlas of normal anatomy and the morbid anatomy
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between the grade of disc degeneration and motion unit of the cervical spine.
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method for deficits of movement control in the cervical spine: reliability and
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96. Grip H, Sundelin G, Gerdle B, et al. Cervical helical axis characteristics and its
center of rotation during active head and upper arm movements-comparisons of
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97. Falla D, Gizzi L, Parsa H, et al. People with chronic neck pain walk with a stiffer
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intensity, neck disability or with fear of motion? Man Ther. 2014;19:252–258.
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4

Neural Tissue in Neck Pain Disorders

Neck pain disorders may include injury to, or pathology of, neural structures. Identifying
involvement of these tissues is essential because it may signal the need for a change in
management strategy, and in more serious cases, a potential safety concern for the patient
requiring immediate medical referral. This chapter discusses the potential mechanisms
underlying the direct involvement of nerve tissue in neck pain disorders, their clinical
manifestations and common conditions.

Nerve injury and neck pain disorders

Specific structural characteristics and pathologies of the cervical spine and upper limb
may render the spinal cord and peripheral nerves susceptible to injury. The term
neuropathy describes abnormal states of the peripheral nerves that may involve numerous
pathological and functional changes in the nervous system. Myelopathy is the relevant
term for similar states of the spinal cord and these terms will be used in this chapter.
Neuropathy may be a manifestation of many health-related or hereditary disorders such
as chronic alcoholism, multiple sclerosis, diabetes mellitus,1 cancer (e.g., Pancoast
tumour),2 metabolic disturbances and nutritional deficits.3,4 Such conditions may result in
polyneuropathies presenting as muscle weakness, atrophy and sensory deficits, but they
may also present in less severe forms mimicking features commonly related to
musculoskeletal conditions. Although it is beyond the scope of this chapter to describe
such conditions in detail, clinicians should be aware of their potential presentation (refer
to Azhary et al.1 for a discussion on differential diagnosis). The focus of this chapter is on
conditions involving neural tissue associated with musculoskeletal conditions of the
cervical spine.

Pathophysiological mechanisms of nerve injury—the

basis for clinical presentation and examination
procedures
This section considers the pathophysiological basis of neuropathy and myelopathy related
to neck pain disorders and the subsequent clinical presentations. Some clinical
presentations have relatively clear indications of nerve involvement, yet others may be
difficult to differentially diagnose. An understanding of pathophysiological processes and
subsequent clinical manifestation may assist the clinical reasoning process. Specific
details regarding examination procedures of nerve tissue are discussed in Chapter 9.
Pathophysiological mechanisms of neuropathy in
neck pain disorders
Neuropathy of variable severity may be secondary to injury or pathology of interfacing
musculoskeletal structures. It may be associated with perineural inflammation and/or
nerve entrapment and compression. Alternately, neuropathy may also arise from direct
trauma to the nerve.

Musculoskeletal injury and perineural inflammation

Injury or pathology of musculoskeletal structures that interface nerves may result in the
release of inflammatory mediators and the development of perineural inflammation. For
example, the release of inflammatory mediators is a feature of cervical disc lesions and is
thought to contribute to the development of cervical radiculopathy.5–7 Animal studies have
shown that perineural inflammation along a nerve trunk can induce pain in the organ
innervated by the nerve8–11 within a few hours of nerve exposure.9,12,13 Nerve-related pain
can result from the presence of chronic mild inflammation even without evidence of nerve
damage, or from a more severe inflammatory process that does result in nerve
damage.11,13,14 Perineural inflammation may induce spontaneous neurophysiological
activity and mechanosensitivity in the affected nerve.15–18

Nerve entrapment and compression

Nerves may be directly entrapped in the cervical spine (e.g., cervical myelopathy, cervical
radiculopathy),19,20 or neck pain disorders may be associated with nerve entrapment in the
upper limb (e.g., cubital tunnel syndrome,21 carpal tunnel syndrome22) in a double crush
scenario.23,24 Degenerative or injured musculoskeletal interfaces within the spine and
periphery may reduce the space containing the nerve, resulting in nerve compression that
may affect nerve tissue both local and remote to the site of compression.
Local compression of peripheral nerves has been shown in animal studies to impair
neural circulation. This may result in: intraneural ischaemia, disturbance of the blood-
nerve-barrier, neuroinflammation and intraneural oedema,25–29 Schwann cell reaction and
demyelination30 and changes in nodal structure.31 Furthermore, there may be reduced
thresholds for firing and ectopic impulse generation from nociceptive fibres and nerve
fibres that have become mechanosensitive.32–35 Nerve compression may affect both
myelinated and unmyelinated fibres.31,36 Animal studies show that even mild compression
can cause degeneration of small diameter axons and demyelination of larger diameter
fibres.36
Changes have also been observed remotely following peripheral nerve injury with the
release of inflammatory mediators36–38 and ectopic activity36,39 of the dorsal root ganglion.
With the close proximity of cell bodies from different peripheral nerves within the dorsal
root ganglion, adjacent intact neurones may also be affected by the neuroinflammatory
process within the dorsal root ganglion, which may alter their firing threshold.40 These
changes in the dorsal root ganglion, together with reported changes within the spinal
cord41 and brain,42,43 are proposed to explain a patient’s spread of symptoms, which are
sometimes well beyond the normal distribution of the injured peripheral nerve.40 For
detailed information regarding pathophysiological processes underlying nerve
compression and the association with neuropathic pain, the reader is directed to very
comprehensive reviews on this topic by Schmid et al.40,44
Injury to a peripheral nerve may occur at more than one site. The term double crush
syndrome was used to explain how injury at one site of a nerve made that nerve more
susceptible to injury at another location.23 In the upper limb, this association has been
often drawn between carpal tunnel syndrome and cervical radiculopathy.45,46 It was
reasoned that compression at one location on a nerve’s axon would predispose that same
axon to injury elsewhere because of disrupted bidirectional transport of essential nutrients
along the axon. The nerve would then be prone to undergoing morphological and
functional changes.23 Although this mechanism has been supported,47 there is still
speculation as to other potential mechanisms underlying the double crush syndrome.48 It
has also been suggested that the term double crush syndrome be replaced with the term
multifocal neuropathy to reflect that nerve injury may occur at more than two sites and can
occur because of stretch and not just compression.24 The term also incorporates the
potential impact that systemic conditions such as diabetes may have on the clinical
sequelae.24

Traumatic nerve injury

Nerve trauma may be catastrophic (such as cervical spinal cord injury), or less severe
(such as brachial neuropraxia). Brachial neuropraxia (stinger) describes a transient episode
of neural symptoms (shooting, electric pain or paraesthesia) and weakness49 in an upper
extremity following a significant blow to the head and/or shoulder, which commonly
occurs in contact sports.50,51 It is thought to mostly reflect a cervical extension-
compression injury,52 usually involving the C5 to C6 nerve roots or the upper trunk of the
brachial plexus.50,53 Brachial neuropraxia may occur recurrently.54
Stretch-induced neuropathies range from a single traumatic tensile strain to the brachial
plexus (e.g., abrupt stop in a bus when the person is standing and holding a handle) to
severe conditions such as a brachial plexus avulsion in a motor bike accident. Prolonged
tensile strain may result in stretch-induced neuropathy such as that reported during
surgical procedures involving sustained upper limb elevation.55,56 Animal studies have
shown that prolonged stretch to a nerve will impair blood flow,57 axonal transport47 and
conduction.58 Nerve injury may also occur during surgical procedures, such as accessory
nerve injury during neck dissection surgery for head and neck cancer with resultant effects
on trapezius function.59 Similarly, trauma to the long thoracic nerve and associated palsy
of the serratus anterior muscle is well documented and may have significant implications
for shoulder girdle function and recovery.60

Clinical manifestations of neuropathy and relationship

to examination findings
The consequences of injury to a nerve and the resultant clinical manifestations (patient-
reported and physical examination findings) are commonly referred to in terms of a gain
(e.g., mechanosensitivity) or loss (e.g., nerve conduction deficit) of nerve function.40
Focus Point
A patient’s pain may not always be associated with nerve compression. Structures such
as the dorsal root ganglion may be involved or the pain may be associated with the
presence of perineural inflammation and the development of nerve mechanosensitivity.

Patient reported symptoms

Patient reported symptoms may be pathognomic of nerve involvement. A loss of nerve
function indicates reduced impulse generation, resulting in numbness (anaesthesia) or
weakness. In contrast, a gain in function reflects reduced inhibition or abnormal
excitability, presenting as paraesthesia, spontaneous pain, hyperalgesia and allodynia.4
Pain may not always be associated with nerve compression and may be dependent on
involvement of certain nerve structures, such as the dorsal root ganglion,61,62 or the
presence of perineural inflammation and the development of nerve mechanosensitivity.
There are characteristic symptoms of nerve-related pain that are distinctive to those
associated with somatic referred pain. Symptoms described as burning, electric shocks,
cold pain in conjunction with paraesthesia, anaesthesia, tingling and itching, may improve
identification of nerve involvement.63 However, caution needs to be taken because
considerable overlap in symptoms has been shown in individuals reporting conditions with
and without nerve involvement.64 This overlap may partly be caused by changes at various
levels of the nervous system which explains the experience of symptoms beyond the
normal distribution of the injured peripheral nerve (e.g., non-dermatomal distribution).40
Differentiation of neuropathic pain may be assisted by the use of specific questionnaires
such as the self-report version of the Leeds Assessment of Neuropathic Symptoms and
Signs65 and the Neuropathic Pain Questionnaire.66

Nerve conduction integrity

A traditional clinical neurological examination (lower tract: spinal reflexes, strength,
sensation; upper tract: Hoffmann’s sign, Babinski, clonus) may detect compromise of
nerve conduction, signalling a loss of nerve function. Similar but more quantitative
evaluation of the integrity of nerve conduction may be undertaken with electrodiagnostic
testing methods.67 Although these forms of evaluation are still warranted in patients with
referred upper limb pain or other reported symptoms (e.g., paraesthesia, anaesthesia,
weakness), their capacity to detect the presence of conduction deficits has limitations.40
For example, electrodiagnostic tests only evaluate large myelinated motor neurons and Aβ
fibres, but not the small diameter fibres (Aδ and C fibres).68 Yet the evidence suggests that
these smaller diameter fibres are affected in entrapment neuropathies, sometimes before
the larger myelinated fibres.36 Because these traditional methods of assessment have
limitations, their findings may correlate poorly with the patients’ symptoms and disability
level.69,70 Elements of Quantitative Sensory Testing may assist the identification of a loss
of nerve function, such as a deterioration in thermal and mechanical detection
thresholds.40,71 Specifically, a loss of function may implicate dysfunction in specific nerve
fibres: elevated vibration detection thresholds implicates Aβ fibres; altered cold detection
threshold implicates Aδ fibres; altered warm detection threshold implicates C-fibres.71 It
should be noted that this is separate to the use of Quantitative Sensory Testing to detect a
gain in nerve function such as allodynia and temporal summation, which may indicate
central mediated pain mechanisms, especially if widespread71–74 (Chapter 2).
Focus Point
Adjacent intact neurones may be affected by neuroinflammatory processes within the
dorsal root ganglion which alters their firing threshold. Together with changes in the
spinal cord and brain, the consequences of neuroinflammation may explain the spread
of symptoms beyond the distribution of the injured peripheral nerve.

Nerve mechanosensitivity
The nervous system slides relative to its interfacing structures during movement of the
body and is subjected to compressive and stretch forces.75–78 As discussed previously,
processes resulting from perineural inflammation or nerve compression from injury to
interfacing musculoskeletal structures may predispose the nerve to mechanosensitivity.
Although healthy nerves can tolerate compressive and stretch forces associated with
movement, animal studies indicate that irritated, inflamed or injured nerves may have
increased mechanical sensitivity, resulting in ectopic impulses in response to movement
and compression.16,17 Elements of the physical examination, such as neurodynamic tests,
active and passive movement examination and nerve palpation,79–81 may identify nerve
mechanosensitivity. Specifically, neurodynamic tests aim to identify the presence of nerve
mechanosensitivity by causing nerve gliding in relationship to interfacing structures76,82–85
and nerve elongation potentially affecting intraneural pressure.86 Ectopic impulse
generation may occur in response to very small amounts of nerve elongation or applied
pressure on inflamed nerves.17 This may reproduce symptoms and aberrant protective
muscle responses during a test and reduce excursion of joint motion.87 Interpretation of
neurodynamic test responses needs to be made with some caution as sensory88 and
protective muscle responses89 during neurodynamic tests are also present in asymptomatic
individuals. Criteria for clinical testing and interpretation of tests of neuro-
mechanosensitivity are described in Chapter 9.
Focus Point
Examination of the neural system attempts to identify altered nerve function such as
nerve conduction deficits (a loss of function) or neural mechanosensitivity (a gain of
function) that is relevant to the neck pain disorder.

Cervical spine-related nerve conditions

The aetiology of nerve-related conditions of the upper body may have a direct relationship
with the cervical spine (e.g., cervical myelopathy, cervical radiculopathy), or conditions of
the cervical spine may potentially contribute to other nerve-related upper limb conditions.
Symptoms and signs of either carpal tunnel or cubital tunnel syndrome may extend
beyond normal territories of the nerves involved if associated with a double crush
mechanism particularly at the cervical spine,45,46 or with neuronal changes in the dorsal
root ganglion and central nervous system41–43 as occurs in some cases of peripheral nerve
injury.40 This section will focus on nerve conditions with a direct relationship to the
cervical spine.

Degenerative cervical myelopathy

Degenerative cervical myelopathy describes a collection of pathological conditions which,
individually, or in combination, cause compression of the cervical spinal cord.19
Degenerative cervical myelopathy incorporates conditions such as cervical spondylotic
myelopathy.90 These non-traumatic degenerative forms of cervical myelopathy are the
most common cause of spinal cord impairment in the elderly.91 Their incidence and
prevalence in North America is estimated at a minimum of 41 and 605 per million people,
respectively.92
The cervical cord is somewhat vulnerable to degenerative change because the width of
the spinal canal reduces from C1 to C6 whereas the width of the cord area increases93
placing the lower cervical cord at increased risk of stenosis and subsequent compression.94
Canal stenosis and subsequent compression may be congenital, the result of trauma or
acquired as a result of cervical spondylosis or neoplasms. Degenerative cervical
myelopathy may result from spondylosis/degenerative osteoarthritic processes (e.g., facet
joint degeneration, degenerative disc disease), non-osteoarthritic ligament degeneration
(hypertrophy, ossification, calcification) or cervical hypermobility (e.g., Ehlers-Danlos
syndrome). Individuals with congenital conditions such as Down syndrome and Klippel-
Feil syndrome are predisposed to cervical myelopathy.92 In any stenotic state, further canal
narrowing during physiological or pathological motion (particularly during cervical
extension), may exacerbate spinal cord compression.90,95–98
Similar to changes in peripheral nerves, compression of the spinal cord may disrupt
blood supply leading to cord ischaemia.96 It has been demonstrated in animal models that
chronic compression of the cervical spinal cord results in spinal cord ischaemia, blood-
spinal cord barrier disruption, neuroinflammation and apoptotic signalling activation.99
Pathological processes within the cord may include grey and white matter degeneration,
anterior horn cell loss, cystic cavitation, Wallerian degeneration and degeneration of the
corticospinal tract.99–101 Reviews by Wilson et al.90 and Nouri et al.92 provide a more
detailed evaluation of the pathological processes associated with degenerative cervical
myelopathy.
Clinical signs associated with cervical myelopathy are varied because of the extensive
and variable changes to the spinal cord. No one clinical finding is pathognomonic, but
cervical myelopathy is typified by gait imbalance, loss of hand dexterity and sphincter
dysfunction.19 Symptoms may also include numbness or paraesthesia of the arms and
hands, weakness of the legs, Lhermitte’s sign (electrical sensation up or down the spine ±
limbs usually with neck flexion). Signs include corticospinal distribution motor deficits,
atrophy of intrinsic hand muscles, hyperreflexia, positive Hoffman sign, up going plantar
responses and lower limb spasticity.102 Cord signal change on MRI may not correlate well
with upper extremity reflex examination findings.103
Natural progression of the condition is highly variable. Some patients remain clinically
stable in the long term, but a large proportion experience clinical deterioration if left
untreated.90 Current evidence suggests that in patients with cervical canal stenosis and
cord compression secondary to spondylosis, but without clinical evidence of myelopathy,
approximately 8% will develop clinical evidence of myelopathy at 1-year follow-up and
23% at a median of 44-months follow-up.104 Furthermore 20% to 60% of patients will
deteriorate neurologically over time without surgical intervention.95
Management of the condition is still uncertain. Evidence supports the efficacy of
surgical treatment for symptomatic patients with degenerative cervical myelopathy;90
however non-surgical management may still be an option for those patients who have
radiological evidence of canal stenosis and cord compression but may not be myelopathic
or have only minimal symptoms. Nevertheless, clinicians need to be aware of the potential
for neurological decline in this patient group that requires immediate medical care.
Continual re-evaluation of clinical presentation including regular neurological evaluation
is indicated for these patients.

Cervicobrachial disorders and cervical radiculopathy

Nerves may be affected by musculoskeletal injury or pathology as they course through and
exit the cervical spine. Cervical nerves exit through the intervertebral foramen, which is
bordered by the pedicles superiorly and inferiorly, by the facet joint and capsule dorsally,
and by the posterolateral disc, uncovertebral joint and vertebral artery ventrally. Pathology
in any of the interfacing musculoskeletal structures may potentially affect the local nerve
structures or, in the presence of stenosis, compress nerves. Coexisting neck and arm pain
is associated with greater levels of self-reported disability than neck pain alone.105
Clinically, there is a spectrum of cervicobrachial conditions. Some present as somatic
referral of arm pain with no apparent nerve involvement, whereas some present with
varying degrees and mix of physical signs of altered nerve conduction and
mechanosensitivity.
Cervical radiculopathy is characterized by objective signs of nerve conduction loss
including some combination of sensory loss, motor loss or impaired reflexes in a
segmental distribution.7 The lower cervical nerve roots (C6, C7) are most vulnerable. This
is consistent with the mismatch in size between the intervertebral foramen and spinal
nerves and the prevalent degenerative changes at the C5-6 and C6-7 motion
segments.106–108 Encroachment of cervical nerve roots as they exit the intervertebral
foramen is from spondylosis in approximately 70% to 75% of cases (reduced disc height,
degenerative zygapophyseal or uncovertebral joints), disc lesions in approximately 20% to
25% of cases or nerve root sleeve fibrosis.107,109,110 Injury to the nerve underlying cervical
radicular pain may be caused by compression of the nerve and/or the presence of
perineural inflammation.5–7
Cervical radiculopathy has a prevalence of 0.10% to 0.35% for the entire population but
mostly affects individuals between 40 and 65 years of age.111,112 Pain may or may not be
present and may be non-dermatomal.113 As discussed, compression of the peripheral nerve
alone may not provoke pain but instead pain may be reliant on factors such as the presence
of perineural inflammation, or the development of intraneural inflammation or the
involvement of the dorsal root ganglion.61 There is also some evidence for altered central
pain processing mechanisms in cervical radiculopathies.72

Occipital neuralgia
Occipital neuralgia is an uncommon cause of occipital pain and headache caused by
irritation of the greater, lesser or third occipital nerves and may be characterized by
paroxysmal lancinating pain.114 It is proposed that irritation and entrapment of the greater
occipital nerve may occur at various locations along its anatomic course including where it
branches from C2 between the axis and atlas, or where it courses between the inferior
oblique and semispinalis muscles or where it pierces the belly of the semispinalis muscle
or aponeurosis of the trapezius.115,116 Although many pathoanatomic aetiologies of
occipital neuralgias have been proposed (trauma, fibrositis, myositis, C1–2 and C2–3
pathology, neural malformations),117 their aetiology is largely unknown and most
presentations are considered idiopathic.114 For a discussion of potential aetiologies
underlying occipital neuralgias, comprehensive reviews on this topic are provided by
Dougherty114 and Cesmebasi et al.117 Although the exact aetiology may be difficult to
identify, from the clinician’s perspective the distribution and nature of headache symptoms
associated with occipital neuralgia justifies a thorough examination of the cervical spine,
including a detailed examination of the nervous system incorporating tests of nerve
conduction and mechanosensitivity.

Thoracic outlet syndrome

Thoracic outlet syndrome still remains a controversial condition.118 It is a blanket term
encapsulating many different clinical entities.119 The syndrome is characterized by pain,
paraesthesia, weakness and discomfort in the upper limb, which is aggravated by elevation
of the arms or by exaggerated movements of the head and neck.120 The thoracic outlet
refers to an area from the supraclavicular fossa to the axilla, through which course the
brachial plexus (C5 to T1 nerve fibres), as well as the subclavian and axillary arteries and
veins.119 Therefore thoracic outlet syndrome may involve compromise of neural tissues,
vascular tissues, or both. Three classifications have been described; (1) neurologic
thoracic outlet syndrome, (2) vascular thoracic outlet syndrome (arterial and venous) and
(3) neurovascular/combined. Vascular thoracic outlet syndrome is rare (< 5% of cases)
with neurologic thoracic outlet syndrome the main contributor.118,121,122 Stewman et al.119
provide a full description of the subcategories and prevalence of subcategories of thoracic
outlet syndrome.
 Potential sites of neurovascular compromise include the interscalene triangle,
costoclavicular space and subcoracoid space,123–125 but there may be significant anatomic
variation in these regions between individuals. There is the potential for compromise as
the brachial plexus and subclavian artery exit through the anterior and middle scalene
muscles that, together with the first rib, form the scalene triangle. The C5 or C6 ventral
rami may penetrate the anterior scalene muscle,126 but most commonly they penetrate the
middle scalene along with the dorsal scapular nerve.127 Atrophy, spasm or the common
presence of the additional scalenus minimus muscle may compromise travel of
neurovascular structures through the scalene triangle.126,128,129 The double crush syndrome
may be a relevant factor for thoracic outlet syndrome with respect to compression of the
brachial plexus and distal sites of nerve compression.130 Overall, there is still uncertainty
about the underlying mechanisms of thoracic outlet. Its diverse presentations underpin
recommendations that diagnoses rely on a thorough examination because there is currently
no gold standard test for its diagnosis.119

Conclusion
Neck pain disorders commonly involve injury or pathology of nerve tissue. The cervical
spine may be directly implicated in some neural conditions such as cervical radiculopathy
or myelopathy. Cervical conditions may also be implicated in some upper limb
neuropathies such as carpal tunnel syndrome. The identification of the presence and nature
of neuropathy in neck pain disorders depends on a judicious structural differential
examination. In particular, determining the relative presence of nerve conduction and
nerve mechanosensitivity features will guide the most appropriate and safe course of
management for these sometimes-complex neck pain presentations.

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5

Neuromuscular Disturbances in Neck

Pain Disorders
The cervical region is equipped with elaborate musculature and the coordinated activity of
all muscles influences the orientation of the cervical spine and head position. The intricate
neural control of the cervical spine dictates that nociception can have a profound influence
on the control of head movement and stability.
A number of theories have been proposed over the years to account for the
neuromuscular adaptations accompanying pain. This includes classic models such as the
pain adaptation model1 and the vicious circle model2 which both predict very stereotypical
changes in the presence of pain. Although a number of experimental findings supported
each model, neither model is able to explain the complexity and diversity of
neuromuscular adaptations seen in people with musculoskeletal pain, including the diverse
neuromuscular adaptations accompanying neck pain. As a result, contemporary theories
have been proposed to better explain motor adaptations to injury/pain, which encompass
the greater diversity of motor adaptations seen in clinical cases.3,4 Some of the key
principles of contemporary theory indicate that;3–5 (1) pain-related neuromuscular
adaptations involve a diversity of changes ranging from subtle redistribution of activity
within a muscle to complete avoidance of movement; (2) despite common features,
individuals will present with their own unique mix of neuromuscular adaptations; (3) pain-
related neuromuscular adaptations have a common aim initially to protect the
painful/threatened body region from real or anticipated further pain/injury; (4)
neuromuscular adaptations can be initiated in the presence of pain/injury but may also be
the initial trigger for the development of pain; and (5) if maintained, neuromuscular
adaptations can lead to secondary adaptations and/or long-term consequences. Such
contemporary theory is underpinned by a wealth of data from experimental and clinical
studies including those in people with neck pain disorders.
The various features of this contemporary understanding of neuromuscular adaptations
to pain will be reviewed in this chapter as it applies to neck pain disorders. Following a
brief overview of anatomic considerations of the cervical musculature, a number of studies
will be considered, which describe varying neuromuscular adaptations in individuals with
neck pain. These changes range from more general modifications such as decreased neck
muscle strength, through to subtle variations in the distribution of activity within and
between neck muscles. There is convincing evidence that nociception/injury is the initial
trigger for such adaptations6–13 although, continued or maladaptive changes in
neuromuscular control can contribute to the chronicity, maintenance and recurrence of
neck pain.14 That is, altered muscle coordination which involves less efficient
combinations of muscle synergies may alter loading on cervical structures including the
muscles themselves and increase the vulnerability of the cervical region to strain resulting
in the maintenance or initiation of nociception.5,6,15 Moreover, neck pain has been
associated with a number of peripheral adaptations within muscle including changes in
muscle cross-sectional area, fatty infiltration of muscle tissue and specific modifications
of muscle fibres, which may in part be driven by ongoing alterations of muscle behaviour.
These adaptations will also be reviewed within this chapter.

Anatomical considerations
There are 44 muscles in the neck which collectively work to control and stabilize head
movement in three-dimensional space while simultaneously executing voluntary
movements. Neck muscles are topographically arranged, with some acting solely over the
upper cervical region, others acting only over the mid and lower cervical region and others
spanning the entire cervical spine. The neck muscles can be further considered according
to their functional roles. Generally speaking, the larger superficial muscles (e.g., splenius
capitis, sternocleidomastoid) have larger lever arms and cross-sectional areas and a greater
capacity to exert torque than deeper muscles (e.g., multifidus, longus colli and longus
capitis).16 In contrast, the deeper muscles are typically segmentally arranged with direct
attachments to the cervical vertebrae and have larger spindle densities.17,18 The
suboccipital (e.g., rectus capitis posterior major and minor) and deep cervical muscles
(e.g., multifidus and longus colli) have the highest density of muscle spindles of all
muscles in the body.17,18 Moreover, the deep muscles are characterized by a greater
proportion of low-threshold slow twitch muscle fibres relative to the superficial muscles
reflecting their contribution to postural support of the cervical spine.17,18 Accordingly, a
model of the cervical spine demonstrated regions of local segmental instability when only
the large superficial muscles of the neck were simulated to produce movement in the
absence of deep muscle activation19 confirming the relevance of the deep muscle layer in
contributing to general postural support. Our recent work using shear wave elastography
revealed that the deep muscle layer has greater passive and active stiffness compared with
the superficial neck muscles.20 These findings are supported by observations of high
passive stiffness of the multifidus muscle, which was demonstrated on muscle fibre bundle
examinations.21 Similar to all deep muscles, the cervical multifidus is predominantly
composed of low-threshold, slow-twitch muscle fibres,17,18 which are stiffer22,23 than fast-
twitch fibres.
The sternocleidomastoid, anterior scalene and hyoid muscles form the superficial layer
of the neck muscles anterolaterally. Bilateral contraction of the sternocleidomastoid
induces extension at the upper cervical region and flexion of the lower cervical region.
Bilateral contraction of the anterior scalene will also contribute to flexion of the neck
whereas ipsilateral contraction induces ipsilateral lateral flexion. During neck extension
(when the neck flexor muscles act eccentrically), it is estimated that the flexor moment
arms of both the sternocleidomastoid and the anterior scalene muscles reduce as extension
progresses such that in extreme extension, their moment arms are less than 25% of their
value in a neutral upright position.16 Thus as extension progresses, the deeper muscles
progressively contribute more to control the position of the head.
The deepest layer of the flexor group consists of the longus capitis, longus colli and
rectus capitis anterior. These muscles act to counter the accentuation of the cervical
lordosis induced by extensor muscle contraction and head weight.19,24,25 The longus capitis
muscle overlaps the superior portion of longus colli and has attachments from the
transverse processes of the third, fourth, fifth and sixth cervical vertebrae to insert on the
inferior surface of the basilar part of the occipital bone. The longus colli has direct
attachment to the anterior surface of the cervical vertebrae and spans from the atlas to the
third thoracic vertebra. An increase in electromyographic (EMG) activity is evident in
these deep cervical flexor muscles either when load is applied to the top of the head, that
is, a load which accentuate the lordosis, or when the lordosis is actively straightened
during postural realignment tasks.26,27
The neck extensor muscles are organized in four layers. Levator scapulae and upper
trapezius constitute the superficial layer and, although they have attachments to the
cranium and cervical spine, they are primarily considered muscles of the shoulder girdle
responsible for bearing the load and absorbing the forces induced on the cervical segments
during upper limb function.28 This implies that the upper trapezius and levator scapulae
muscles may induce compressive loading on cervical motion segments because of their
attachments. Compared with the levator scapulae, the mechanical effects of upper
trapezius are less owing to its relatively small cross sectional area and attachments
primarily to the ligamentum nuchae.29–31 However, the vertical orientation of the levator
scapulae fibres and direct attachments to the upper four cervical vertebrae may induce
compressive forces on the cervical spine.32 Understandably, forces imposed on the cervical
spine from excessive or aberrant axioscapular muscle activity may be potentially adverse
and contribute to the development of neck pain during static work postures and/or tasks
imposing repetitive arm movements.28,32
Splenius capitis forms the second layer and acts on the head to produce extension,
ipsilateral rotation and ipsilateral lateral flexion of the neck.33 The semispinalis capitis
forms the third layer, and semispinalis cervicis, multifidus and rotatores muscles form the
deepest layer together with the suboccipital muscle group. The rotatores are small and
short muscles lying close to the vertebral arch and spinous process and act to rotate the
vertebra to the opposite side. Multifidus has direct attachments to the cervical vertebrae
and similarly the fibres of semispinalis cervicis originate from the transverse processes of
T1 to T5–T6 inserting on to the spinous processes of C2 to C5 respectively down to C7.
Collectively, the multifidus, rotatores and semispinalis cervicis form the transversospinalis
muscle which produces extension, ipsilateral lateral flexion and contralateral rotation of
the neck.
The suboccipital muscle group includes the rectus capitis posterior major and minor,
and the obliquus capitis superior and inferior. These muscles contribute to the fine control
of head movement in addition to providing support for the upper cervical segments, which
is accredited to their relatively small moment arms, direct attachments to the cervical
vertebrae, high proportion of slow-twitch fibres and high density of muscle spindles.34–39
 The knowledge on the differing functional roles of the neck muscles is relevant because
studies in people with neck pain disorders support a differential effect of pain on the
deeper postural muscles of the neck versus the larger torque producing muscles. These
differential effects are reviewed in this chapter.

Changes in motor output in people with neck pain

Several biomechanical disturbances are noted in people with neck pain including reduced
range of motion,40–42 reduced concurrent motions in the associated planes,43 slower
movement speed44,45 and reduced smoothness of movement44,42 as reviewed in Chapters 3.
In addition to these biomechanical disturbances, people with neck pain commonly display
other impairments in motor output including reduced neck muscle strength, endurance and
force steadiness.
Decreased neck strength is a common physical feature in people with neck pain
regardless of the aetiology of their symptoms, and is typically diminished around all
axes.46 The extent to which neck strength is affected in people with neck pain varies
widely with reports ranging from a 13% to 90% reduction compared with asymptomatic
people.47,48 Neck muscle endurance is also commonly affected and multiple studies have
confirmed poor endurance of the neck flexors, extensors and craniocervical flexor muscles
in people with neck pain across a range of contraction intensities.49–52 Similar to
observations for neck strength, reduced endurance appears to be independent of the
aetiology of the patient’s symptoms and has been documented for people with different
neck pain disorders including cervicogenic headache,51 cervical radiculopathy,53 and
idiopathic neck pain.50,54 A loss of endurance in the craniocervical flexor muscles has also
been observed indirectly as a reduced ability to maintain an upright sitting posture.55 That
is, compared with asymptomatic people, those with neck pain drift into a more forward
head position during prolonged sitting.55
An impaired ability to maintain a steady force output around a target force value during
isometric contractions is a further indicator of disturbed motor output in people with neck
pain.50,56,57 As an example, note the larger fluctuations in force illustrated in Fig. 5.1 when
the patient with chronic neck pain attempts to control a force at 15 N while performing a
circular contraction of their head and neck as compared with the representative example
from an asymptomatic person.56 Reduced ability to maintain a steady force output has
been documented for people with neck pain across a range of contraction intensities.50,56,57
 FIG. 5.1 Representative force traces obtained for a control subject and a patient
performing a circular contraction at 15 N. Note that the patient presents with less
accuracy in producing the circular contraction compared with the control subject, which
is reflected in a greater coefficient of variation of force for the patient compared with
the control subject. In this example, the coefficient of variation of force is 7.4% and
17.5% for the control and patient respectively. (From Schomacher J, Farina D, Lindstroem R, et
al. Chronic trauma-induced neck pain impairs the neural control of the deep semispinalis cervicis muscle.
Clin Neurophysiol 2012;123:1403–1408.)

Some of the variability in neck muscle functional performance seen in people with neck
pain can be explained by the presence of psychological features. For instance,
approximately 13% of the variability in neck muscle strength in a group of patients with
chronic neck pain could be explained by their level of fear avoidance.46 Nevertheless,
when their current pain during the neck muscle strength testing was taken into account,
current pain and fear avoidance explained around 27% of the variance in neck muscle
strength.46 A recent study also showed that most of the variability in performance on
physical tests of neck muscle function in people with whiplash-associated disorders could
be best explained by their level of pain intensity and disability rather than their scores on
various psychological questionnaires.58
Underlying these general changes in motor output, there may be numerous
modifications in muscle behaviour including altered coordination both between and within
muscles as now explored.

Changes in the coordination between muscles

As indicated, there are 44 muscles in the neck which collectively facilitate the control and
support of the cervical spine while simultaneously executing voluntary movements. Our
central nervous system (CNS) copes with the anatomic complexity and redundancy of the
neck muscles by developing consistent muscle synergies to generate multidirectional
patterns of force.6,59–61 Normally, the neck muscles show well-defined preferred directions
of activation, which are in accordance with their anatomic position relative to the
spine.30,56,61,62 The recruitment of neck muscles for a given movement or task is therefore
optimized and dependent on the task requirements. This changes when pain or anticipated
pain is present.
Studies have shown that people with neck pain display distinct changes in neck muscle
coordination including reduced specificity of neck muscle activity with respect to
asymptomatic individuals56,63,64 (Fig. 5.2). This includes people with chronic whiplash-
associated disorders in addition to those with idiopathic neck pain. The reduced specificity
of neck muscle activity is associated with a reduced modulation in the discharge rate of
individual motor units with force direction.56 Notably, reduced specificity of neck muscle
activity also implies an increase in neck flexor and extensor coactivation as seen in Fig.
5.2, because a high level of antagonistic neck muscle activity is present in association with
neck pain. Greater coactivation of the superficial cervical flexor and extensor muscles has
also been observed in people with chronic neck pain and headache during isometric neck
contractions64,65 and in office workers with neck pain during a typing task.66 Increased
coactivation of the neck flexor and extensor muscles is inversely correlated with total neck
strength and positively correlated with levels of pain and perceived disability.64

FIG. 5.2 Representative directional activation curves obtained from the

sternocleidomastoid, splenius capitis and semispinalis cervicis muscles during a
circular contraction performed at 15 N presented for a control subject and a patient
with chronic neck pain. Note the defined activation of the sternocleidomastoid, splenius
capitis and semispinalis cervicis for the control subject with minimal activity during the
antagonist phase of the task. Conversely, the directional activation curves for the
patient indicate more even activation levels of each muscle for all directions. (From Falla
D, Lindstrom R, Rechter L, et al. Effect of pain on the modulation in discharge rate of sternocleidomastoid
motor units with force direction. Clin Neurophysiol 2010;121:744–753; Schomacher J, Farina D, Lindstroem
R, et al. Chronic trauma-induced neck pain impairs the neural control of the deep semispinalis cervicis
muscle. Clin Neurophysiol 2012;123:1403–1408; Lindstrom R, Schomacher J, Farina D, et al. Association
between neck muscle co-activation, pain, and strength in women with neck pain. Man Ther 2011;16:80–
86.)

Higher levels of neck muscle coactivation may serve to initially protect a painful neck,
that is, increased neck muscle coactivation may reflect an attempt to voluntarily increase
the stability of the head/neck for the fear of performing potentially painful movements.
This fits with the contemporary theory that motor adaptation to pain has a general aim (at
least in the short term) to protect the painful/threatened body part from real or anticipated
further pain/injury.3 However, if maintained, this may ultimately lead to excessive loading
on cervical structures further perpetuating neck symptoms and may act to facilitate
ongoing nociception.
A number of additional studies support the observation of heightened activity of the
superficial neck muscles in people with neck pain disorders. In particular, increased
activation of the sternocleidomastoid and anterior scalene muscles is commonly observed
during performance of the craniocervical flexion test; an observation that has been made
in a number of studies evaluating different patient populations including cervicogenic
headache,67,68 idiopathic neck pain,69,70 whiplash-induced neck pain70–72 and
occupationally-induced neck pain73,74 (Fig. 5.3). The heightened activity of the superficial
flexors was thought to reflect a compensatory strategy for weakness or inhibition of the
longus colli and longus capitis reflecting a reorganization of the motor strategy to perform
the task. Reduced activation of the deep cervical flexors was subsequently confirmed via
direct measures of the EMG amplitude of longus colli and longus capitis during
performance of this test in people with chronic neck pain.69 Recent work confirmed the
interpretation that higher activity of the superficial flexor muscles during performance of
this test, is an indicator of reduced activity of the deep cervical flexors.75 That is, a
moderate negative correlation was identified between the average EMG amplitude of the
deep cervical flexors and sternocleidomastoid across all stages of the craniocervical
flexion test.
 FIG. 5.3 Normalized electromyograph amplitude (root mean square, RMS) recorded
for the sternocleidomastoid muscle (SCM) during performance of the craniocervical
flexion test (C-CFT) in people with neck pain (dark blue) versus healthy controls (light
blue). Note the higher activity of the sternocleidomastoid muscle for the patients
regardless of the aetiology of their neck pain. (A) cervicogenic headache,67 (B)
whiplash-induced neck pain,72 (C) occupationally-induced neck pain73 and (D)
idiopathic neck pain.69

Increased activation of the superficial neck flexors is not unique to the task of
craniocervical flexion. Indeed, several studies have reported augmented activation of these
muscles as people with neck pain perform other tasks including repeated upper limb
movements66,76 and isometric neck contractions.56,77 Moreover, a recent study which
examined the behaviour of sternocleidomastoid motor units, found that the people with
mechanical neck pain showed significantly higher initial and mean firing rates during
isometric cervical flexion contractions,78 which supports earlier observations from surface
EMG studies of greater sternocleidomastoid muscle activity in people with neck pain
disorders. Additional findings of reduced modulation of the discharge rates of
sternocleidomastoid motor units56 (Fig. 5.4) and decreased sternocleidomastoid motor unit
short-term synchronization78 further support an altered neuromuscular control strategy in
people with chronic neck pain. Interestingly, a recent study using real-time, ultrasound
measurements of muscle deformation showed reduced variability in the interplay between
different neck flexor muscles in people with whiplash-associated disorders during repeated
arm elevation.79
 FIG. 5.4 Mean and standard deviation of left and right sternocleidomastoid motor unit
discharge rate for a group of control subjects and patients with chronic neck pain
during 10-second contractions performed at 15 N of force in eight directions (45-
degree intervals from 0–360 degrees) in the horizontal plane. The symbols at the top of
the image illustrate the directions of force. The asymptomatic subjects display a
modulation in discharge of motor units depending on the direction of force. In contrast,
the patient group displayed the same neural drive to the sternocleidomastoid muscle
for all force directions. PPS, Pulses per second. (From Falla D, Lindstrom R, Rechter L, et al.
Effect of pain on the modulation in discharge rate of sternocleidomastoid motor units with force direction. Clin
Neurophysiol 2010;121:744–753.)

Consistent with the observation of reduced activation of the deep cervical flexor
muscles, studies have also demonstrated that people with neck pain commonly present
with reduced activation of the deep extensors, semispinalis cervicis and multifidus. This
has been demonstrated in several studies applying different methodologies including
functional magnetic resonance imaging80 and intramuscular EMG.63,81 In contrast, higher
activity of the superficial extensors (e.g., splenius capitis) is frequently seen in people with
neck pain and this has been demonstrated in a number of tasks including typing on a
keyboard,82 isometric neck extension and lateral flexion,83 repetitive upper limb
movement66 and isometric circular contractions in the horizontal plane.64
These seemingly contrasting effects on deep and superficial muscle activity suggests
that more deeply and superficially situated muscles may be affected differentially by either
central or peripheral mechanisms.15 Another explanation could be that the CNS prioritizes
a solution of increased stiffness/protection by coactivating the larger, superficial muscles84
yet this comes at the expense of loss of control of the deeper postural muscles. Similar
hypotheses have been proposed to explain trunk muscle adaptations in people with low-
back pain.84
Besides changes in neck muscle activation, altered axioscapular muscle activation may
be present in people with neck pain despite the absence of shoulder or arm pain76,85–88 and
can be induced experimentally with injection of hypertonic saline into neck muscles.89,90
For instance, changes in upper trapezius muscle activity have been observed in patients
with neck pain of both traumatic and non-traumatic origin66,76,86 during repetitive
movements of the upper limb. Likewise, altered masticatory muscle activation has been
observed in people with persistent neck pain despite the absence of orofacial pain or
temporomandibular disorders.91,92
Subtle variations in the distribution of activity within
muscles
High density, two-dimensional surface EMG provides a measure of the electrical potential
distribution over a large surface area during muscle contraction and unlike classic bipolar
surface EMG applications, provides a topographic representation of EMG amplitude.93
This method can be used to evaluate the distribution of activity within a muscle and can
identify relative adaptations in the intensity of activity within regions of a muscle during
both static and dynamic contractions.
One of the most relevant findings revealed by high-density EMG over the last decade is
spatial heterogeneity of muscle activity and how it changes during sustained constant-
force contractions,94,95 contractions of increasing load,95,96 and dynamic contractions.10,97
These findings likely indicate a nonuniform distribution of motor units or spatial
dependency in the control of motor units.98,99 Importantly, studies in healthy individuals
have shown that this spatial reorganization of muscle activity during contractions has the
physiological significance of minimizing muscle fatigue, that is, prolonging endurance,
and is potentially relevant to avoid overload of the same muscle fibres during prolonged
activation.94 For example, a progressive shift of activity occurs towards the cranial region
of the upper trapezius muscle when healthy individuals perform sustained shoulder
abduction9,94,100,101 resulting in a total shift of the centre of activity within the muscle. This
response reflects a greater progressive recruitment of motor units within the cranial region
of the upper trapezius muscle99,102 and likely reflects an optimization of the neural strategy
with fatigue. Variability is an important neural strategy because variation effectively
shares the load so that one tissue or structure is not repeatedly loaded.
In the presence of either experimentally induced muscle pain9,10,101,103 or clinical
pain,91,92,97,100 there is less redistribution of activity to different muscle regions during
sustained and/or dynamic contractions. Thus when pain is present, muscle contractions are
performed by increasing the activation of a region within the muscle over the duration of
the task, that is, without the normal variability of muscle activity characteristic for
asymptomatic subjects. These findings suggest that nociception interferes with the normal
adaptation of activity within a muscle, which may ultimately induce overuse of similar
muscle compartments with fatigue. Our recent work also revealed that neck muscle pain
induces a shift of the spatial distribution of upper trapezius muscle activity during a
repetitive task, which may help to explain the perpetuation of pain with repetitive activity.
The study identified that regions of the trapezius muscle, which would not normally be as
active, became active in the painful condition and that regions, which would normally be
active (based on their anatomical action), became less active. This new motor strategy
may be seen as an effective mechanism to “protect” the painful region. However, this
“new” pattern of trapezius muscle activation in the painful condition can be seen as an
inefficient motor strategy and would likely be relevant for perpetuation of symptoms.
Changes in the temporal characteristics of neck
muscle activity
Besides changes in the extent of neck muscle activation, alterations in the timing of neck
muscle activity may occur in association with neck pain. Alterations in the temporal
aspects of neck muscle activation have been explored by evaluating both the onset of
muscle activity, typically via perturbations, and the offset of muscle activity, typically as
time to relaxation following voluntary contractions.

Delayed onset of neck muscle activity

The onset of neck muscle activation has been tested during both internal and external
perturbations. Internal perturbations, such as a rapid movement of the arm, produce
reactive forces, which are of equal magnitude and opposite direction to the forces
produced by the arm movement.104 These forces are transferred to body segments eliciting
a series of postural adjustments to maintain equilibrium. One strategy of the nervous
system, which is detectable by EMG during internal perturbations, is feed-forward muscle
activation. This mechanism helps to maintain or regain stability in the presence of external
forces, or when a body part is required to act as a steady base for movement to occur.
When asymptomatic people perform rapid arm movements in standing, both the deep and
superficial neck muscles are activated in a feed-forward manner.105,106 In contrast, the onset
of neck muscle activity is delayed in people with neck pain.106 Notably, the delay in onset
exceeds the criteria for feed-forward contraction. Moreover, unlike observations in
asymptomatic people, the activation of the deep cervical flexors adopts a direction specific
response suggesting that the change is not simply a delay that could be explained by
factors such as decreased motor neuron excitability, but instead is consistent with the
change in the strategy used by the CNS to control the cervical spine.106
More recent work has shown that when people with neck pain are exposed to rapid,
full-body postural perturbations, they demonstrate delayed activation of the
sternocleidomastoid and splenius capitis muscles with respect to asymptomatic people107
(Fig. 5.5). The reduced ability to activate neck muscles in response to an unexpected
event, such as a trip, slip or jolt, may leave the neck vulnerable to further injury.
 FIG. 5.5 Patients with chronic neck pain and healthy controls stood on a moveable
platform and were exposed to randomized full body postural perturbations (8-cm
forward slides [FS], 8-cm backward slides [BS], 10-degrees forward tilts [FT], and 10-
degrees backward tilts [BT]). (B) Mean and standard deviation of the onset of the
sternocleidomastoid and splenius capitis muscles in response to the perturbations.
Note the significantly (*P < 0.05) delayed onset time of the neck muscles for the
patients with neck pain regardless of the perturbation direction. (From Boudreau S, Farina D,
Kongstad L, et al. The relative timing of trunk muscle activation is retained in response to unanticipated
postural-perturbations during acute low back pain. Exp Brain Res 2011;210:259–267.)

Delayed offset of muscle activity

Delayed muscle relaxation has been documented after neck108 and upper limb
contractions109 in people with neck pain. For instance, a significant reduction in the ability
to relax the upper trapezius and infraspinatus muscles was observed in people with chronic
whiplash-associated disorders as they performed repetitive shoulder flexion.110 Lower
relative rest times have also been observed for people with occupationally-induced neck
pain during the performance of standardized short-term computer work.111 A number of
other studies have confirmed that people with neck pain may have difficulty relaxing the
upper trapezius both between and following repetitive arm movements.76,112 It has also
shown that this muscle is generally susceptible to increased activity during tasks involving
mental demand.113 Similarly, there is some evidence to suggest that people with neck pain
may have difficulty relaxing their anterior scalene and sternocleidomastoid muscles
following activation.76
In a recent study examining the flexion-relaxation phenomenon and flexion-relaxation
ratios of the cervical extensor muscles using surface EMG in computer workers with and
without chronic neck pain, a lower flexion-relaxation ratio was observed for the
semispinalis capitis muscle in the symptomatic group. This change was attributed to pain-
induced overactivity of the semispinalis capitis muscle.114 In another study, the flexion-
relaxation phenomenon for the cervical extensors was observed in around 85% of the
asymptomatic subjects whereas it was only present in around 36% of the participants with
chronic neck pain.115 Moreover, for the patients who did show the phenomenon, the period
between onset and offset was reduced. A lower cervical flexion-relaxation ratio has also
been documented in people with subclinical neck pain.116

Individual variability in motor adaptations to pain

The earlier sections of this chapter have outlined common features of neuromuscular
impairment in people with neck pain, yet it must be noted that there is considerable
variability between individuals. This is typically evident when considering the large
standard deviation of EMG data reported for people with neck pain relative to healthy
control groups. Not every person with neck pain will present with such changes in
neuromuscular control and certainly not to the same extent. There is some evidence
suggesting that the variability existing between individuals with neck pain is partially
related to the magnitude of their pain and perceived disability.76,117,118 For instance, the
level of activity of the sternocleidomastoid and anterior scalene muscles during a repeated
upper limb task was shown to be greatest for those reporting higher levels of perceived
pain and disability as reflected by their Neck Disability Index score.76 Higher levels of
pain intensity were also associated with slower onset of the deep cervical flexors during
rapid flexion shoulder and lower activation of these muscles during the craniocervical
flexion test.118 Besides the relation to symptom severity, the variability between
individuals likely also relates to the presence and magnitude of attendant stress reactions
and may even relate to different functional histories, experiences with pain, or habitual
postures/movement patterns.
Supporting the variability observed in clinical studies, there is convincing evidence
from experimental pain studies that nociception will trigger individual specific
neuromuscular adaptations.6,119,120 For instance, in a study which examined the effects of
experimentally induced neck muscle pain on multi-muscle control of neck movements
during an aiming task,6 each subject in the study adopted an individual control strategy to
cope with the painful stimulus. This allowed each subject to perform the task in the
painful condition without altering their neck kinematics but rather taking advantage of the
redundancy of neck muscle activation and changing their control strategy (Fig. 5.6).
Interestingly, on average across the group, the sternocleidomastoid muscle displayed
increased activity in the painful condition. Yet inspection of the individual data presented
in Fig. 5.6 shows that for some people, their “new” motor strategy involved reduced
activation of the sternocleidomastoid. Thus even though at a group level it was a common
strategy to increase the activation of the sternocleidomastoid, this was not universal for all
subjects. This example supports the contemporary theory of a heterogeneous adaptation of
motor control in response to pain despite common changes on average3,121 and clearly has
important implications for management.
FIG. 5.6 (A) Participants performed multidirectional, multiplanar aiming movements of
the head. Nine circular targets (one “central target” plus eight “peripheral targets”) were
placed on a whitewall following a circular trajectory. Participants wore a helmet
mounted with laser pointers and the task consisted of moving their head and neck to
aim laser pointers from the central target to each peripheral target following the tempo
provided by a metronome. Electromyography (EMG) was recorded from multiple neck
muscles. (B) The task was completed at baseline (no pain) and immediately following
the injection of hypertonic saline into the right splenius capitis muscle (painful
condition). (C) Mean and standard deviation of the EMG amplitude recorded for each
muscle in the painful condition normalized relative to the baseline condition. The blue
dotted line indicates the level of activity which would be comparable between
conditions. The injected muscle, the right splenius capitis, is highlighted in grey; note
the overall decreased activity of this muscle. Other muscles showed either an increase
or decrease of activity when averaged across all subjects. (D) Individual data for each
of the eight subjects showing the direction of change in EMG amplitude of each muscle
between the baseline and painful condition. Dark blue indicates an increase of EMG
amplitude in the painful condition compared with baseline, grey indicates decreased
 EMG amplitude and white indicates no change. Note the individual specific patterns of
modulation of muscle activity. No two subjects showed the same strategy. HYO,
Sternohyoid; L, left; LTR, lower trapezius; R, Right; SCA, anterior scalene; SPL,
splenius capitis; STER, sternocleidomastoid; UTR, upper trapezius). (From Gizzi L, Muceli
S, Petzke F, et al. Experimental muscle pain impairs the synergistic modular control of neck muscles. PLoS
One 2015;18:e0137844.)

Changes in peripheral properties of neck muscles

Besides changes in neck muscle behaviour, a number of biochemical, histological and
morphological muscle adaptations have been observed in people with chronic neck pain.
Biochemical alterations include increased interstitial levels of glutamate detected in the
upper division of the trapezius muscle in people with trapezius myalgia122 and higher
interstitial interleukin and serotonin in those with chronic whiplash-associated disorders.123
Additional observations in people with trapezius myalgia include morphological signs of
disturbed mitochondrial function (ragged red and cytochrome-c oxidase negative
fibres),124–126 and increased cross-sectional area of type I muscle fibres despite a lower
capillary to fibre area ratio.127–129
Further specific changes to muscle fibres include a significant increase in the proportion
of type IIC fibres in both the neck flexors and extensors of people with chronic neck pain,
suggesting preferential atrophy of slow-twitch oxidative type I fibres.130 Interestingly, this
observation was found to be independent from the type of neck pathology130 and may
partially explain the greater myoelectrical manifestations of fatigue detected for the
cervical and axioscapular muscles in people with neck pain during both static and dynamic
conditions.53,131–133
Elevated fatty infiltration of neck muscles has been observed in people with neck pain
following a whiplash trauma.134–137 This has been most notable in muscles known to
possess a larger proportion of type I fibres and a higher density of muscle spindles, that is,
the deep sleeve of cervical muscles including the rectus capitis minor and major, longus
capitis, longus colli, semispinalis cervicis and multifidus.134–137 This degeneration of
muscle tissue has been noted particularly in people with persistent moderate to severe
levels of pain following the injury135,137 and in contrast, is not a common finding in people
with insidious-onset neck pain.138 However, a recent study showed larger amounts of fat
infiltrates in the rectus capitis posterior major and minor and splenius capitis muscles in
elders with cervicogenic headache.139 Of interest, the total amount of fat within the neck
extensor muscles in people with chronic whiplash-associated disorders was shown to be
correlated to sensory, physical, kinaesthetic and psychological features, with cold
hyperalgesia showing the strongest correlation.135 Elevated levels of neck muscle fatty
infiltration has also been associated with poor functional recovery.137 The mechanisms
underlying the development of fat within the neck muscles following trauma is not fully
understood and could be attributed to a number of factors ranging from generalized disuse
of the muscles to chronic denervation of the muscle. Considering that these changes are
not typically identified in people with idiopathic neck pain, it is likely that the actual
trauma plays a role.
Atrophy has been noted for some muscles in people with chronic neck pain disorders
and may be present in both deep (e.g., multifidus139–141) and superficial muscles (e.g.,
semispinalis capitis142). Some studies have reported the opposite, that is, a larger cross-
sectional area of the multifidus muscles was documented in people with whiplash-induced
neck pain143 and a larger cross-sectional area was noted for the semispinalis cervicis and
multifidus in fighter pilots with chronic neck pain.144 In whiplash, the larger cross-
sectional area probably represents muscle pseudohypertrophy because of the higher fat
content of the muscles.145 A measure of relative muscle cross-sectional area was
introduced to account for the presence of fatty tissue infiltration and one study reported
that for 93% of muscles examined, the relative muscle cross-sectional area was the same
or even smaller for the patients compared with the control subjects.145

Time course for development of neuromuscular

dysfunction
Muscle behaviour adapts very rapidly to the presence of nociception. This has been
demonstrated experimentally in a number of studies6–9,13,90,103 and the type of adaptations
seen in people with chronic neck pain can be artificially induced through experimental
pain models.7,9,103 As an example, local excitation of nociceptive afferents in the upper
trapezius muscle unilaterally, induced a significant decrease in longus colli and longus
capitis activation;7 a common finding in people with chronic neck pain disorders.69 In
addition to this experimental data, clinical observations in patients with acute neck pain
also support the presence of early neuromuscular adaptations. For instance, increased
activation of the sternocleidomastoid muscle has been observed in people with acute pain
following a whiplash trauma when they perform the craniocervical flexion test.72 As
detailed earlier, increased activation of the sternocleidomastoid muscle on this test is a
direct reflection of lower activation of the deep cervical flexors.75 For these reasons,
exercise is advocated as an essential component of management from the outset, as is
discussed in Chapter 15.
In contrast, it appears that the peripheral adaptations do not occur immediately and may
take several months, if not longer, to develop. An example is the presence of fatty tissue
infiltration of the extensor muscle group which first becomes apparent three months after
the injury in those suffering with moderate to severe pain.137 Consider also the example
presented in Fig. 5.7, which shows a greater relative increase in the proportion of type II
fibres with increasing pain duration.130,146 Although the mechanisms underlying the
development of these peripheral changes are not entirely known, they may at least be, in
part, considered secondary adaptations of disrupted muscle behaviour. This knowledge
provides an even greater incentive to ensure early and effective exercise for people with
acute neck pain with the aim of preventing these adaptations.
 FIG. 5.7 Biopsy taken from the sternocleidomastoid (SCM) muscle shows a greater
relative increase in the proportion of type II fibres with increasing pain duration. (A)
SCM after 12 months of pain with 6% of type-IIB fibres (dark). (B) SCM after 36
months of pain with 44% of type-IIB fibres (dark). (From Uhlig Y, Weber BR, Grob D, et al. Fiber
composition and fiber transformations in neck muscles of patients with dysfunction of the cervical spine. J
Orthop Res 1995;13:240–249.)

Implications for management

Exercise is recommended for people with neck pain and is likely the most widely used
conservative intervention.147 Systematic reviews confirm its effectiveness in relieving neck
pain 147–151 and also for the prevention of pain.152 In addition, there is strong evidence that
exercise is effective for restoring or enhancing neuromuscular function.55,153–158 When
considering the analgesic effect of exercise, multiple forms of exercise have been
proposed to relieve neck pain including general strength and endurance training, exercises
for flexibility and range of motion, graded activity, motor control, and aerobic exercise for
general fitness. In terms of the effect on pain, then there is little evidence to support one
type of exercise over another and the same holds true for low-back pain.121 For example,
higher-load resistance training for the neck flexor muscles provides the same degree of
pain relief compared with low-load motor control exercises for the neck flexors.153 It is
suggested that the decision on the type of exercise to use should be dictated by clinician
and patient preference.
Nevertheless, although various exercises may be effective for relief of chronic neck
pain, some exercises have superior immediate analgesic effects and become particularly
relevant and a greater priority for those with acute symptoms. For instance, one study159
compared the immediate effects of a low-load craniocervical flexion exercise versus a
head lift exercise on neck pain intensity at rest and during active cervical motion, and on
pressure pain thresholds (PPT) and thermal pain thresholds measured over the cervical
spine and at a remote site over the tibialis anterior muscle. Additional measures of
sympathetic nervous system function were evaluated including blood flux, skin
conductance, skin temperature, heart rate and blood pressure. The study revealed that the
craniocervical exercise produced the most significant immediate hypoalgesic effect. This
improvement was in the order of 14% to 21% of pre-exercise PPT levels measured over
the neck as opposed to only a 3% to 7% change for the head lift exercise. Neither exercise
influenced pressure pain sensitivity at the remote site. There was no indication of
sympathetic nervous system excitation following exercise which would have been
indicative of a systemic effect. There was a significant reduction in pain during active
movement post-exercise following the craniocervical flexion exercise only. Other studies
have confirmed an immediate reduction in neck pain intensity and increase in PPT over
the neck region following craniocervical flexion exercise.160 In addition, gentle active
scapular retraction and depression has been shown to induce an immediate reduction in
neck pain intensity and increase in PPT over the neck region.161 Although these specific
neck exercises did not induce immediate systemic pain modulating effects, the immediate
localized hypoalgesia that can be gained from these exercises has important implications
for exercise prescription.

Variability in symptomatic response to exercise

Although clinical trials confirm that standardized exercise programs are effective on
average for people with neck pain, a review of individual responses often reveals that
some patients have an excellent outcome with complete relief of their symptoms and
others have only minimal or even no benefit.162 Thus the often applied “one size fits all”
exercise for neck pain is usually inadequate. There are a number of reasons for such
variability in outcome. One, is the presence of central sensitization which may impede
positive exercise outcomes.163 Psychological factors have also been shown to impede a
favourable outcome from neck exercise programs.164
A further important consideration is the type and degree of neuromuscular impairments
present in the individual before the commencement of training, which can be an important
determinant of symptom relief. As reviewed in this chapter, although there are common
features of neuromuscular impairment in people with neck pain, there is considerable
variability between individuals. Not every person with neck pain will present with the
same changes in neuromuscular control and not to the same extent. Thus it is not
surprising that standardized exercise programs provide varying results in people with neck
pain given that some of the patients in a trial would display minimal impairment in the
targeted neuromuscular function. The data presented in Fig. 5.8A and B supports this
reasoning. It presents the results of a study162 in which the physiological effects of a 6-
week craniocervical flexion exercise program for people with chronic neck pain were
examined. Participants, regardless of their baseline performance in the craniocervical
flexion test, performed this exercise over a 6-week period and were instructed to perform
their exercise twice daily, with supervized sessions with a physiotherapist once a week.
Fig. 5.8A shows the relation between their baseline level of deep cervical flexor muscle
activity versus the amount of improvement in deep cervical flexor muscle activity
following the exercise intervention. As predicted, those with the least activation of their
deep cervical flexor muscles before training were those who had the greatest increase in
activation following training. Fig. 5.8B shows the relation between change in pain
following the exercise intervention and the amount of improvement in the activation of
their deep cervical flexor muscles post-intervention. Once again, a linear relation is
observed. That is, the patients who showed the greatest improvement in the activation of
their deep cervical flexor muscles were those who gained the greatest pain relief from
training. Some patients had no change or only minimal change in pain despite
participating in a 6-week exercise program. It is likely that those patients had other more
relevant features that were not targeted by the exercise. Thus to optimize exercise
prescription and outcome for people with neck pain, exercises must be assessment-driven
and targeted to the patient’s unique mix of presenting features for more effective
management of neck pain.121

FIG. 5.8 (A) Scatter plot of pre-training normalized deep cervical flexor (DCF)
electromyography (EMG) amplitude and the percentage change in DCF EMG
amplitude values after 6 weeks of craniocervical flexion training in a group of patients
with chronic neck pain. (B) Scatter plot of post-training normalized DCF EMG
amplitude and change in average neck pain intensity rated on a visual analogue scale
(VAS) post-training. RMS, Root mean square. (From Falla D, O’Leary S, Farina D, et al. The
change in deep cervical flexor activity after training is associated with the degree of pain reduction in patients
with chronic neck pain. Clin J Pain 2012;28:628–634.)

A recent study further supported the benefit of tailored exercise interventions.165 The
only factor significantly associated with a reduction of both neck pain and neck-related
disability at 3 and 12 months following different exercise interventions for chronic
whiplash-associated disorders, was participation in a specific neck exercise program,
based on a detailed assessment of the patient and tailored to each individual. Patients
allocated to this group had up to 5.3 times higher odds of achieving disability reduction,
and 3.9 times higher odds of achieving pain reduction compared with those who
participated in general physical activity, even if both groups did have a significant benefit
from exercise overall.165 This data further supports the benefit of tailoring and targeting
exercises according to detailed assessment of neuromuscular function to account for the
variability in people with neck pain disorders.

Neuromuscular adaptations to exercise

Reductions in pain and disability are often the main outcome measures in randomized
controlled trials for various types of exercise programs in patients with neck pain and as
illustrated previously, various training approaches can relieve neck pain. Nevertheless,
when managing people with neck pain, relief of pain is only one consideration. Equally
important is the restoration of function. This is particularly relevant considering that many
people develop recurrent pain following their first episode of neck pain.166 Thus the
challenge with treatment is not only to resolve an acute episode of pain, which can be
achieved relatively easily via a number of different techniques, but to prevent or limit its
recurrence for future quality of life. In that respect, exercise to restore neuromuscular
function plays a critical role in the long-term management of the neck pain disorder with
aims to prevent or lessen recurrent episodes of pain. Its prescription and application have
to be thought about in quite different terms compared with exercise for its analgesic
effects.
There is convincing evidence that neuromuscular function of the neck can be enhanced
by training. However, although multiple forms of exercise have been shown to relieve
neck pain, there is evidence supporting the need for specificity in training when the aim is
for rehabilitation of neuromuscular function. For example, low-load exercise to facilitate
activation of the deep cervical flexor muscles is effective at increasing the activation of
these muscles,156 restoring the coordination between the deep and superficial flexors,156,160
enhancing the speed of activation of the deep cervical flexor muscles when challenged by
a postural perturbation156 and improving the patient’s ability to maintain an upright posture
of the cervical spine during prolonged sitting.55 These improvements of neuromuscular
function were not obtained when people with chronic neck pain participated in a strength
and endurance training program for their neck flexor muscles, despite comparable changes
in pain and perceived disability.55,156 In contrast, exercise programs using higher-load
endurance and strength protocols for the neck flexors induce superior gains in neck muscle
strength, endurance and resistance to fatigue compared with craniocervical exercises.153,155
This is hardly surprising because the low-load nature of craniocervical flexion exercises
would not be expected to substantially change strength and fatigability of the superficial
cervical flexors especially when an aim of the exercise is to decrease the relative activity
of these muscles during performance of the task. Thus the provision of a load to challenge
the neck muscles is required to induce a change in higher-load function. These
observations are in line with multiple studies examining neuromuscular adaptations to
training which confirm that specific neuronal, muscle and functional changes in motor
output in response to exercise are specific to the mode of exercise.167–170 This knowledge
further supports the need for assessment-driven targeted exercises for people with neck
pain if neuromuscular function is to be improved.

Conclusion
Neuromuscular adaptations are a common and expected reaction to nociception. There is
an abundance of literature describing such changes in people with various neck pain
disorders and some of the common features are summarized in Fig. 5.9. Although these
changes may have some short-term benefit by acting to protect a painful neck, in the
longer term such adaptations become maladaptive and can contribute to persistence and
recurrence of symptoms. This could occur, for example, if the adaptation to protect the
neck results in increased load on cervical structures (e.g., greater coactivation of the neck
muscles) or if there is an increased risk of further injury (e.g., delayed neck muscle
activation during body perturbations). Potentially, changes in muscle behaviour may lead
to altered muscle structure further contributing to ongoing symptoms and affecting
functional recovery. Chapter 15 is devoted to the effective management of neuromuscular
dysfunction, a critical component of rehabilitation for any neck pain disorder.
 FIG. 5.9 Overview of common neuromuscular adaptations in people with neck pain
disorders.

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6

Sensorimotor Control Disturbances in

Neck Pain Disorders
Cervical afferent input is vital for the control of head and eye movement and postural
stability. This chapter reviews the morphology, the central and reflex connections of
cervical mechanoreceptors and the signs and symptoms caused when they are disturbed
artificially. How disturbed cervical afferent input influences sensorimotor control is
discussed, as well as the possible mechanisms and aetiology of disturbed cervical afferent
input in people with neck pain disorders. Altered cervical afferent input may not only
impair sensorimotor control but may also result in symptoms such as dizziness and visual
disturbances. Understanding how and why sensorimotor control may be affected in people
with neck pain, as well as being able to quantify sensorimotor impairments, provides
direction for precise assessment and interventions for persons with neck pain disorders
(see Chapters 9 and 16).

Cervical mechanoreceptors
Morphology
Receptors in the cervical ligaments, joints and muscles convey afferent information that
contributes to sensorimotor control. Muscle spindles are probably the most significant
receptors. They are found in high densities, especially in the upper cervical region.1,2 Joint
and ligament receptors, via their influence on muscle spindles and the gamma motor
neurons, initiate protective muscle activation to prevent joint degeneration and
instability.3,4
The density of muscle spindles is highest in the suboccipital muscles. The average
number of muscle spindles per gram of muscle is 242 in the obliquus capitis inferior, 190
in obliquus capitis superior, 98 in the rectus capitis posterior minor, 49 in the longus colli
and 24 in the multifidus.1,2 For comparison, the first lumbrical in the hand has 16 and the
superficial region of the trapezius muscle contains 2 muscle spindles per gram of
muscle.1,2 Cervical muscle spindles, especially in the suboccipital muscles, are uniquely
arranged and have high numbers of slow-twitch muscle fibres5–7 to facilitate their role in
movement precision, proprioception, control of head position and eye-head
coordination.5,8,9

Central connections
Cervical afferents provide input to several areas of the spinal cord and central nervous
system (CNS) to integrate and formulate appropriate efferent neuromuscular responses.10
Areas include the central cervical nucleus, thalamus, cerebellum and somatosensory
cortex. Cervical afferents also have unique connections to both the visual and vestibular
systems via projections to the medial and lateral vestibular nuclei, as well as the superior
colliculus, which is a reflex centre for coordination between eye and neck movement (Fig.
6.1).11,12 The deep suboccipital muscles, in tandem with their important proprioceptive
role, are vital for relaying and receiving this information to and from these CNS
connections. Much of the descending information for head and eye movement control
projects specifically to these muscles.5,13

FIG. 6.1 Central connections from the cervical afferents.

Focus Point
Assessment and management of cervical proprioception in people with neck pain is just
as important as proprioceptive management of the lower limb following an ankle or
knee injury. Afferent information from the vestibular, visual and the somatosensory
systems converges in multiple areas within the central nervous system and is important
for general equilibrium, body orientation and oculomotor control. The abundance of
mechanoreceptors in the muscles and joints of the cervical spine and the central and
reflex connections from cervical afferents to the vestibular, visual and the sensorimotor
control systems, indicate that cervical proprioceptive information provides important
somatosensory information. Abnormal cervical afferent input is considered to underlie
symptoms of dizziness or unsteadiness, problems in maintaining a stable upright
posture and measurable deficits in head and eye movement control in people with neck
pain.

Reflex-mediated activity
Synaptic connections from the cervical receptors to other areas of the CNS also play an
important role in neck reflex activity. Neck afferents are involved in reflexes, which
influence head orientation, eye movement control and postural stability. These reflexes
work in conjunction with other cervical, vestibular and visual reflexes acting on the neck
or eye musculature, to coordinate postural stability and head and eye movement (Fig. 6.2).

FIG. 6.2 Sensorimotor control reflex activity relating to the cervical spine. Bold lines
indicate reflex activity specific to the cervical spine. Dashed lines indicate reflex activity
relating to the visual or vestibular system.

The cervico-collic reflex (CCR) activates the neck muscles when they are stretched by
head movement in relation to the body. The CCR is integrated with the vestibulo-collic
reflex (VCR) to activate neck muscles to maintain head position and to limit unintentional
head rotation displacements.14,15 The CCR has high sensitivity to smaller, rather than larger
neck rotations, which suggests that muscle spindles, rather than joint receptors, provide
most input to the CCR.16 The VCR is evoked by vestibular stimuli acting on the neck
muscles, and is similar to the CCR, but responds to faster neck movements.14,15
The cervico-ocular reflex (COR) is evoked by stretch of the neck muscles. It acts
together with the vestibulo-ocular (VOR) and optokinetic reflexes (OKR) to control the
extraocular muscles. The COR serves to assist in maintaining eye position such that head
movement results in equal but opposite movement of the eyes, creating clear vision with
low-frequency movement.17 Its importance in humans has been debated, but it can
compensate when the VOR, which controls eye movement at higher head speeds, is
impaired or diminished.17–21 The OKR activates eye muscles in response to movement of
the visual field over the retina.
Ocular influences on cervical muscles in humans are mediated by the frontal eye fields
and the superior colliculus. They activate neck muscles in response to eye movements
while the head is still. A close relationship has been observed between activity in the deep
cervical extensor muscles and horizontal eye movement.22,23 Functional coupling between
the eye-neck and scapular muscles is also thought to occur.24,25
Focus Point
The numerous reflex connections between the neck, vestibular and visual systems
implies that changes in somatosensory information could result in disturbances in reflex
activity relating to postural stability and coordinated stability of the head and eyes in
the presence of neck pain.
 The tonic neck reflex (TNR) is responsible for alteration in limb muscle activity when
the body moves with respect to the head. The TNR integrates with the vestibulospinal
reflex to achieve postural stability.26

Artificial disturbance to cervical somatosensory input

Experimental studies on healthy subjects have clearly demonstrated the nature of signs
and symptoms that can be attributed to altered cervical afferent input. The association
between disturbances of cervical afferent input and altered sensorimotor control has been
demonstrated in several ways. For instance, injection of anaesthetic or sectioning of
nerves in the upper cervical region has caused disequilibrium, ataxia and nystagmus.27
Less invasive techniques, such as vibrating the neck muscles, which stimulates the muscle
spindles, or restricting neck motion can induce eye position changes, illusory visual and
head movements as well as altered velocity and direction of gait.8,28–33 Furthermore,
sustained isometric contraction causing neck muscle fatigue, affects postural sway, gait
and head position awareness in healthy persons.34–39 These findings demonstrate the
significance of the cervical sensory system’s contribution to head and eye movement
control and postural stability.

Mechanisms underlying disturbances in sensorimotor

control
The likely mechanism for disturbances in sensorimotor control in individuals with neck
pain is conflict between converging inputs from the different sensory systems when
cervical afferent activity is altered.40 A changed or disturbed sensitivity of the muscle
spindles may result in dizziness, altered head position or movement sense, eye-head
coordination or postural stability. There is also some evidence that the neck may directly
influence vestibular function41,42 and may cause asymmetry of the VOR.43,44 Any
disturbance, either a decrease or increase of cervical somatosensory input, may result in
altered sensorimotor control.45,46
Focus Point
Considering collectively, the cervical muscle spindle characteristics, central connections
and their role in reflex pathways, it is apparent that the sensory properties of the
cervical region are vital both for somatosensory information and for their influence on
postural stability and eye-head coordination.

Possible causes of altered cervical afferent input

Many mechanisms may disturb cervical afferent input in people with neck pain disorders,
particularly after neck injury (Table 6.1). Afferent information from cervical receptors
(mechanoreceptors and nociceptors) can be altered either by direct trauma or as a
consequence of impaired or adapted muscle function,47 for example, neck extensor and
scapular muscle fatigue deleteriously affect standing balance.34–37,39 Inflammatory
mediators may activate chemosensitive nerve endings in joints and muscles leading to
altered muscle spindle activity. For instance, several studies in cats show experimentally
induced, long-lasting, increased muscle spindle activity following excitation of
chemosensitive afferents in and around the cervical joint complex.48–51
TABLE 6.1

Possible Mechanisms of Disturbed Cervical Afferent Input in Neck Pain Disorders

Direct damage Functional impairment Morphological change Pain
Mechanical Altered protective muscle Changes from slow to fast twitch Muscle inhibition
disruption179,180 responses55 fibers181
Excessive joint Inhibition of deep musculature184 Fatty infiltration into muscle8,52 Increased nociceptor input185,186
loading182,183
Muscle damage187 Altered feed-forward Muscle atrophy (reduced cross- Somatosensory reorganization59–61
neuromuscular control188 sectional area)
Local ischaemia189 Increase in superficial muscle Decreased non-nociceptive
activity190,191 input186,192
Joint Altered neuromuscular Decreased primary motor cortex
inflammation193,194 efficiency195 representation54
Muscle fatigue196 Central inhibition
Sympathetic nervous system Central sensitization185
activation62,63

Morphological changes may occur in neck muscles, particularly in the suboccipital

muscles8,52,53 which could affect their proprioceptive capability. Relationships between
poor standing balance and fatty infiltrate in the rectus capitis posterior major muscle have
been demonstrated in people with chronic neck pain.53 Further, pain may affect
sensorimotor control by modulating proprioceptive input at many levels; in the periphery
(local information from mechanoreceptors), in the spinal cord and during supraspinal
control and evaluation of cervical somatosensory information.3,54 Experimentally induced
neck pain can change cervical muscle activity54–56 (including reflex activity57,58) and
muscle spindle sensitivity. Pain may have a role in subcortical and cortical reorganization
at many levels of the human somatosensory system.59–61 There is also some evidence
linking psychological stress and activation of the sympathetic nervous system, which may
affect muscle spindle activity.62 Experimental activation of the cervical sympathetic nerve
has been shown to depress cervical muscle spindle afferents in animals.63
Focus Point
Altered head and eye movement control and postural stability are evident in neck
disorders and should be considered in the examination of a patient with neck pain.
It is most probable that a combination of causes leads to an immediate, sustained
alteration in cervical afferent input, which in turn influences sensorimotor control in
individuals with neck pain disorders. The specific mechanisms for change are likely to be
different between individuals.

Symptoms of altered cervical sensorimotor control

Dizziness or, more specifically, light headedness and unsteadiness are common symptoms
associated with neck pain and disability, especially in people with chronic whiplash-
associated disorders (WAD) where the incidence is up to 75%.64–67 Visual complaints may
also occur. We explored a number of possible visual symptoms and found that light
sensitivity, needing to concentrate to read and visual fatigue were the most prevalent (>
50%) and troublesome in patients with both idiopathic and traumatic onset neck pain.68
Tinnitus may likewise be a consequence of disturbed cervical afferent input in some
patients.69–71

Signs of altered cervical sensorimotor control

Altered sensorimotor control can encompass head and eye movement control, postural
stability and coordination. Tests of head movement control primarily assess cervical
proprioception either directly or indirectly, whereas tests of postural stability, eye
movement control and coordination assess how a potential disturbance of cervical afferent
information may have indirectly influenced each of these areas. Changes in sensorimotor
control seem to occur to a greater extent in persons with neck pain of traumatic origin and
in those complaining of dizziness. The presence of symptoms probably reflects a greater
disturbance to cervical afferent input. Nevertheless, signs of altered sensorimotor control
can be present in persons with neck pain of insidious onset and in some patients who do
not specifically complain of dizziness and unsteadiness.

Cervical proprioception
Cervical proprioception is assessed traditionally by conscious tests, namely tests of
cervical position, movement and force sense.72 To date, most research on neck pain has
evaluated position and movement sense. A systematic review of these measurements and
their clinometric properties73 found that test-retest reliability for joint position sense (JPS)
was fair to excellent (Intraclass Correlation Co-efficients [ICC]: 0.35–0.87) and movement
sense, using the fly test,74 was moderate to excellent (ICC: 0.60–0.86). Both tests
demonstrated discriminant validity.

Cervical joint position sense

The measure of JPS tests a patient’s ability to relocate their head back to a natural head
posture or to a predetermined target while vision is occluded.19,73,75,76 There is now
consistent evidence that JPS can be impaired in persons with neck pain regardless of the
aetiology.77,78 Evidence suggests that patients with greater pain, a traumatic onset of neck
pain and symptoms of dizziness have poorer JPS.67,79–82
JPS testing is used as a measure of cervical proprioception, but deficits in JPS can be
observed in association with vestibular pathology, although not always a consistent
finding.83,84 We recently investigated a test of trunk relocation with the head held still to
stimulate cervical proprioceptors but limit vestibular involvement. Results suggested that
this test was more specific to neck proprioception.85 It has recently been used to identify
cervical proprioceptive deficits associated with concussion risk.86 These promising
outcomes encourage more research to find tests which differentiate cervical from
vestibular origins of symptoms.
Interestingly, JPS deficits may not be isolated to the neck. Proprioceptive deficits have
also been measured at the shoulder, elbow and hand in persons with neck pain.87–89 Such
deficits are reasoned to reflect altered cervical afferent input affecting the coordination and
movement of the upper limb.

Cervical movement sense or accuracy

Another measure of proprioception which tests fine control of neck movement is a test of
movement sense, that is, the accuracy to follow either a stationary or moving target.
Kristjansson and colleagues74,90 found that persons with WAD had less accuracy in tracing
a computer-generated moving pattern (the fly) when compared with both control and
idiopathic neck pain groups. Woodhouse et al.91 used a stationary movement pattern and
again found that individuals with WAD demonstrated decreased accuracy to follow the
pattern compared with idiopathic neck pain and control subjects. Sarig Bahat and
colleagues92 used a virtual environment to test accuracy to follow a moving target. The test
depicted persons with neck pain but did not discriminate between traumatic onset and
idiopathic neck pain.

Cervical force sense

Little research has been conducted to evaluate whether cervical force sense, a third
dimension of proprioception, is affected in people with neck pain. Reduced force
steadiness has been demonstrated during cervical muscle contractions especially at low
load.93,94 In addition, an inability to hold different pressure (force) levels steady in the
craniocervical flexion test is evident in persons with neck pain.95

Kinematic disturbances
Other measures that could be related to altered cervical proprioception include
disturbances in movement quality,96–98 for example, changes in movement velocity
profile.96,99,100 Velocity profile includes the mean and peak velocity of movement as well as
its smoothness and symmetry. Persons with neck pain consistently display deficits in most
elements of the velocity profile. Symmetry of motion, measured as the time to peak
velocity or the acceleration/deceleration ratio, may99 or may not101,102 be disturbed.

Vertical perception
The ability to correctly identify the true vertical, using the rod and frame test, is deemed to
be another test of cervical proprioception.103 Greater deficits have been found in
association with WAD103 whereas our study found altered vertical perception in
participants with idiopathic neck pain but not WAD.104 The measure has complexities, and
in its current form, it may not be a suitable measure of cervical proprioception.104
Sensorimotor incongruence
Sensorimotor incongruence may occur as a result of impaired cervical proprioception and
is more of an indirect measure exploring the cortical spatial representation of the body and
motor planning.105 Tests of sensorimotor incongruence are considered to assess the central
tuning or regulation of proprioceptive information. It is tested by either perception of
distorted visual feedback or judgement in laterality tasks. Participants with acute or
chronic neck pain have demonstrated sensorimotor incongruence by either experiencing
increased symptoms during a distorted arm coordination task or by having an impaired
ability to identify incongruence between true head motion and a false visual
reference.106–108 In concert with vertical perception tasks, laterality judgement tasks were
found to be impaired in idiopathic neck pain105 but not WAD.109 Indeed Richter et al.,110
found that those with WAD had better laterality judgement reaction times and similar
accuracy to controls, which they believe were strategies to compensate for altered
proprioception.

Postural stability
Disturbed postural stability includes tests of various static standing tasks under several
different conditions such as type of stance, visual and stability conditions. Dynamic
measures such as influences on gait and functional balance tasks can also reveal impaired
function.

Static measures
Disturbed postural control, commonly measured as increased sway in quiet stance, is not
uncommon in patients with neck pain, and is common in the elderly with neck pain,111–122
in patients with WAD and patients who have dizziness with their neck pain.112,122 Deficits
are demonstrated consistently in most standing tasks, namely comfortable, narrow and
tandem stances, especially when vision is occluded. Sway is usually increased in the
anterior posterior direction, which is indicative of somatosensory impairment.123
Nevertheless in more difficult tests, some patients display less sway (a stiffening
strategy).124 These static balance disturbances in all likelihood reflect cervical afferent
dysfunction rather than a disturbance of vestibular function because sway patterns are
usually different in unilateral vestibular pathology (increased sway in the medial lateral
direction).125 Persons with neck pain also fail to maintain stability for 30 seconds in the
more challenging tandem stance position more frequently than healthy
individuals.112,115,121,122 Changes in cervical muscle activity and in muscle composition may
make important contributions to altered postural stability. Relationships have been
demonstrated between poorer postural stability and increased superficial muscle
activity,126 cervical muscle fatigue127 and fatty infiltration of the suboccipital muscles.53
Although age is a factor that affects balance, we have determined that elderly subjects
with neck pain have greater balance disturbances compared with elders without neck
pain.117,128 These deficits do not appear to be associated with age-related changes in vision
or vestibular function. Rather they appear to be caused by the neck pain disorder.129 Older
patients have more profound deficits in balance than younger patients with neck pain. The
impacts on balance of normal age-related changes in vision and in the vestibular system in
addition to the impact of neck pain should be considered in assessment and management.
Recent studies have investigated the potential for adding a cervical spine bias to a
balance test to help identify balance disturbances caused by altered cervical proprioception
rather than for example, a vestibular cause. The bias was adding neck torsion to the
balance test, that is, rotating the trunk on a stationary head to rotate the neck. Neck torsion
has also been added to tests of cervical JPS85 and smooth pursuit eye movement.130 Adding
neck torsion to the balance test revealed a greater balance deficit than when the neck was
in neutral but only in persons with WAD, not in healthy controls131 and not in persons with
vestibular pathology.132 This suggests that adding torsion to a balance test may make the
test more specific to cervical-related balance deficits.
There is also interest in transforming postural sway signal into various frequency bands
in an attempt to isolate proprioceptive disturbances. Different frequency bands are thought
to represent different types of sensorimotor regulation with higher frequencies
representing proprioceptive control.118,119 Results of research to date suggest that persons
with WAD and older adults with neck pain tend to use altered strategies to maintain
balance or use low frequencies bands.118,119 Research is in its infancy at this time, but these
trends suggest that transforming postural sway signals into various frequency bands may
be useful to identify the contribution of cervical afferent dysfunction to balance
impairment in the future.

Dynamic and functional tasks

Postural control has also been investigated using functional tasks. Persons with WAD have
demonstrated significant differences in the timed 10-m walk with head turns, the step test
and tandem walk as well as delayed responses to perturbations while sitting and stepping
on the spot.133–135 Most research in the area has involved working age populations with
WAD, yet similar findings for gait speed are observed in elders with neck pain.128,136,137
This has important implications for falls assessment and prevention in the older
population, especially because neck pain has been identified as a risk factor of concern for
falling in elders.138,139

Eye movement control

Disturbances in eye movement control have been demonstrated across several types of eye
movements particularly in persons with traumatic neck pain and in those reporting
dizziness and/or visual disturbances. Control of vision can be divided into voluntary or
involuntary eye movements to stabilize, fix or shift the gaze to track or maintain focus on
visual stimuli. Gaze shift occurs when using either smooth pursuit (i.e., eye follow) to
track a slow-moving target, or by using saccadic (rapid) eye movements to rapidly change
a point of fixation. Vestibular ocular reflex, COR and OKR involuntarily move the eyes in
the opposite direction to head movement so that images remain stable during head
movements. Vergence eye movements differ. Here, each eye moves in the opposite
direction, to maintain the image on each retina when targets are at different distances.
Vergence eye movements (e.g., convergence and divergence) are used when focusing on
objects at a distance or when objects are moving towards or away from the visual field.
Vergence movements work with accommodation reflexes to change lens shape and pupil
size to allow focusing between near and far targets. Deficits in eye movement control can
lead to obvious symptoms as blurred vision, but such deficits can cause other symptoms
including visual fatigue, sensitivity to light or headache as a result of increased load on the
visual system as the individual struggles to maintain focus. It is possible that this may lead
to a vicious circle where altered visual conditions lead to secondary cervical muscle
overload and subsequent neck pain exacerbation.140,141
To date, deficits in oculomotor control such as decreased smooth pursuit velocity gain,
altered velocity and latency of saccadic eye movements, altered convergence and an
increased gain in the COR have been demonstrated in people with both insidious onset
neck pain and WAD. Nevertheless, the majority of research has been conducted on people
with WAD.130,142–151 Convergence and accommodation insufficiency and eye alignment
malfunctions occur in some individuals with either WAD,148,152 or with idiopathic neck
pain.153 In addition, abnormal cervical muscle activity during eye movements with the
head still was observed in persons with WAD when compared with control subjects,154 as
was a reduction in range of head movement during gaze fixation.155,156
An increased gain in the COR has been shown in individuals with WAD over a wide
range of neck movement velocities but especially during slower movements.145,146 This
increased gain has also been observed in persons with idiopathic neck pain,157 which
supports the theory that cervical afferent disturbance is the cause of the deficits.
Interestingly, when increased gain of the COR is observed in the elderly and in people
with vestibular pathology, it is regarded as a compensation for a decrease in the VOR
gain.158 However, this compensatory response has not been observed in WAD and may be
an important cause of disturbances to the visual system.158
Eye movement dysfunction may have prognostic value in WAD.144,159 Hildingsson and
colleagues 159 found that persons with eye movement dysfunction on smooth pursuit
and/or saccadic eye movement on initial assessment soon after the car crash continued to
have persistent disabling neck pain and disability at least 8 months postinjury. In contrast,
individuals with normal eye movement on initial assessment recovered fully or had only
minor discomfort at follow-up. It is possible that cognitive disturbance, another common
complaint after whiplash, may manifest from disturbances in sensorimotor control as a
result of abnormal cervical somatosensory input. Gimse et al.160 found a close correlation
between technical reading ability, information uptake and performance in the smooth
pursuit neck torsion test. Similarly driving skills were associated with altered eye
movement control in the absence of many other possible causes such as premorbid state
and brain injury.161

Smooth pursuit neck torsion

Because there are several potential causes of oculomotor disturbances, Tjell and
colleagues149 developed the smooth pursuit neck torsion test (SPNT) to specifically
differentiate eye movement disturbances related to altered cervical afferent input. The use
of torsion in this test was the basis for investigating the use of torsion in the JPS and
balance tests. A semiautomated analysis is used to measure the difference in smooth
pursuit eye movement control with the head and trunk in a neutral position compared with
when the trunk and neck are rotated relative to the stationary head.150 A decrease in
smooth pursuit velocity gain when the head is torsioned compared with the neutral
position is only seen in individuals with neck pain, not in those with vestibular or CNS
disorders or healthy controls.125,149,150 SPNT deficits have been found in insidious onset
neck pain particularly of upper cervical origin,162 cervical vertigo and spondylosis but
deficits are most evident in persons with WAD and in those complaining of
dizziness.130,149,150
There is some debate about the SPNT because researchers using a fully automated
analysis163–165 have not found deficits to the same extent. This may reflect the importance
of trained observers to extract the appropriate elements of the signal for analysis, by
differentiating appropriate signals from blinks, square waves and other artefacts, rather
than rely on a fully automated analysis. Alternatives have been explored. L’Heureux-
Lebeau and colleagues83 compared results with the SPNT and a test called the cervical
torsion test where they monitored nystagmus following sustained neck torsion positions to
left, neutral and the right. They found that both SPNT and nystagmus of greater than 2
degrees in any neck position was present in persons with neck pain and cervicogenic
dizziness but not in those with a peripheral vestibular disorder. The authors suggested that
the cervical torsion test might be an alternative method to the SPNT to demonstrate
cervical afferent influence on eye movement control. To date, only individuals with
cervicogenic dizziness have been studied and more research is required, particularly to
differentiate vertebral artery insufficiency from cervical afferent dysfunction in this test.
Most tests of eye movement require quantification using sophisticated equipment.
Recently, physiotherapists’ ratings of visually assessed head and eye movement control
tests (gaze stability and eye-head coordination) were evaluated. Impairments were
detected in persons with neck pain and importantly they were reliably detected in the
clinical examination.166 We recently expanded on this study and demonstrated the
suitability of assessing the SPNT by clinical observational assessment compared with
sophisticated measurement of eye movement (electro-oculography). Good agreement was
present between electro-oculography and visual observation of blinded video analysis of
the corrective saccadic eye movements.167 Adding symptom reproduction is likely to
enhance this clinical test, in a similar way to augmenting visual observation of eye
movement in concussion.168,169

Coordination
Eye-head coordination
Altered eye-head coordination has been demonstrated in a variety of tasks in patients with
neck pain. Patients with idiopathic neck pain have displayed an altered velocity profile in
an eye-head coordination task involving moving their head to look at targets as fast and
accurately as possible.170 Patients with WAD displayed decreased head velocity during
tasks of eye-head coordination and had compensatory head movements when requested to
only rotate their eyes to the left or right.156 Patients with both idiopathic neck pain and
WAD displayed reduced precision in an eye-head-hand coordination task involving fast
pointing movements to a visual target.171

Trunk-head coordination
Patients with neck pain can have impaired trunk-head coordination, that is, moving the
head and trunk independently.172 Specifically, they find it difficult to keep the head still
while moving the trunk, which potentially could be related to altered CCR reflex activity.

Onset of disturbances in sensorimotor control

Most studies investigating changes in sensorimotor control have been conducted in people
with chronic neck pain disorders. Nevertheless, reports of dizziness and disturbances in
balance, oculomotor control and JPS are found in patients in the acute phase following a
whiplash injury 82,159,173–175 and often align with poorer outcomes and with higher levels of
pain and disability. This evidence that disturbances in sensorimotor control begin early in
the history of the disorder indicates that they are not a consequence of chronic pain.
Cervical movement sense disorders in contrast, seem to develop over time, they often
persist but again do not relate specifically to other signs and symptoms such as pain and
disability of WAD.176
Focus Point
The observed changes in balance and head and eye movement control in persons with
neck pain may reflect altered somatosensory input from a variety of structures in the
cervical spine. Alterations in cervical somatosensory information in neck pain may be
arising from a number of causes including direct trauma, functional impairment or
morphological changes in the cervical muscles and the direct effects that pain has at
many levels of the nervous system. Psychosocial and or work-related stresses may also
affect cervical somatosensory function via activation of the sympathetic nervous
system.

Relationships between sensorimotor measures

Disturbed cervical somatosensory input associated with neck pain may affect postural
stability as well as head and eye movement control. A relationship between these
measures might be expected because of similar mechanisms, however correlations
between measures are not high,177,178 even within tests with similar constructs, such as tests
of cervical JPS and movement sense.178 As a consequence, a patient with neck pain may
present with disturbances to eye movement control but may not have any disturbance in
cervical JPS or postural stability. This may reflect different control strategies and physical
demands in the different tests. Thus assessment of each area is recommended. Further, the
degree of dizziness reported by the patient does not necessarily determine the outcome of
the physical measures. Although subjects with WAD complaining of dizziness appear to
have greater deficits, 50% of subjects with WAD who did not complain of dizziness were
shown to have deficits in two or more sensorimotor control tests.177 At this time it is not
known whether dizziness reflects an overall greater degree of cervical somatosensory
dysfunction or relates to more specific areas of dysfunction (Fig. 6.3).

FIG. 6.3 Impact of cervical somatosensory dysfunction on sensorimotor control.

Several peripheral mechanisms can alter mechanoreceptor function and thus cervical
somatosensory input to the sensorimotor control system. Such changes can alter the
central nervous system and subsequent descending information, which further
contributes to altered somatosensory input. Visual and vestibular input can be
indirectly affected from altered cervical somatosensory input.

There is some evidence that patients with upper cervical impairment might be more
prone to sensorimotor disturbances.162 Assessment of cervical proprioception should
always be undertaken in patients presenting with symptoms of dizziness, unsteadiness or
visual disturbances. However, patients with sensorimotor deficits may not have overt
symptoms.112 Thus assessment of cervical proprioception should also be undertaken when
patients are not responding as expected to traditional management.

Conclusion
Deficits in cervical JPS, balance and eye movement control have been demonstrated in
patients with both insidious onset and traumatic neck pain and are, in all likelihood,
reflecting disturbances in cervical somatosensory information. Cervical joint position and
movement sense, eye movement control, coordination and postural stability need to be
considered in the clinical reasoning process in patients with neck pain disorders. The lack
of direct relationships between these measures and the lack of a direct relationship to
patients’ reported pain and disability indicates that each aspect of sensorimotor function
should be assessed. The clinician should also be aware of other possible causes of
dizziness (see Chapter 10). We advocate that assessment and management be tailored
specifically to deficits in sensorimotor control. Concurrently, the potential causes of
abnormal cervical somatosensory input need to be addressed. Rehabilitation strategies to
enhance cervical proprioception, balance and eye movement control related to altered
cervical afferent input are offered in Chapter 16.

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7

Psychological and Social Considerations

in Neck Pain Disorders
The interest in psychosocial aspects of pain disorders has grown considerably over recent
decades among researchers and clinicians alike. This reflects the move across all health
professionals to consider behavioural, psychological and social dimensions in addition to
biological features in understanding an individual’s presenting pain disorder.1,2 Unhelpful
emotional, behavioural and cognitive features may influence management and prognosis.
This chapter overviews a selection of psychological and social features that have been
investigated in association with neck pain disorders, noting that it is artificial to separate
them from biological features, as embraced in the biopsychosocial model. Nociception
cannot be separated from emotions and behaviours. Likewise, emotions cannot be
separated from a range of physiological responses, for example, anxiety and increased
heart rate, stress and cortisol production. Indeed, much current research is focussing on
psychophysical interactions towards better understanding and management of neck pain
and other musculoskeletal disorders.3–7

Psychological features
Many emotions, behaviours and cognitions have been investigated in association with
neck pain disorders. Commonly, these have included psychological distress (anxiety,
depression and stress, including posttraumatic stress) as well as cognitive factors as
catastrophizing, hypervigilance, fear avoidance beliefs (kinesiophobia, fear of pain), self-
efficacy (general or pain self-efficacy) and expectations of recovery. The diverse nature of
studies makes it difficult to make general overall statements about the role of each of these
features in the presentation or prognosis of neck pain disorders.8 Neck pain populations
have differed as have the psychological features investigated. Measurement tools differ
and for some questionnaires there are no predetermined cut-off points, thus outcomes and
interpretations of findings from these instruments differ. Psychological features often
coexist and interact to moderate or mediate particular symptoms, behaviours or thoughts.
They may be risk factors for chronicity.9,10 Although recognizing these complexities, for
clarity, selected, single psychological features will be considered, acknowledging that they
frequently interact.
What is clearly evident is that there is variability in the frequency and magnitude of
adverse psychological features within and between neck pain disorders and the individuals
who present with them. For instance, two studies considering depression illustrate this
variability. In a study of patients with chronic cervical radiculopathy attending a
neurosurgery clinic, depression was not a major feature contributing to the disability or
health status. Depression together with anxiety and catastrophizing, explained only 7.6%
of the variance, and anxiety was the strongest-loading variable of the three.11 In contrast,
in a group of patients with chronic neck pain attending an interventional pain management
clinic, a greater level of depression was the strongest predictor of clinical insomnia, and
28% of the group exceeded threshold scores for symptoms of depression.12 Of note, both
groups were described as suffering a chronic neck condition on the basis of pain for longer
than 3 months. The findings not only illustrate the heterogeneity in psychological features
among patients with neck pain disorders but illustrate the inadequacy of a time-based
definition of chronicity to characterize a disorder (see Chapter 1).

Depression
Depression is commonly considered in studies of neck pain. Studies of general neck pain
populations reveal that mean scores from questionnaires for depressive symptoms or low
mood are well below threshold for depressive symptoms.6,11,13,14 Thus the majority of
individuals with neck pain (albeit not all) do not have significant depressive symptoms.
Nevertheless, the frequency and level of depressive symptoms can be higher in particular
patient groups, such as those with high pain levels relating to trauma induced neck pain
(e.g., persisting whiplash-associated disorders or other recalcitrant neck pain
disorders.10,12,15–17) It is therefore important to assess each patient on an individual basis.

Stress and anxiety

Stress and anxiety are common emotions associated with any pain, particularly in the
acute phase. A systematic review and meta-analysis confirmed these relationships across
various neck pain disorders.18 Stress was found to be more frequently associated with neck
pain than elevated anxiety, but there was insufficient evidence to support stress as a risk
factor for chronic neck pain because of the low quality of the results in the studies
reviewed at this time. Nevertheless, symptoms of posttrauma stress have been increasingly
associated with recovery and nonrecovery in persons who have sustained a whiplash
injury. Recovery trajectories have shown up to 20% of persons seeking treatment for
whiplash-associated disorders (WAD) will have persisting and significant symptoms of
posttrauma stress 12 months following the injury.19 In particular, the hyperarousal subscale
of the Posttraumatic Stress Diagnostic Scale has been shown to be one of the predictive
factors for recovery or nonrecovery following a whiplash injury.20 Symptoms such as
stress and anxiety may be the result of pain. Conversely, premorbid anxiety may increase
the risk of developing chronic pain as shown in the large longitudinal Norwegian Nord-
Trøndelag Health Study (HUNT) where preaccident baseline measures of anxiety were
available.21 Of the populations who did and did not develop a chronic WAD, 23.8% and
13.8% respectively exceeded the cut-off score for anxiety, suggesting that those
individuals with preexisting anxiety are more likely to experience prolonged suffering.
Nevertheless, anxiety levels are not necessarily high, even in individuals with chronic
WAD.22
Catastrophization
Catastrophization is an emotion in which a negative perspective is placed on situations, for
instance, believing that the neck pain or injury is far worse than it actually is and a feeling
of hopelessness about the future. Similar to other psychological features, levels of pain
catastrophization vary considerably.22,23 In several studies, pain catastrophization has been
reported to be low level with no major impact on pain or disability or treatment
outcome.11,14 Yet in another,24 catastrophizing together with higher pain severity were
found to modify treatment success, but the mean catastrophization score in this study was
well below that regarded as clinically relevant catastrophization. Although less of a feature
in idiopathic neck pain groups, higher pain catastrophization is one of the prognostic
factors for poor outcome following a whiplash injury.25 It appears to be a more frequent
feature when pain originates from trauma as in a road traffic crash.26 Higher levels of pain
catastrophization in these patients may influence the likelihood of return to work,9
although expectations for return to work partially mediate this relationship. High pain
catastrophization can be associated with depression.26,27 On a positive note,
catastrophization levels can decrease as pain decreases and function returns, even in cases
of recalcitrant WAD.14,28

Fear avoidance
Fear avoidance represents pain-related fear and anxiety causing an individual to avoid
activities, to expect increased pain and to report more disability.29,30 Fear of movement is a
very normal reaction to acute neck pain and pain-related fear-avoidance beliefs and
kinesiophobia are commonly found to be associated with neck pain disorders.11,14,31–33 Fear
of movement is one of several features that can mediate the relationship between pain
intensity and disability.34,35 As with other features, levels of avoidance and kinesiophobia
are highly variable between individuals and range from negligible to well above
threshold.36–38 Notably, fear-avoidance beliefs and kinesiophobia seem to be the most
consistent psychological feature(s) associated with neck pain disorders,14,33,39 and
unhelpful beliefs can influence outcomes.39

Patient expectations
Expectations should always be elicited from the patient in the initial interview because
they can impact on the way the clinician communicates with the patient.40 Positive and
negative patient expectations about treatment outcomes can influence (albeit varaibly)
recovery and nonrecovery respectively.41–44 There may be a direct link between an
expectation and the outcome of a treatment technique,41 but often several factors shape an
expectancy. For example, Ozegovic et al.45 found that 10 different factors had an influence
on expectations of recovery from a whiplash injury, the strongest being initial neck pain
intensity and symptoms of depression. Similarly positive and negative expectations for
return to work are shaped by several features.46 In turn, patient expectations may mediate
other associations, for example, the way in which pain catastrophizing and fear of
movement affect return-to-work outcomes after a whiplash injury.9
Self-efficacy
Self-efficacy refers to a person’s own beliefs about their ability to manage tasks and
activities, even when difficulties are present.47 Pain self-efficacy is related to the
individual’s beliefs about performing activities and tasks despite pain.48 Low self-efficacy
can directly affect neck pain and pain-related disability13,49 and work ability.50 Levels of
self-efficacy again vary quite markedly between individuals and circumstances as
reflected in dichotomous findings of relative minor to significant roles of self-efficacy in
different neck pain groups.11,49,51 Lower self-efficacy need not be a barrier to recovery as
revealed by a negative association between pain self-efficacy at baseline and
improvements in pain intensity and disability following a structured exercise
intervention.14 The authors reasoned that the professionally supported, structured exercise
program might have offered effective support and relieved the participant’s uncertainties
in performing tasks in spite of pain.

Implications for assessment and management of

psychological features
There are robust calls for consideration of various psychological features in the
assessment and management of patients with neck pain10,39,43,45 and this concurs with the
biopsychosocial model. Patients are not inanimate objects, and the experience of neck pain
will evoke various emotions, behaviours and thoughts. It is important to gain perspective
on the balance between physical and mental/psychological health across the whole
spectrum of individuals with neck pain.
A recent longitudinal study of 1100 community-based individuals with neck pain
determined that neck pain was negativity associated with physical but not mental health
related quality of life.52 When the spectrum of individuals with neck pain is considered,
the evidence suggests that it is the minority who have psychological features that are well
outside population norms or cut-off values. The scores on various questionnaires of the
studies reviewed for this chapter are frequently either well below thresholds for a certain
psychological feature or are in the mild category, implying that many patients do not have
substantive adverse emotions or behaviours. This is consistent with findings of a
prospective study of 917 patients presenting to 97 chiropractic primary care practices for
management of neck or low-back pain.53 Only a minority of patients had high scores on
psychological variables (for patients with neck pain, between <1% to 7.5% depending on
the feature measured). Furthermore psychological features had little added value (about
1%) for predicting the outcome of treatment. The authors, in consequence, counselled
against the use of extensive psychological screening tools at initial assessment.
The low incidence of persons with substantive psychological features presenting to
community-based practices does not necessarily reflect the incidence in patients with neck
pain disorders who are attending pain clinics or specialized intervention clinics12,54 In
addition, patients with persistent neck pain induced by trauma (e.g., whiplash) tend on
average, to have greater sensory, physical and psychological responses than groups with
insidious onset neck pain55 and some may have other specific issues such as perceived
injustice associated with loss and suffering.10,26 A clinical trial of management for acute
whiplash determined that general distress was one of the factors moderating neck pain and
disability at baseline through to 12 months.37 Yet, other trials of management of patients
with chronic WAD found that psychological features were not associated with
outcome.56,57 This reinforces the fact that there can be no automatic assumptions about
individual patients or conditions.
The opposite question to consider is whether treating psychological features improves
outcomes for patients with neck pain disorders. Cognitive behaviour therapy can
positively change emotions and behaviours associated with chronic musculoskeletal
pain.36,58,59 Yet, recent systematic reviews reveal that there is no strong or consistent
evidence that psychological interventions for acute or chronic neck pain or WAD make
any clinically relevant changes to neck pain and disability.60–63 Topically, recent trials
determined that the addition of cognitive behavioural therapy to an exercise program for
patients with chronic neck pain compared with exercise alone produced no superior
outcomes in neck pain and disability22,64 or disability.65 Nevertheless, in the latter trial,
more participants made clinically meaningful reductions in pain with the combined
program, and there were superior benefits in functional self-efficacy and pain-related fear.
A further trial showed no differences postintervention, but there were significant
advantages of the combined cognitive behavioural and exercise treatment at the 12 month
follow-up across pain and disability and psychological features.58 These results encourage
further work on the nature of the combined intervention as well as who delivers the
intervention. Other features such as “acceptance” are being studied for its potential role in
rehabilitation outcomes of persons with chronic neck pain.66
Currently, information about psychosocial features is rather piecemeal and tends to be
context specific for particular neck pain disorders at particular time points. Data at present
is rather disparate. The ideal would be to develop an international mega database to build
a full-bodied picture of psychological features across all domains of neck pain considering
multiple variables including: neck disorders with pain and disability of mild, moderate to
severe levels; whether neck pain is episodic or continuous; the stage of the condition;
whether neck pain is of insidious onset or traumatic onset; whether the condition is
compensable or non-compensable; whether the neck pain population is community based
or attending specialized or tertiary clinics. Most importantly, a clear picture is needed of
the incidence of “above threshold” scores within neck pain populations or preferably, the
incidence of responses indicating normal, low, moderate or severe levels for the
psychological features, which is currently unclear when population means only are
presented.
The current lack of robust epidemiological data on the incidence of psychological
features that are above normal thresholds does not detract from the need to help the patient
with neck pain resolve unhelpful emotions, behaviours and beliefs when present, possibly
even in sub-threshold levels. Variously, studies advocate the importance of addressing fear
of movement,33,39,67 catastrophization,24,68 self-efficacy,49,51 and expectations of recovery.44
Neck pain disorders are heterogeneous in nature. There is variability in the nature and
extent of emotional, behavioural and cognitive responses because there is variability in
features as pain intensity, range of movement and muscle performance. Box 7.1 offers
some factors that could be borne in mind when assessing and interpreting psychological
features in a patient with a neck pain disorder.

Box 7.1

Some factors to consider when reasoning the role of

psychological features in neck pain patients

■ Many emotional reactions are normal responses rather than abnormal behaviours
■ It is understandable that a person may be anxious when they develop
significant neck pain and they do not understand its cause. Normal
anxiety is usually time limited. A patient’s anxiety should lessen when
the clinician explains the nature of their neck disorder and the pain,
assures them of its benign nature and empowers the patient to be an
active participant in their recovery.
■ Fear of movement or activity is understandable in an acute or severe state
when, for example, a movement causes a sharp nauseating pain. There
would be grave concerns about a patient who had no respect for their
neck condition, and deliberately moved to cause themselves acute pain.
When fear of movement is a normal response to pain, movement and
activity usually return as pain resolves.37,114,115
■ The clinician must recognize when patients have unhelpful fear-
avoidance beliefs and help them to modify these beliefs because they can
be unhelpful to recovery.
■ The clinician can assist the patient quell emotional reactions through
insightful explanations, education, assurance and due empathy and
importantly, effective pain-relieving management.
■ Differentiate between emotional and behavioural responses and psychopathologies
■ The diagnosis and management of the true psychopathologies is well
beyond the scope of practice of the musculoskeletal clinician.
■ Temporary or mild low mood associated with neck pain should
reasonably resolve with assurance and as pain, activity and participation
in regular activities improve.
■ The diagnosis and management of a person with significant low mood,
suggesting clinical depression requires the expertise of a clinical
psychologist or psychiatrist.
■ Questionnaires provide information on symptoms, not a diagnosis of a
psychological disorder
■ Diagnoses of depression and a posttraumatic stress disorder, as examples,
can only be made from a clinical examination by a trained practitioner.
The scores on questionnaire only indicate the presence of symptoms.
 ■ People and neck pain disorders are characterized by their heterogeneity
■ Pain is a personal experience.
■ Psychological responses and social determinants are not uniform. How a
person perceives and reacts to a neck pain disorder is quite individual.

Social features–the work environment

Social contexts can influence both the neck pain experience and the cervical spine
disorder. Social features include aspects such as relationships with family and friends,
cultural traditions, access to health care, education, socioeconomic status, work
environment and lifestyle factors such as hobbies or recreational interests. Research has
been undertaken into most of these features, but the area of greatest activity has been in
relation to work environment. Social and psychological factors are inherently interwoven
in the work environment and this will be the focus of this section. Both will be discussed,
and biological associates will be included where relevant. Not surprisingly, each factor
contributes to greater or lesser degrees and there is great variability in circumstances and
individual features.

The changing face of work

The technological and digital revolutions are very rapidly changing the nature of work
worldwide across the spectrum of occupations. Robots can make cars and perform
complex surgical procedures. The human role has in many circumstances, evolved to a
sedentary occupation interfacing with a computer. The downside is that computer use has
been linked with an increasing prevalence of neck pain.69,70 No more than 6 hours
computer use per day is linked to risk for developing neck pain.71 In line with this, Shahidi
and colleagues6 found that 21% of workers commencing full-time office work, using a
computer 75% of the time, developed chronic neck pain within the first 12 months of
work. All work is not of a sedentary, sitting nature but there is an increased frequency of
sedentary work compounded by the rapid rise in sedentary leisure pursuits across all ages
with social media and other electronic devices. This work and lifestyle increases loads on
the neck and contributes to other health problems. It is likely that the current sedentary
nature of work and leisure, together with the aging population and possibly the need to
work longer, has contributed to neck pain joining back pain as the world’s leading cause of
years lived with a disability.72
Neck pain does not belong to any occupational category. Occupations involving
sustained neck postures or awkward neck postures, high mechanical workload, lifting in
awkward postures, working with the arms raised to, or above shoulder level, working with
the arms in sustained positions have all been associated with neck pain.73–78 Many
occupations across the spectrum of work are linked with significant neck pain including
the professions (e.g., dentists and dental assistants, laparoscopic surgeons; nurses,
ophthalmologists and optometrists, ultra-sonographers), the trades (e.g., hairdressing,
electricians, plumbers, dress makers), desk and office workers as well as craft
workers.74–77,79–83 Nevertheless, office workers appear to be particularly prone to neck
pain.69,70,84
Although various features combine to be associated with neck pain, the physical nature
of the work is one of the major risk factors.73,76,78,81,85 A clinician must thoroughly
understand the work undertaken by their patient and the physical requirements and
demands of that work. Often, modifications can be made to the work, or to how the
individual performs the work, to limit adverse strains on the neck and shoulders. Likewise,
simple preventative strategies can be helpful to break up any prolonged work activity. This
was illustrated with surgeons’ reports of lessening of pain and fatigue in the neck and
shoulder region with the inclusion of simple, targeted, stretching micro breaks within an
operative procedure.82 How easily neck pain can develop was illustrated in a longitudinal
study by Hanvold and colleagues.76 They tracked young adults over 6.5 years as they
proceeded through technical training college, apprenticeship and into the work
environment. They found that the transition from technical school to working life was
accompanied by increased neck and shoulder pain in several occupations. Time alone
increased the tendency to develop moderate to severe pain levels. It is logical to try to
prevent this predictable work-related pain onset. Prevention is the ideal and it might be
possible with the provision not only of information about ways to protect the body from
undue strains, but with the routine inclusion of supervised practice in good work technique
in technical and professional training programs of occupations where there is a known risk
of developing neck pain.

Workplace psychosocial factors and the development

of neck pain
Several social issues have been investigated around work for their association with neck
pain. Studies vary in the breadth and nature of the features measured, the occupations
investigated and the population considered. Findings, not surprisingly, differ and illustrate
the variety of psychosocial features that can potentially influence the neck pain
experience. As examples, Yang et al.86 derived data for nearly 14,000 Americans from the
2010 National Health Interview and Occupational Health Supplementary Surveys. Their
analysis indicated that workplace risk factors for neck pain included work-family
imbalance, exposure to a hostile work environment, job insecurity, non-standard work
arrangements, multiple jobs and long work hours. The large prospective Norwegian
HUNT study of 29,496 workers87 found that work stress was an independent predictor of
chronic neck pain, although more so in men than women, but poor job control was not a
risk factor. Christian et al.73 in another large population study (> 4000 workers) found that
initially the greatest social risk factor for neck pain was role conflict. Over a period of 4
years, the risk factors for the pain persisting or a new episode of neck pain developing,
were role conflict, social climate and decision control.85 Factors that also seem to be fairly
consistently associated with neck pain are high job demands and low levels of supportive
leadership (i.e., job strain).78,81 Socioeconomic circumstances seem not to be a major
factor,88 which is understandable given the variety of occupations linked with neck pain.
Factors that may protect a worker from neck pain are of particular interest in
establishing optimal work environments. These, as could be expected, are the opposite to
provocative factors. For instance, Christensen and colleagues73 found that empowering
leadership and decision control protected against neck pain. A Swedish study,89 albeit in
relation to musculoskeletal pain in general, found that less sickness leave was associated
with less stress, more support from superiors, having an influence on working hours and,
as opposed to common logic, working long and irregular hours. Certainly, prospective
studies have shown a preventative effect of higher social support in reducing the
development of neck pain.90,91 The clinician must be aware of the variables in social
features that might come into play with neck pain disorders, assess the individual patient’s
circumstances and, when in a position to do so, discuss issues with management.

Biological associates of work-related social and

psychological factors
Within the spirit of the biopsychosocial model, investigators have been considering
possible biological associates of neck pain associated with psychological and social
features. Several studies have identified perceived muscular tension as either an early sign
of musculoskeletal symptoms or a predictive factor for future neck pain.76,92,93 The feeling
of muscle tension might be a physical manifestation related to work stress, or could reflect
altered neuromuscular control via increased co-contraction of neck muscles, identified in
individuals with neck pain including office workers.94,95 There is functional coupling
between vision and the neck, thus the muscle tension perceived could reflect the effect on
neck musculature, of unfavourable visual conditions such as glare exposure.96–98 Lesser
neck extensor endurance at baseline, has also been found to be a risk factor for developing
new onset, chronic neck pain within 12 months of commencing work.6
Greater pain intensity and disability at baseline are usually strong predictors of
persisting pain or poorer outcomes.8,99 Pain mechanisms are starting to be measured in
association with other psychological or social variables to determine any influence of
changes in central nervous system processing in a worker’s pain state. Although there is
variability between studies, minor signs of widespread mechanical and cold hyperalgesia
have been found in office workers with neck pain.100 Reduced diffuse noxious inhibitory
controls or impaired endogenous pain inhibition were also found to be a predisposing
factor for neck pain in office workers.6 In addition, the level of pain experienced in
response to a physical task, termed sensitivity to movement-evoked pain, was shown to be
related to work disability level following a whiplash injury.101 The findings of these
studies are beginning to reveal the potential role of psychophysical features and highlight
the need to consider variables and their interactions within a biopsychosocial context.
An area of rapidly increasing interest in neck and low-back pain is sleeping patterns and
pain-associated sleep interference. Sleep disturbances can impact on neck pain and neck
pain can impact on sleep quality.102 Psychological features, such as low mood, may
contribute to poor sleep as may social factors, such as low support at work and imbalances
in effort and reward.12,103 Sleep disturbance is also associated with increased sick leave104
and, not surprisingly, poorer response to physical therapy treatments.105,106 Thus it is
important that patients are questioned about their sleep quality and that any sleep
disturbances or insomnia are addressed as part of pain management.

Return to work
Individuals with neck pain often continue to work (presenteeism) rather than take time off
work (absenteeism), which is opposite to many cases of low-back pain. Presenteeism,
regardless of the reason, is associated with costs in terms of lost productivity,107 as well as
social costs, for instance, straining worker relationships if extra work has to be taken on by
colleagues for a prolonged period. It appears that the costs of presenteeism may exceed
those of absenteeism when all factors are considered.108
Studies examining features associated with return to work often included cohorts of
people with either neck pain or low-back pain,99,109 and thus have obvious limitations from
physical perspectives. Yet there does appear to be commonalties in relation to individual
and social perspectives. Factors associated with a greater likelihood of return to work
include positive expectations, greater self-efficacy, active coping skills, higher education
and socioeconomic status and lower severity of pain/injury/functional disability.9,99,101,109,110
Lesser likelihood of return to work is associated with the opposite attributes. In addition,
older age, female gender, depression and higher physical work demands can mitigate
against return to work or return to full-time work.46,99,111
It is vital for the clinician to understand the work status of the patient. Some features are
nonmodifiable, such as age and gender but others are modifiable. The clinician can assist
with strategies to either improve workplace performance or facilitate return to work, with
good management methods to alleviate pain, to restore physical function and to encourage
active coping through effective self-management strategies for work and home. It seems
that such an approach is more effective, or at least as effective, as work-focused
interventions.112,113

Conclusion
Neck pain and disability can be moderated or mediated by psychological and social
factors. It is clear that the relative contributions of biological, psychological and social
features vary remarkably between and within patients depending on changing
circumstances, within and between various disorders, and in acute and persistent pain
states. Each patient must be understood as an individual and there should be no
preconceived judgements. More research is required that considers, simultaneously, the
relative contributions of a range of biological, psychological and social features, rather
consider them in relative isolation. Such research is proceeding.

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SECTION 3

Clinical Assessment
OUTLINE

Introduction
8 Clinical Assessment The Patient Interview
9 Clinical Assessment Physical Examination
10 The Differential Diagnosis of Symptoms and Signs of Sensorimotor
Control Disturbances
11 Headache The Differential Diagnosis of Cervical Musculoskeletal
Causes or Contributors
Introduction
8 CLINICAL ASSESSMENT: THE PATIENT INTERVIEW 101
9 CLINICAL ASSESSMENT: THE PHYSICAL EXAMINATION 111
10 THE DIFFERENTIAL DIAGNOSIS OF SYMPTOMS AND SIGNS OF
SENSORIMOTOR CONTROL DISTURBANCES 149
11 HEADACHE: THE DIFFERENTIAL DIAGNOSIS OF CERVICAL
MUSCULOSKELETAL CAUSES OR CONTRIBUTORS 161

This section on clinical assessment considers the interview and physical examination of
patients with neck pain disorders and emphasizes the importance of skills in clinical
reasoning. High level skills in clinical reasoning ensures an accurate interpretation of the
patient’s presenting disorder and is the basis for developing a relevant and comprehensive
patient-centred management program.
Chapters within this section have also been devoted to the differential diagnosis of
dizziness and sensorimotor control disturbances as well as the differential diagnosis of
headache. These symptoms have multiple potential causes, one of which is a cervical
musculoskeletal cause. Accurate examination is required to rule a cervical cause in or out
so that patients receive relevant care for their disorders.
8

Clinical Assessment

The Patient Interview

Skill in clinical reasoning is one of the pillars for good clinical practice. It is a constant
and ongoing process through all facets of the examination and patient management
program. Clinical reasoning in the patient interview is an intricate process that requires
integration of multiple features from many different perspectives. There are many layers
of enquiry to gain an understanding of the patient, their needs and preferences, their neck
pain disorder and how it is impacting on them personally and in their activities of daily
living and work. Information is used to propose provisional diagnoses, to direct the
physical examination, to establish patient-centred goals of treatment, to identify relevant
outcome measures and to plan management.
The clinical reasoning process is now well imbedded in physiotherapy education and
practice.1 Research is continuing in various aspects of clinical reasoning from clinician2,3
and patient management perspectives4,5 and in different practice environments.6 In this
chapter, the elements of the clinical interview of a patient with a neck pain disorder will be
outlined and desired outcomes of the interview will be discussed.

Elements of the patient interview

Patient-centred care is advocated as a best-practice model,7 in which patients are involved
in decisions about their care, and care is provided that respects and responds to their
individual preferences, needs, beliefs and treatment goals. The elements of the patient
interview begin to establish the patient-clinician relationship and provide a comprehensive
understanding of the patient, their neck pain disorder, its impact on their work and quality
of life, as well as diagnostic, physical examination and treatment directives. The reader is
referred to established texts to review the structuring of questions.1,8 Common models of
clinical reasoning are hypothetico-deductive reasoning, pattern recognition and narrative
reasoning.1 These models are not mutually exclusive and a clinician could use parts of all
three methods in their assessment. Whatever reasoning model(s) are used, there is some
assurance “when the pattern fits” or, in other words, when the mechanism of onset fits
with the nature of symptoms, when symptoms fit with the nature of physical or
participation limitations, and ultimately when the pattern of symptoms and functional
limitations fit with the findings of the physical examination. When the pattern fits, there is
greater confidence in interpretation and in constructing a management program. When the
pattern does not fit, the clinician should use hypothetico-deductive reasoning, reset and
test new hypotheses and rethink the whole case to ensure an accurate understanding of the
patient and their neck pain disorder.

Outcomes of the patient interview

There are several outcomes desired from the patient interview, and information gained
about one feature often informs several outcomes (Box 8.1). For each outcome, examples
will be given on how decisions are derived. Importantly, the patient interview directs the
physical examination. The discussion is by no means exhaustive, rather the aim is to give
some insight into the process.

Box 8.1

Patient interview
The constructs of the patient interview

■ History and temporal pattern of neck pain disorder

■ Area and quality of pain
■ Other symptoms
■ Behaviour of all symptoms; provocative, relieving postures, movements, activities
■ General wellbeing; sleep, general activity levels
■ Impact on work and social participation
■ Psychological or individual features
■ General health; medications
■ Investigations; imaging; laboratory tests
■ Patient’s expectations

Outcomes

■ Patient: good rapport and therapeutic alliance; knowledge of patient’s concerns,

needs and beliefs
■ Musculoskeletal disorder recognition
■ Red flag recognition
■ Provisional decision on pain mechanism(s)
■ Provisional decision on other symptoms
■ Knowledge of physical provocative factors, functional limitations, levels of
participation
■ Knowledge of psychological or social moderators
■ Provisional diagnosis
■ Prognostic features
 ■ Treatment goals and outcome measures

The patient-clinician rapport and collaborative

relationship
The clinical examination lays the basis for the therapeutic relationship between patient and
clinician and the importance of this initial communication cannot be overestimated.
Excellent communication is vital to the success of management. Although specific
information is required about the patient’s neck pain, the clinician should not dominate the
interview.9 Rather in the spirit of patient-centred care, clinicians should let the patient tell
their story, listen attentively, clarify points and request more detail or specific information
as required. Patients wish to be listened to, be understood and be assured that their neck
pain is acknowledged or validated.10 For instance, patients might rightfully perceive
injustice if their neck symptoms are doubted following a whiplash injury.11 They may feel
that their pain and disability has not been understood or acknowledged if the discord
between their disabling neck pain and “normal” findings x-rays is not explained well.
Likewise, statements such as: “Your pain is in your brain” can easily be misinterpreted
leaving the patient quite distressed, thinking that the clinician feels their pain is “in their
head”.
Engaging with the patient, demonstrating empathy, interest and friendliness are
important clinician attributes.12 As the patient tells their story, the clinician must listen and
interpret the meaning of the information towards making clinical decisions. When
focusing on gaining specific information, the clinician must be mindful not to ignore or
fail to respond to any concerns or fears that the patient may express.13 Sensitivity to
patients’ concerns and needs works towards developing a successful collaborative
relationship.

Musculoskeletal disorder recognition

Neck pain is a symptom of various origins. Even though musculoskeletal causes or
“mechanical neck pain” is by far the most common, neck pain can also be a symptom of
non-musculoskeletal sources. A primary outcome of the initial examination is to be
assured that the patient is presenting with a musculoskeletal disorder. Even though
presentations and pain syndromes may be complex in some patients, initial basic
assurance can be gained if pain is felt in the posterior neck region (with or without spread
to neighbouring areas) and symptoms have familiar patterns of being aggravated or eased
with neck movements and postures. Likewise, a clear understanding of history of onset
and its relation to adverse mechanical loading whether insidious onset (postures or
activities) or trauma (minor or major) adds to the picture of a musculoskeletal disorder.
Neck pain disorders are often recurrent, and it is important to understand the pattern or
temporal behaviour of this recurrence and provocative features. There is usually a familiar
pattern of exacerbations and remissions. The clinician needs to beware when histories of
onset do not fit a familiar pattern. Thus in the patient interview, the clinician must listen
for a history, presenting features and behaviours of symptoms that are consistent with a
“mechanical” cervical musculoskeletal disorder.

Red flag recognition

Recognition of unusual histories, symptoms or symptom behaviours is essential to identify
any potential “red flags” that may indicate either serious underlying musculoskeletal
pathology (e.g., a fracture) or non-musculoskeletal pathologies. Fractures must be
considered in cases of neck trauma especially in older persons or when there is a
dangerous injuring mechanism and when neurological signs are present.14 Red flag
pathologies do occur in the cervical spine but are relatively rare. Nevertheless the cervical
spine can be the site of primary tumours and metastases,15,16 but these are not common in
patients presenting primarily with posterior neck pain without other neurological or
systemic symptoms.17 Clinicians are very aware of the potentially devastating
consequences of a vertebral or carotid arterial dissection. Recent onset, moderate to severe
unusual headache or neck pain that is progressing, a history of transient neurological
symptoms and recent exposure to infection or even minor head/neck trauma should alert
the clinician to possible arterial dissection.18,19 The neck can also be a site of referred
visceral pain. Cardiac pain may be felt in the anterior neck region.20 Immediate referral for
medical investigation is mandatory when there is any indication or suspicion of serious
underlying pathology and the pattern does not fit a musculoskeletal disorder.
Vertebral and ligament anomalies of the upper cervical spine are well documented in
congenital conditions such as Down syndrome.21 Children presenting with acute torticollis
(wry neck) may require referral for radiology because imaging is necessary to confirm or
rule out atlanto-axial rotary fixation.22 Atlanto-axial rotary fixation is not common but can
occur spontaneously after trivial trauma. It also might occur secondary to ligamentous
laxity and inflammation following infection (e.g., tonsillitis) or head or neck surgery (e.g.,
adeno-tonsillectomy) (Grisel syndrome). Atlanto-axial rotary fixation is usually treated
conservatively, but on occasions surgical fixation is required.23

Conditions requiring caution

Some neurological and rheumatological conditions do not negate physiotherapy
management but require due care. As examples, cervical dystonia has many causes and is
characterized by abnormal head posture, involuntary muscle contractions of the neck
muscles (which causes abnormal movements) and awkward posture of the head and neck.
Neck pain may be a feature. First-line treatment is usually botulinum toxin type A
injections but other methods (electromyography biofeedback training, muscular
elongation, postural exercises and electrotherapy) can be helpful adjunct treatments.24
Neck pain can present in inflammatory arthropathies, such as rheumatoid arthritis or
ankylosing spondylitis.25,26 Upper cervical involvement is not uncommon in rheumatoid
arthritis and may result in atlanto-axial subluxation. Such conditions require that any
treatment proceed with due safety.
Questions are also asked about the patient’s general health, medications and any
relevant surgical or medical history to seek any comorbidities or other considerations that
require proper regard and care when management plans for the neck disorder are
developed.

Provisional decision on pain mechanism(s)

The patient is asked to describe many aspects of their pain to provide information on its
distribution, intensity and quality, how it reacts to movements and postures, its general
pattern over 24 hours and history of onset. This information has several functions
including an initial estimate of the pain severity and the possible regional source of pain
(upper, mid, lower cervical region). An important interpretation relates to pain
mechanisms (nociceptive, inflammatory, neuropathic, peripheral and central nervous
system sensitization). Pain mechanisms (Chapter 2) inform assessment. For instance, the
presence of severe pain and pain with associated central sensitization indicates caution in
the physical examination because pain may be easily exacerbated. Central sensitization
may occur in any condition. It is not uniquely associated with chronic pain and can be
present in acute pain states.27 It is more prevalent following trauma and is present in a
small proportion of patients with whiplash-associated disorders (WAD) and in patients
with cervical radiculopathy.28 It is rarely found in patients with idiopathic neck pain.29
The clinician listens for pain descriptors and behaviours, which help to characterize
each pain mechanism. Nociceptive pain is suspected with reports of local pain in the neck
shoulder region (there may be referral into the arm and/or thorax), the pain in any 24 hours
is intermittent or a continuous dull ache often interspersed with sharp pains. There is a
typical mechanical pattern with movements and postures aggravating and easing
symptoms.30 Inflammatory pain is considered in association with nociceptive pain
especially when there is pronounced or prolonged aching with or following activity.
Peripheral neuropathic pain is present in cervical radiculopathy. The pain is referred
usually, but not always, into the arm in a dermatomal distribution. The quality is a sharp
shooting pain or a burning pain, it is often relentless and difficult to obtain relief. There
may be other sensations such as pins and needles or numbness.31
Peripheral and central nervous system sensitization is suspected when there is a wider
spread of pain and allodynia and hyperalgesia (mechanical, thermal) are present. There is
often marked pain sensitivity to movement and once pain is aggravated, it may take hours
to subside.
Multiple mechanisms may be present simultaneously in a patient’s neck pain disorder,
for example, local neck pain on movement (nociceptive) in the presence of a cervical
radiculopathy (neuropathic). Local nociceptive pain, neuropathic pain and central
sensitization may present in patients with moderate to severe pain in both acute and
chronic WAD.27,32 In cervicogenic headache, there is nociception from local joint
dysfunction (C0–1, C1–2 or C2–3) although it is thought that the headache reflects a
rostral neuraxial spread of central sensitization to the trigeminocervical nucleus.33
Provisional decision on other symptoms
Sensorimotor disturbances
There is a variety of symptoms other than pain that may accompany neck pain disorders.
These include symptoms of light headedness or dizziness, unsteadiness, visual
disturbances and cognitive deficits such as decreased concentration. They are frequently
associated with impaired cervical sensorimotor control when closely related to neck pain.
Nevertheless, dizziness is a common symptom and can be associated with a mild brain
injury in traumatic origin neck pain (motor vehicle crash, concussion in a sporting injury),
a central or peripheral vestibular disorder or vascular disorders (such as vertebral artery
insufficiency or cervical arterial dissection). The origins and differential diagnoses of
these symptoms are explored in detail in Chapters 6 and 10. The clinician must carefully
elicit the nature and behaviour of presenting symptoms to provisionally decide on their
possible source as well as direct further physical examination.

Sleep
Fatigue is another symptom state and patients’ sleep patterns should be explored routinely
in questions concerning general wellbeing. The role of poor sleep is receiving extensive
interest in relation to musculoskeletal pain states. There is evidence to indicate that
persons with neck pain who report poor sleep quality are less likely to respond to
treatment than those with good sleep quality.34,35 Poor sleep quality may not only affect
neck health but general health.36 In patients with chronic neck pain receiving
interventional pain management, greater levels of depression were linked with clinical
insomnia.37 If patients report problems with sleep, the relationship between poor sleep
quality and neck pain needs to be explored because neck pain may be contributing to
interruption of sleep or conversely a sleep disorder may be adversely affecting the neck
pain condition. Improving sleep should become an important aspect of overall patient
management and referral to an appropriate specialist may be required especially if the
patient has a primary sleep disorder.

Knowledge of physical provocative factors and

functional limitations
Understanding which movements, postures or activities aggravate as well as ease
symptoms informs on several factors. One, as mentioned, is pain mechanisms, another is
which movement directions, forces or loads are not being tolerated by the structures of the
cervical region. A third is to inform on meaningful outcomes by which the impact of
interventions can be determined. Box 8.2 gives examples of provocative factors and
possible interpretations, which in turn begin to direct the physical examination and what
findings might be expected. If the expected findings are confirmed in the physical
examination, then clinical reasoning is accurate and importantly, “the pattern fits”. It is of
equal value to understand what postures, movements and activities ease symptoms. This
information can contribute to physical diagnosis and provides material to help patients
problem solve on neck care.

Box 8.2

Possible interpretations of provocative factor

1. Neck pain when looking down reading or using a device for a prolonged period
■ adverse strain on posterior elements, compression of anterior elements
■ neck extensor endurance inadequate for the task
2. Catching pain, suboccipital region on quick turning, (e.g., driving)
■ C1–2 dysfunction
■ poor movement sense
3. Neck pain and later headache develops with prolonged computer use
■ adverse loading and dysfunction upper cervical joints
■ poor control of posture
■ poor endurance of deep neck flexors
■ poor scapular muscle control
4. Looking up causes neck pain and light headedness, unsteadiness
■ upper cervical joint dysfunction
■ poor control and strength of neck flexors
■ poor sensorimotor function – proprioception, balance
■ rule out Vertebrobasilar insufficiency (VBI)
5. Carrying bags of groceries increases neck pain
■ excessive compressive loads on cervical joints
■ poor scapular muscle control
■ poor neck flexor and extensor control
■ adverse load on the brachial plexus
6. Neck and arm pain on reaching backwards
■ adverse strain on neural tissues
■ adverse loading on cervical joints
■ adverse strain on glenohumeral joint

The history should provide a clear understanding of movements, functional activities

and work practices that might be possible sources of adverse strains contributing to the
development of the neck pain disorder.38 Health care is often reactive and the focus is on
the acute episode rather than being concerned with the bigger picture. The bigger picture
is that neck pain is a recurrent disorder and perpetuation of any adverse strains from work
or recreational postures and practices must be addressed if there is any possibility to lessen
recurrences and slow progression of the neck disorder. An important management
outcome will be to successfully reduce adverse strains and achieve more suitable work or
recreational practices towards a concerted and comprehensive rehabilitation effort to
manage the disorder in the long term.
The clinician must not only understand which features aggravate neck pain but have a
full appreciation of the impact of the condition on a patient’s participation in work,
activities of daily living and recreation. Has the patient withdrawn, reduced or modified
their work or general activities as a result of their neck pain disorder? Likewise, what are
their expectations regarding return to former participation levels? Both the clinician and
the patient should discuss whether expectations are a realistic outcome goal.

Knowledge of psychological or social moderators

There are several emotions that may be associated with a neck pain disorder. Listening to
the patient is important as what a clinician believes will be psychological
features/concerns does not always match the patient’s actual concerns.39 Clinicians must
be mindful that many emotions are normal and reasonable behaviours for a person who is
experiencing a neck pain disorder, especially in the early stages. “Pathologizing” patient’s
emotions must be avoided.40 Labelling normal behaviours as maladaptive can be harmful
for the patient and counterproductive to good rehabilitation.41
There are abundant psychological questionnaires available to provide indications of
various emotional states. They have been used extensively in research to better understand
the moderating role of psychological features on treatment effectiveness and prognosis.
Nevertheless, the extensive use of these questionnaires in clinical trials and prognostic
studies should not be misunderstood as endorsing their routine use in everyday clinical
practice. Rather, psychological questionnaires should be used judiciously, and not
routinely especially in initial consultations. The clinician should carefully consider if and
when their use is indicated as well as the timing of their use. Psychological questionnaires
have limitations and are not diagnostic. Inappropriate use and interpretation of
questionnaires can lead to a poor service for the patient.40,41
Some patients may have unhelpful emotions and beliefs that can hinder/moderate their
recovery from the neck pain disorder but better therapeutic alliances are likely to result if
the clinician focusses on listening to and understanding the patient, their condition and
their beliefs in the first instance.41 Hearing how the patient describes their condition, if
they are guarding their necks, how neck pain is affecting their work, how they are coping
at work and home as well as asking questions about any concerns, their expectancies of
treatments and outcome goals provides the clinician with an initial sound insight into
patient’s anxieties, fears, mood and coping skills. Initial patient management can be
designed and implemented on this knowledge. In addition, when patients consult a
clinician for treatment of their neck pain, they have an expectation of receiving advice,
hands-on physical examination and treatment and exercise, that is, physical therapies. If,
with this expectation, patients are suddenly confronted with questionnaires probing them
about their psychological state, they may well react with thoughts of: “I have come to
have my neck treated, not my head”. Therapeutic relationships can be irrevocably harmed,
and patients may not be assured that their neck pain is acknowledged.10
If at a later stage in treatment, patients are not progressing as expected and the clinician
is concerned that psychological features such as depression, an anxiety state, posttraumatic
stress or a personal trait are adversely moderating symptoms and hindering recovery, the
clinician can explain their concerns to the patient and, in context, ask them to complete a
relevant questionnaire to allay or confirm the clinician’s concerns. This lays a cooperative
basis for managing emotional features that might influence recovery, with the help of the
clinician or other appropriate practitioner.

Provisional diagnosis
Patients desire a diagnosis so they understand “what is wrong” with their neck, and
clinicians require a diagnosis to implement an appropriate treatment program.
Physiotherapists make a diagnosis based on presenting symptoms, functional limitations,
movement dysfunctions and pathophysiological processes to direct their management (i.e.,
pain mechanisms, impaired kinematics, impaired neuromuscular and sensorimotor
control).
Pathological or pathoanatomic diagnoses are discouraged in many quarters, but this
“blanket ban” could be questioned. The terms nonspecific neck pain or nonspecific low-
back pain have been adopted to express a limited understanding of the pathological source
of pain in a patient presenting with spinal pain especially because radiological imaging
often cannot identify a lesion of proven relevance, and clinical tests are not sensitive or
specific enough to define a pathoanatomic lesion. The adoption of the biopsychosocial
model may have suppressed research in investigations into pathology as an important
component of the spinal pain experience;42 as possibly, have opinions that peripheral
nociception automatically ceases after the usual time for tissue healing has passed. Indeed,
there have been increasing calls to put the “bio” back into the biopsychosocial model in
both neck pain and low-back pain.42–44
Pathological processes do occur in particular anatomic structures in the generation of
neck pain as noted in painful extremity disorders. Lesions in discs, zygapophysial joints,
ligaments and bone can result from injury.45 Some research is proceeding to understand the
relationships between structural change and neck pain.46,47 Medical interventional
management, whether surgery or radiofrequency neurotomies, relies on accurately
identifying the anatomic source of symptoms. Surgery relies on a clinical presentation
which is complemented by radiological identification of pathoanatomy such as lateral
canal stenosis from a disc fragment or osteophyte. Neither plain x-rays nor clinical tests
can identify lesser pathologies, but clinical examination methods can reliably detect a
segmental source of symptoms when present. The flexion rotation test has proven validity
to identify C1–-2 segmental dysfunction.48,49 Manual examination can identify a
symptomatic zygapophysial joint and its accuracy has been proven against anaesthetic
blocks.50–52 Manual examination may also be able to determine painful central joint
(discal) dysfunction when present, but this has not been tested because there is no gold
standard on which it can be judged.
Clinical tests cannot provide a pathoanatomic diagnosis but an argument can be put for
the value of a basic segmental diagnosis to complement the physical diagnosis of
pathophysiological mechanisms. A clinical examination of the cervical region, which
includes a skilled manual examination, can provide at the least a basic diagnosis of painful
facet (zygapophysial) joint dysfunction or possibly central joint (discal) dysfunction as
relevant. This is valuable from several perspectives. First, it can direct local active and
passive management techniques and guide advice on management. Second, manual
examination can assist to determine pain processes (e.g., the presence or not of a
peripheral nociceptive source of pain). Third, it can inform on the extent to which the
cervical spine is involved in complaints such as headache and dizziness by determining
the presence or not of cervical segmental dysfunction and if present, matching the severity
of the symptoms with the degree of dysfunction (i.e., does the pattern fit). Fourth, the
manual skill to examine the neck and accurately identify the symptomatic segment is
invaluable in cost-effective diagnostic screening for anaesthetic blocks or radiofrequency
neurotomies for cervical zygapophysial pain.53,54 Fifth, patients desire a diagnosis, and
nonspecific neck pain is an unsatisfactory label and does not necessarily validate their
neck pain with some form of tangible evidence.10 Eliciting symptomatic joint dysfunction
with manual examination effectively serves this purpose and provides a very basic
diagnosis that the clinician can discuss with the patient.

Prognostic features
Prognosis is a key component of clinical decision making. Knowing which features
indicate a good, fair or poor prognosis helps in understanding the possible course of a
patient’s complaint. It may also help in deciding who requires more in-depth
investigations and targeted intervention in the early stages to potentially influence
prognosis and prevent a transition to a recurrent or persistent pain state. Knowledge of
features consistently indicating a good, fair or poor prognosis is far from absolute. Many
features have been researched and at this stage many of the predictors identified have low
or very low confidence or have inconclusive predictive value. More research is required to
confirm or discard them as important features.55 Perhaps not unexpectedly, different
features are nominated depending on whether occupational neck pain, whiplash-induced
neck pain or nontraumatic neck pain is being investigated.55–60
There is little evidence as yet of the benefits of making decisions about management of
neck pain based on prognostic indicators. A challenge is that many prognostic features are
not modifiable, for instance, being female or having a previous history of neck pain.58,61
High initial neck pain intensity and high disability are two factors with high confidence to
foreshadow a poor prognosis. Yet at present, there is a lack of evidence and consensus on
effective pharmacological management of severe musculoskeletal pain. Likewise, every
person with high initial pain intensity does not have a poor prognosis, some recover well
as we have identified in our clinical trials.62
Prognostic studies are important, and more research is required to document features in
which there can be strong confidence. Likewise, research is necessary to determine any
benefit of targeted intervention based on prognostic features that might help meet the great
challenge of preventing transition from an acute state to a recurrent or persistent pain state.

Treatment goals and outcome measures

Goal setting is an important component of patient-centred care.63,64 Active engagement of
the patient in goal setting and management planning is considered to promote compliance
and to facilitate ongoing self-management or maintenance programs, which is so
important with the recurrent nature of neck pain disorders.65 Goal setting takes place
initially after the patient interview and physical examination. A helpful outcome measure
that can be an initial basis for discussing goal setting is the Patient Specific Functional
Scale (PSFS) where the patient nominates and rates the functions with which they are
having difficulty.66 The scale can be used to set and evaluate progress in achieving goal.
Goals should focus on activity and participation and it is often helpful to set and attain
progressive goals to reach a desired outcome.
In tandem, a clear set of outcomes should be established at the conclusion of the
interview that will capture, as relevant to the individual patient and their goals, changes in
symptoms, physical functioning, psychological functioning as well as work and social
participation. There are several well-established measures that the clinician can use,
including measures of pain intensity (numerical rating scale), the PSFS,66 the Neck
Disability Index67 and a less used, but region-specific questionnaire, the Pictorial Fear of
Activity Scale-Cervical.68 Other outcomes and goals depend on patient circumstances and
could be, for instance, related to dizziness severity and its impact on function (Dizziness
Handicap Inventory),69 fatigue, posttraumatic stress symptoms, return to customary
participation levels or return to work. Carroll and colleagues70 confirmed the value of a
simple single outcome question: “How well are you recovering?” to obtain a brief overall
assessment of recovery especially of patients with longer recovery periods as with some
persons with WAD. Recovery was rated using six response options from “all better” to
“getting much worse”. Outcome measures must be as patient specific as possible and
capable of measuring relevant clinical change.

Conclusion
An effective and quality patient interview fulfils several principal functions. It begins to
establish the important patient-clinician relationship. It allows the patient to tell their story
and express any concerns. It provides the clinician with a comprehensive understanding of
the patient and the neck pain disorder on which they can plan the physical examination as
well as begin to plan management strategies. The patient and clinician, as part of this
initial communication, should be beginning to discuss expectancies and goals of
management to have a clear pathway of rehabilitation.

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9

Clinical Assessment

Physical Examination
The physical examination of the patient with a neck pain disorder includes a local and
regional examination. There is an interdependency in posture and motion between the
different regions of the cervical spine, as well as between the cervical, thoracic,
craniomandibular and shoulder girdle regions.
The clinical reasoning process continues in the physical examination. The hypotheses
formed from the patient interview are tested and are either accepted or rejected and
reformulated. The desired outcomes of the physical examination are: (1) a physical
diagnosis that identifies the source of symptoms, confirms pain mechanisms and defines
associated impairments in the sensory, articular, nervous, neuromuscular and sensorimotor
systems; (2) a functional diagnosis which defines how postures, movement and activity
immediately aggravate or relieve neck pain; (3) a practical understanding of how work
practices, the work environment, sport or functional activity could be contributing to the
disorder; (4) clear directions for the development of a management program, (5) a suite of
appropriate outcome measures on which to evaluate and progress treatment.
Sound clinical reasoning throughout the physical examination is paramount for good
decision making. Normal variations from an ideal posture are common and there is
variability in cervical range of movement and muscle strength between healthy
individuals. Thus the relevance of findings to the patient’s neck pain condition must
always be considered. An indicator of relevance that is commonly used is “reproduction of
the patient’s pain” on a particular test. At a deeper level, relevance is evident when a clear
pattern emerges between the patient’s presenting complaint, the aggravating features and
findings from the physical examination. No decision can or should be made on single or
isolated findings. Presentation of a single, isolated impairment is not the nature of
musculoskeletal disorders. The questions: ”Is a pattern present?” or “Does the pattern fit?”
should be foremost in the clinician’s thoughts.
The physical examination is a continual process of evaluation, intervention,
reevaluation and reflection.1 Patient-centred outcome measures such as estimates of
symptom change on a numeric rating scale or changes in scores on the Patient Specific
Functional Scale2,3 are important and relevant. However, symptom resolution does not
mean that the impairments contributing to those symptoms have resolved automatically.4–6
It is essential to derive a suite of outcome measures from the physical examination
relevant to patients’ symptoms and functional complaints, when aims of management are
not just symptom relief but to rehabilitate the person’s neck pain disorder. Such a suite of
outcome measures also directs treatment progression and dosage, as well as providing
target goals for the patient, which can offer incentives for compliance with self-
management programs.
On the theme of incentives for compliance with self-management, the physical
examination is an excellent opportunity for patient education. Demonstrating the link
between symptoms and functional complaints, such as a poor posture, altered movement
or muscle function, is a powerful tool in helping the patient both understand their
condition and the treatment rationale. Showing how a change in a static or functional
posture can decrease their neck pain is a convincing lesson. It provides the basis for a
change in behaviour (e.g., how they sit or work) as well as highlighting the need for their
participation in a self-management program to address the features that may be
contributing, or perpetuating, to their neck pain.
In this chapter, we present a comprehensive physical examination of the cervical region,
which considers postural analysis and examination of articular, nervous, neuromuscular
and sensorimotor systems as well as consideration of adjacent regions as necessary. An
order for testing is suggested (Table 9.1). It avoids excess positional changes for the
patient and importantly, it facilitates understanding of how findings of different elements
may interact. The examination will be presented in this order, but the order can be
changed depending on the patient’s presentation and the clinician’s line of reasoning.
Although the examination proforma is comprehensive, in practice, the information gained
from the patient interview should guide the direction of the physical examination. Not all
tests are relevant or necessary for all patients. Clinicians should prioritize examination
procedures as part of the clinical reasoning process, matching the physical examination to
the patient’s complaint and most importantly, then matching the examination findings to a
meaningful management approach. Case examples are presented in Chapter 18 to
demonstrate this process.
TABLE 9.1

Scheme for a comprehensive examination of the cervical region

Position Assessment
Standing, sitting
Patient reported provocative movement or posture
Postural analysis

Sitting
Postural analysis
Analysis of active range of motion
Assessment of cardinal planes of motion
Movement speed and velocity profile
Movement tests to further direct management
Movement diagnostic tests
Positional tests for vertebral artery insufficiency

Supine
Sensory testing and pain mechanisms
Examination of the nervous system
Clinical neurological examination
Tests of nerve tissue mechanosensitivity
Nerve palpation
Manual examination
Passive physiological intervertebral movements
Craniocervical ligament tests

Prone
Manual examination
Posteroanterior glides
Muscle tests
Scapular muscle tests

Supine
Scapular muscle tests
Craniocervical flexion test
Neck flexor strength and endurance

Four-point kneeling
Neck extensor tests
Neck extensor strength and endurance

Sensorimotor tests
Cervical position and movement sense
Cervical position sense
Cervical movement sense
Standing balance
Oculomotor assessment
Gaze stability
Eye follow: smooth pursuit neck torsion
Eye-head coordination; trunk-head coordination

Analysis of provocative movement or posture

One of the most patient-centred and relevant analyses in the physical examination is the
analysis of the posture, movement or activity that the patient reports is provocative of their
symptoms. Such an analysis often reveals the heart of the problem and leads the clinician
to other tests. Fig. 9.1 presents examples of a possible analysis of a patient’s provocative
activity and illustrates initial clinical reasoning in the physical examination, including first
thoughts on possible management options. This analysis often guides the direction of
further examination, making it relevant to the patient’s presentation. Placing first priority
on the analysis of the patient’s nominated provocative activity is not only a crucial
examination strategy, but it also assures the patient that the clinician is listening and
hearing their concerns and giving them significance in examination and management. The
patient’s nominated activity also becomes an outcome measure.

FIG. 9.1 Example of clinical reasoning of a patient’s provocative activity. CCFT,

Craniocervical flexion test; O/E, on examination; Tx, treatment.

Analysis of posture
The forward head posture (FHP) has traditionally received attention as the adverse
postural position in neck pain disorders. The FHP places the upper cervical spine in
extension and flexes the lower cervical region. In tandem, modelling has confirmed that a
FHP is associated with shortness of the suboccipital extensors and lengthening of the
longus capitis, multifidus and semispinalis cervicis.7 The FHP is usually associated with a
greater thoracic or cervicothoracic kyphosis8,9 and reduced cervical range of motion.9,10
However, not all patients with neck pain disorders have a FHP and the strength of its
association is debatable.8,11–13 Although initial observation of posture may be undertaken in
standing, it is important that the head and neck posture is assessed in sitting, particularly
when patients nominate activities in sitting as aggravating their disorder. People without a
FHP in standing often display a FHP when sitting.14 The adoption of a FHP in sitting
seems to be the major problem as verified in several studies of neck pain patients
undertaking computer work.14–17 Pertinently, a slouched FHP is associated with higher
neck extensor activity (and load on cervical structures).18 As a positive point,
rehabilitation of a patient’s habitual FHP posture has a better chance of success than trying
to change a fixed or structural posture.
Other postures may be problematic. The head flexed posture has likewise been
associated with neck pain especially in this era of technology with prolific use of various
mobile handheld devices.19 In the flexed posture, the mechanical demand on extensor
muscles increases 3 to 5 times.20 A posture that does not seem to necessarily relate to neck
pain is a radiological measure of a straightened or even slightly kyphotic cervical curve.
Lordotic, straight and kyphotic cervical curves have all been measured in healthy men,
women and children.21,22
Spinal posture is analyzed in standing by judging the posture of the lumbopelvic region,
the shape of the thoracic and cervical spinal curves, the position of the head and shoulder
girdle. Aberrant postures (e.g., a poor scapular or thoracic posture) may be immediately
modified to determine if correction lessens symptoms. Posture is then assessed in
unsupported sitting. The patient may sit with the lumbopelvic region and spine in the
preferred neutral position or they may sit in an undesirable extended or, conversely and
commonly, a slumped or flexed posture. The patient is asked to sit in what they consider a
perfect posture. The better strategy to observe is the pelvis rolling up into a neutral
position restoring the normal lumbar lordosis (with evident use of the lumbar multifidus).
The kyphosis forms in the thoracic region and there is a neutral head on neck posture. It is
undesirable when an upright posture is gained with dominant use of the thoracolumbar
extensors, and the lordosis forms in the thoracolumbar or the lower thoracic region while
the lumbopelvic region remains in a flexed position.23 This pattern of correction is
considered to signify a poor pattern of control in the lumbar region.24
Scapular posture is observed. The “ideal” scapular posture is such that the superior
angles are level with the T2 or T3 spinous process, the spines of the scapulae are level
with the T3 or T4 spinous process and the inferior angles are level with the T7–9 spinous
process.25 The spine of the scapulae and clavicles have a slight superolateral orientation
and the scapulae sit flush against the chest wall in both the sagittal and transverse planes.
Variations in scapular orientation and asymmetries are common and are often seen in
asymptomatic people. Common observations in people with neck pain, often in
combinations, include a downward scapular rotation, scapular protraction, winging of the
medial border (excessive internal scapular rotation) or a prominence of the inferior angle
(excessive anterior tilt). Change in orientation may indicate dysfunction in scapular
muscles and thus scapular position is observed in association with changes in muscle
form. Overactivity or altered resting tone of muscles, such as the levator scapulae,
rhomboids and pectoralis minor may be implicated in a downwardly rotated and
protracted scapular position in association with impaired activity in the tripartite trapezius
and serratus anterior muscles. An elevated scapular position might reflect shortness in the
upper trapezius, but it may be a posture protective of mechanosensitive nerve tissue. In the
latter case, the scapula appears to be held in a raised position. It is associated with a
“thickening” appearance of the anterior scalene muscle or an apparent subtle lateral shift
of the mid to lower cervical region (towards the side of the mechanosensitivity). The
initial interpretation of a protective posture is later confirmed with neurodynamic tests
(see subsequent section). When changes in scapular posture are protective of nerve
mechanosensitivity, attempts to correct it may aggravate symptoms. In this case, attention
to scapular posture correction is delayed until the nerve mechanosensitivity has been
addressed.
 There is considerable individual variation in spinal posture and positions of the
scapulae. Thus it is necessary to investigate the relevance of any spinal or scapular
postural variation to the patient’s presenting neck pain. The relevance is gauged by
determining any difference in neck pain and range of cervical rotation when tested in the
patient’s natural posture compared with a corrected postural position (Fig. 9.2A–C).
Cervical rotation is the movement direction chosen for testing because it is affected by
both an FHP 9,10 and the length of axioscapular muscles.26,27 A working interpretation is
made from the outcome that may help to direct treatment. Alternatives are that correction
of posture (spinal or scapular) results in the following.

FIG. 9.2 (A) Spinal and scapular posture is assessed in sitting. The patient is
requested to rotate their head to each side. The clinician notes the range and any pain
provoked. (B) Facilitation of spinal posture. An upright neutral spinal posture is
facilitated by the clinician with manual guidance through L5 and the lumbopelvic
region. Cervical rotation is then reassessed to both directions in the upright neutral
spinal posture and any change in range and pain is noted. (C)Testing the effect of
positioning the scapula in a neutral position. Scapular posture is observed. Each
scapula is then positioned manually so that the scapula sits flush on the chest wall
(neutral position). The clinician notes the movement corrections necessary to achieve
this neutral scapular posture as these will inform the postural correction strategy in
management. Cervical rotation is reassessed to both directions in the corrected
scapular posture and any change in range and pain is noted. Scapular correction is
performed on both sides.

■ A marked reduction in pain and increase in range of cervical rotation.

Interpretation: poor spinal and/or scapular posture is adversely
loading cervical structures; it is a significant contributor to the
neck pain disorder; segmental joint pain may be a consequence
of this adverse loading.
Implication for management: train a neutral posture (1) to
decrease cervical segmental loading and pain; (2) as an exercise
for the deep cervical flexors and/or axioscapular postural
muscles (see Chapter 15).
■ A slight reduction in pain and slight increase in range of cervical
 rotation
Interpretation: poor spinal and/or scapular posture is a part
contributor to the neck pain disorder. It is probable that other
factors (e.g., painful segmental dysfunction) are also relevant to
the disorder.
Implication for management: train a neutral posture (1) to
decrease cervical segmental loading and pain and (2) as an
exercise for the deep cervical flexors and/or axioscapular
postural muscles.
■ No reduction in pain and no increase in range of cervical rotation
Interpretation: poor spinal/scapular posture has little or no direct
role in the neck pain disorder. Other factors are more relevant to
the disorder (e.g., painful segment dysfunction, nerve
mechanosensitivity).
Implication for management: train a neutral posture as an exercise
for the deep cervical flexors and/or axioscapular postural
muscles.

Control of scapular posture

Control of scapular posture is further explored, particularly when scapular postures were
linked with pain in the previous test. A lack of active scapular control may become more
obvious when the scapulae are loaded. Three functional tests are performed. First, the
patient is asked to slowly flex, abduct and then externally rotate the arms. Arm
movements should be less than 30 degrees to assess scapular control in a neutral
functional position. In the first 30 to 40 degrees of arm elevation, minimal scapular motion
is expected.28 Thus the scapulae should remain relatively stable if the scapular muscles are
providing adequate control. Second, the patient performs isometric contractions against
mild resistance with the shoulder held in minimal elevation. Gently resisted isometric
shoulder abduction may expose an inability to maintain upward rotation of the scapula,
suggesting weakness of the upper trapezius. If resisted flexion reveals an inability to
maintain posterior tilt of the scapular, it suggests weakness in lower trapezius, serratus
anterior and if resisted external rotation shows an inability to control internal rotation of
the scapula (winging), it suggest weakness in serratus anterior and the lower trapezius
(Fig. 9.3). Second, scapular control is assessed under low load in a closed chain condition
in a small wall push up. The shoulders are held in the same minimally elevated position to
that of the isometric tests. Third, scapular control is assessed through the full range of
upper limb elevation during which the scapula should progressively upwardly rotate,
posteriorly tilt and externally rotate. The clinician observes for reduced or delayed
scapular rotation in arm elevation and lowering which signals poor function of the
trapezius-serratus anterior force couple.29 Scapular rotation is manually facilitated in
different planes of motion (i.e., scapular upward rotation, external rotation, posterior tilt)
to identify the specific direction of any loss of scapular control during arm elevation and
its relationship to symptoms.

FIG. 9.3 The clinician gently resists isometric shoulder abduction and observes for
movement of the scapula. Tests are also performed for arm flexion and external
rotation.

Adjacent regions
There are neurophysiological, biomechanical and functional links between the cervical
spine and both the craniomandibular complex and upper limb. The cervical spine has been
implicated in craniomandibular disorders,30–35 shoulder disorders,36 lateral epicondylalgia37
and carpal tunnel.38 Thus a screening examination of the neck (active movement
examination and a manual segmental examination) is an essential first step in the presence
of any of these disorders. The examination can be extended to a more detailed assessment
of the cervical region if these examinations reveal positive results. Likewise, adjacent
regions should be examined in patients presenting with primarily a neck complaint (e.g., a
screening examination of the craniomandibular complex in a patient presenting with a
cervicogenic headache.34)
The biomechanical relationships between spinal and arm movement are revealed when
full arm elevation is impossible without motion occurring in the cervicothoracic, thoracic
and even the lumbar spine.39–42 However, there is inconsistency in reports for
biomechanical, postural, kinesiological and functional links between disorders of the
craniomandibular complex and the neck, which probably reflects the heterogeneity in
nature and presentation of craniomandibular disorders,32 a problem shared by neck pain
disorders. There is popular opinion that neurophysiological interrelationships and the
presence and influence of central nervous system sensitization commonly underpin links
between neck pain and pain in the craniomandibular complex or indeed painful disorders
of the shoulder or elbow.32,35,37,43 A neurophysiological link would explain findings of neck
tenderness or mechanical hyperalgesia and a general restriction of motion but without
signs of cervical musculoskeletal dysfunction (e.g., no deficit when performing the
craniocervical flexion test, no positive cervical flexion rotation test) in a
temporomandibular disorder.32,35 Clinical reasoning can be complex in determining the
origin of symptoms in such patients and where to direct primary treatment. Often a trial of
treatment with careful assessment of effect over the first one to two treatments provides
the answer.

Analysis of cervical motion

The analysis of cervical motion is a fundamental component of the examination of a
patient presenting with neck pain. Changes in motion are pathognomic of a cervical
disorder.44,45 The range, pain provoked, the nature and pattern of motion loss help to define
the disorder and directly informs management as well as provide an outcome measure.
The analysis of cervical motion provides information on the following.

■ Range of available motion and its relationship to symptoms.

■ Reasons for limitations of motion: biological (pain, articular
restrictions, neural mechanosensitivity or extensibility, poor
neuromuscular control, muscular restrictions [spasm, extensibility]),
psychological (fear of movement).
■ Patterns of movement restriction for diagnostic and management
purposes.46–48
■ Disturbances in control of movement (acceleration, velocity, movement
smoothness).49–51

Motion analysis is designed to consider all components of the functional cervical spine,
the craniocervical (C0–2) cervical (C2–7), and cervicothoracic regions (C7–T4). Even
though there is some interdependence between the regions, each region is assessed
separately, recognizing the independence of the regions (see Chapter 3). The focus on
cervical regions does not dismiss any assessment of the thoracic or lumbar regions as
relevant to the individual patient.

Assessment of cardinal planes of motion

The relationship between movement and pain or other symptoms such as light headedness
is documented for all movement tests. Here, we describe possible observations and
analyses of motion and neuromuscular control of movement.

Cervical and craniocervical motion

Cervical flexion.
Request the patient to look down to flex the cervical region. A smooth flattening of the
cervical lordosis should be observed down to the upper thoracic region with the head
remaining in a neutral position. Points to note include the following.

■ A tendency to extend the craniocervical region beyond that expected

from passive restraints of the posterior structures as full flexion is
approached could be protective of nerve tissue mechanosensitivity. To
confirm, ask the patient to flex their chin and assess pain response; or add
a nerve tissue sensitizing, straight leg raise position and assess any change
in pain.
■ The pattern of return is usually initiated from the lower cervical region
with the head in a neutral position. Initiation of return with excessive
craniocervical extension (chin up first) may signal dominance by the
superficial extensor muscles (e.g., splenius capitis, semispinalis capitis).

Cervical extension.
Request the patient to look up towards the ceiling and follow the ceiling back with their
eyes as far as possible. Points to note include the following.

■ The mass of the head should be posterior to the line of the shoulders. If
it remains in line with the shoulder, the patient is probably moving largely
in their upper cervical region only (Fig. 9.4A and B). Possible reasons for
this pattern include reluctance to move a painful segment into extension
and/or weakness of the flexors and an inability to eccentrically control the
weight of the head.
 FIG. 9.4 (A) The patient displays an appropriate pattern of cervical extension
and the head’s centre of gravity is posterior to the line of the shoulders. (B)
Extension is principally occurring in the upper cervical region only. Note the
head’s centre of gravity is in the line of the shoulders, not posterior to them.

■ The head moves backwards but at a point of extension, the neck appears
to “translate backwards”. Possible reasons are “segmental instability” or
more commonly, poor control of the head movement by the deep and
superficial cervical flexors. The moment arm of sternocleidomastoid
(SCM) reduces with progressive extension and if there is weakness of the
deep cervical flexors, they cannot control the movement.52 Occasionally
the patient may passively assist their head back to the upright position.
■ The return of the head from a fully extended position to a neutral
upright position should be initiated with craniocervical flexion. If the
return to the neutral position is initiated by an anterior translation type
movement in the lower cervical region (SCM action) and craniocervical
flexion is the last movement, this indicates weakness of the deep cervical
flexors.

Craniocervical flexion and extension.

The cervical spine remains in neutral and the patient is requested to first, nod their chin
down and second to lift their chin up as far as possible. Points to note include the
following.

■ Upper cervical flexion: restriction of range and a pulling sensation.

Possible reasons are articular restrictions, shortness of the suboccipital
extensors, neural tissue mechanosensitivity. The latter is differentiated by
 presensitizing neural tissues with either the addition of a straight leg raise,
flexion of the trunk (slump sitting) or presetting craniocervical flexion and
adding cervical flexion.53
■ Upper cervical extension: restriction of range. The most common reason
is articular. Note any production of dizziness or light headedness.
■ Upper cervical flexion or extension: symptoms of dizziness or light
headedness. Possible reasons are cervicogenic dizziness, or possible signs
of altered blood flow in the vertebral artery. Relate to the nature of the
dizziness and other symptoms and historical factors in differential
diagnosis (see Chapter 10).

Craniocervical and cervical lateral flexion.

Request the patient to curl their head sideways towards their shoulder. The movement is
tested bilaterally. Points to note include the following.

■ Lateral flexion of the head on the neck (C0–2). Most lateral flexion in
the craniocervical region is at C0–1. Note the contralateral pattern of
lateral flexion and rotation in the two upper cervical joints. If there is a
restriction in (L) craniocervical lateral flexion, the pattern would fit with a
reduction in (R) craniocervical rotation.
■ Observe the shape of the lateral curve of the neck. A segmental
restriction may be relatively discreet and can be identified by an
interruption to the shape of the curve.
■ Lateral flexion of the cervical region appears restricted en-bloc from C2
downwards, as a result of hypertonicity or shortness of the scalene
muscles. Possible reasons include: (1) a protective response to
mechanosensitive nerve tissue (the range of lateral flexion and pain
response will be altered when neural tissue is presensitized by placing the
arm in slight abduction and external rotation with the wrist and fingers in
extension); (2) an upper costal breathing pattern; and (3) compensatory
activity for weak deep cervical flexors.54

Craniocervical and cervical rotation.

Request the patient to turn their head to look over the shoulder. Points to consider include
the following.

■ C1–2 provides almost one-half of the range of head rotation and the
movement should be initiated with the head. When motion is limited, a
lack of free spin of the head suggests an upper cervical restriction; the
presence of free spin suggests a lower cervical restriction. In the latter
 case, the head may rotate with some ipsilateral lateral flexion, reflecting a
loss of the normal C0–2 contralateral lateral flexion that accompanies C0–
2 rotation.
■ Rotation at C1–2 can be tested specifically with the flexion-rotation
test.55
■ The head cannot rotate fully unless there is up to a 10-degree
contribution from the upper thoracic spine.56

Movement speed and velocity profile

Assessment of axial rotation provides the opportunity to test for other qualities of
movement performance. To this point of the assessment, the patient has performed
movements at self-selected speeds. Impairments in the mean and peak velocity of neck
motion have been identified in people with neck pain disorders, that is, they have slower
neck movements but not necessarily reduced range of motion. This deficit has significant
implications for dynamic functional tasks such as involved with driving and reacting to
visual and auditory stimuli.51,57 It is important to identify.
For an initial qualitative assessment of neck movement velocity profile:

■ Request the patient to move as quickly as they can to a specific point in

range (i.e., 45-degree rotation), stop, hold the position and then return to
the starting position as quickly as possible. Judge the speed of the
movement.
■ Assess overall speed and velocity profile. Observe how quickly and
how smoothly the movement is performed. The clinician should observe a
smooth acceleration followed by a smooth deceleration rather than stilted
movements.

Cervicothoracic region
Adequate mobility in the cervicothoracic and thoracic spinal regions is necessary for
normal motion in the cervical spine and shoulder complex.

Cervicothoracic flexion and extension.

Movement at the cervicothoracic region is examined in conjunction with cervical flexion
and extension. Points to consider include the following.

■ Observe for a spreading (flexion) and closing (extension) of the

interspinous spaces from C7 to approximately T3–4.
■ In extension, note any hinging appearance through the lower cervical
region which may occur when the cervicothoracic region is hypomobile.
■ If observation is unsatisfactory, the clinician may palpate the
 interspinous motion at each segment during the movement.

Cervicothoracic rotation and lateral flexion.

Movement at the cervicothoracic region is examined in conjunction with cervical rotation
and arm elevation. Palpation of spinous process movement with these tests is an easier and
more exacting assessment than observation.

■ Palpate for the lateral displacement of the thoracic spinous processes

(rotation) while the patient rotates the head (Fig. 9.5).

FIG. 9.5 The patient performs repeated head rotation while the clinician
palpates for the lateral displacement of the thoracic spinous processes (rotation)
at each thoracic segment (C7–T1 to T3–4 or T4–5). Movement is examined in
each direction. This examination technique can be used as a treatment
technique. The clinician performs a transverse glide through the spinous process
of the hypomobile thoracic segments as the patient rotates the head.

■ Single arm elevation induces rotation and ipsilateral lateral flexion in

the upper thoracic segments.41,42 Palpate for the displacement of the
thoracic spinous processes while the patient performs assisted unilateral
arm elevation (see Fig. 3.4).

Movement tests to further direct management

Two movement examination schemes extend examination of movement in cardinal planes
to further direct specific management approaches. One scheme is the combined movement
examination which was originally described by Edwards.46 It is built on a theory which
considers the combined nature of functional movements, the coupled nature of spinal
segmental movements and the relationship between movements that load the segments in
similar ways. A comprehensive theory has developed to underpin the combined movement
approach.58 The active movement component of the approach aims to identify the primary
movement and the primary combination of movements that most accurately reproduce the
patients’ pain, or in the case of severe pain, most accurately relieves pain. It provides the
basis and rationale for the starting position and progression of manipulative therapy
techniques. Inter-examiner reliability has been established for the main components of the
active combined movements assessment.59
Another scheme of active movement examination is related to the mechanical diagnosis
and therapy approach. The primary objective is to determine if neck pain or related arm
symptoms can be abolished or reduced with the use of repeated movements or sustained
postures. A principal of assessment is the use of direction-specific loading strategies to
relieve pain or stimulate “centralization”, that is, shift peripherally located pain to a more
central location. Any movement direction might be used, based on a patient’s presentation
but a key movement is neck retraction. Assessment outcomes may help classify patients
into one of three syndromes, derangement, dysfunction or postural syndrome, which
assists in directing treatment. The reliability of the assessment method has been
established for persons trained in the McKenzie method.60

Movement diagnostic tests

There is often contention about the ability of physical examination tests to assist
diagnosis. There is now evidence that either a single test or a combination of physical tests
can reliably detect cervical facet/zygapophysial joint dysfunction.

Cervical flexion rotation test.

The flexion rotation test will identify C1–2 dysfunction. Its basis is that C1–2 axial
rotation is separated from cervical axial rotation by fully flexing the neck before
performing head rotation (see Fig. 3.1A and B).61 The test was first described some 40
years ago,62 but more recent research has proven its construct validity, reliability and
discriminant ability.47,55,63,64 It is a valuable test to identify cervicogenic headache
associated with C1–2 dysfunction and to discriminate persons with cervicogenic headache
from those with migraine or no headache complaint.47,64

Extension rotation test, manual segmental examination, palpation of

segmental tenderness.
This combination of tests is able to detect a symptomatic cervical zygapophysial joint as
tested against diagnostic facet joint anaesthetic blocks: sensitivity (79% confidence
interval [CI], 72–86), specificity (84% CI, 77–90), positive likelihood ratio 4.94 (CI 2.80–
8.20) and negative likelihood ratio .25 (CI .15–43).48 The study was conducted with
people with chronic neck pain attending an interventional pain management clinic.
Interestingly, the presence of catastrophization and psychological distress did not modify
or confound the outcome of the physical examination. The validity of this clinical
examination contributes both to diagnosis of the neck pain disorder, and to identify
patients potentially suitable for facet joint interventions.65

Spurling’s test.
This test is used to help identify if a patient’s arm pain is related to a cervical
radiculopathy. The neck is placed in either rotation or lateral flexion and extension is
added, which narrows the intervertebral foramen. The clinician applies a compressive
force through the head. A positive test response is reproduction of arm pain. It is a
vigorous test and is only indicated when the presence of a cervical radiculopathy is not
obvious from other aspects of the examination. Although Spurling’s test has high
specificity, it has low sensitivity.66 Thus at best, the test is only able to contribute to a
clinical diagnosis.

Positional tests for vertebral artery insufficiency

The presence of dizziness or unsteadiness in association with neck pain may have its
origins in vestibular, cervical or vascular disorders (see Chapter 10). The vascular
disorders of concern include the relatively rare presentation of cervical arterial dissection
(CAD) or vertebrobasilar insufficiency (VBI). Points to note include the following.

■ When there are any concerns about the presence of CAD or VBI, then
priority must be given to investigating these factors before conducting any
other part of the physical examination.
■ In the rare event of a strong suspicion of CAD, clinicians are advised
not to undertake a potentially provocative cervical movement
examination. Rather, the patient should be referred immediately to a
hospital emergency department with documentation about the concerns
(younger patients aged under 55 years, acute, sudden onset of unfamiliar
moderate to severe headache or neck pain often progressing, history of
recent minor neck or head trauma, respiratory infection or onset of
neurological features [e.g., 5Ds—dizziness and/or unsteadiness; diplopia;
dysarthria/dysphasia; dysphagia; drop attacks or 3Ns—nystagmus;
nausea; perioral numbness or paraesthesia], disturbances to balance or
vision).67
■ Perform VBI tests as the first tests when there is suspicion of VBI;
usually an older patient who reports symptoms of the 5Ds or 3Ns.
Historically, there have been many tests proposed for VBI. None have
high sensitivity and specificity or predictive value to identify risk of CAD
or adverse events associated with manipulative therapy. Nevertheless,
sustained end-range rotation is regarded as the most provocative and
 reliable test for those individuals with VBI.68 The test is performed in
sitting and end range rotation is sustained for at least 10 seconds. Positive
responses include the production of dizziness, feelings of faintness,
nystagmus which does not settle within a few seconds, or any of the 5Ds.
A period of 10 seconds is advocated before rotation is tested to the other
side in case there is any latency in responses.

The second indication for VBI testing is in patients for whom cervical manipulation or
end range, firm mobilization techniques are considered in management. Premanipulative
screening includes the sustained rotation test and also sustaining the position of the neck
in which manipulation is to be performed to potentially identify any individuals with
asymptomatic VBI. A comprehensive framework was developed by the International
Federation of Orthopaedic Manipulative Physical Therapists for the examination of the
cervical region in patients with suspected vascular dysfunction,69 and readers are referred
to this framework and its scheduled updates.

Sensory testing and pain mechanisms

Quantitative sensory testing (QST) can assist in understanding pain mechanisms (see
Chapter 2). These tests are undertaken particularly in those patients whose history and
pain descriptions suggest the possibility of central pain mechanisms. This occurs in some
subjects with whiplash-associated disorders (WAD),70 cervical radiculopathy,71 headache
including cervicogenic headache72 or another neuropathic pain state. These sensory
changes occur early so testing is relevant in patients both in acute and persistent stages of
their disorder.70 There are many sensory tests that can be performed but two that have been
used extensively in research into neck pain disorders are tests to elicit signs of mechanical
and thermal hyperalgesia. Tests are conducted over the local neck region to detect any
potential peripheral sensitization and tests are also conducted at remote sites, commonly
over the tibialis anterior, to detect evidence of widespread hyperalgesia which suggest the
presence of central sensitization.
Measures of mechanical pain thresholds can be made with commercially available, low-
cost pressure algometers. Thermal sensitivity (heat and cold pain thresholds) can be
examined with thermorollers, which can be set at predetermined temperatures.73 Cold
hyperalgesia is proving to be important in identifying central sensitization and also as a
potential predictor of recovery following a whiplash injury. Maxwell and Sterling74 rated a
simple, clinically friendly, ice application over the neck (two ice cubes in a plastic bag)
against a laboratory thermotest system. They found that a pain intensity rating of greater
than 5 out of 10 with the ice test gave a positive likelihood ratio of 8.44 suggesting the
likely presence of cold hyperalgesia.

Examination of the nervous system

A battery of tests is undertaken to detect the presence of neuropathy and changes in nerve
function. Multiple tests, as opposed to any single test, improves diagnostic accuracy for
cervical radiculopathy75 and upper limb neuropathy.76,77 The test battery routinely includes
a clinical neurological examination and tests of nerve tissue mechanosensitivity. Elements
of QST may be included to investigate nerve conduction integrity (e.g., small fibre
function).

Clinical neurological examination

A neurological examination is undertaken to evaluate nerve conduction integrity when
symptoms (1) extend beyond the shoulder into the upper limb, or (2) include
paranesthesia, anaesthesia, weakness, reduced dexterity within the upper quadrant or (3) if
there are specific descriptions of pain indicating nerve irritation (e.g., burning, shooting,
itching). These symptoms may have been reported in specific questionnaires for
neuropathic pain (e.g., Self-Administered Leeds Assessment of Neuropathic Symptoms
and Signs (S-LANSS); Neuropathic Pain Questionnaire (NPQ); painDETECT
questionnaire).78,79 Other factors such as muscle wasting or changes in balance and gait
also indicate the need for a neurological examination.
A standard neurological examination includes evaluation of spinal reflexes (biceps C5,
C6; brachioradialis C6; triceps C7), strength of muscles in related myotomes (upper
trapezius C4; middle deltoid C5; biceps brachii C6; triceps brachii C7; extensor pollicis
longus C8; palmer interossei T1), and tests of sensation in related dermatomes80 (light
touch, pin prick, vibration). The clinical neurological examination has acceptable test
reliability.81
The neurological examination may expand in response to variations in clinical
presentation. Examples include the following.

■ Sensory testing to differentiate dermatomal80,82 from peripheral nerve

distribution when nerve entrapment is suspected (e.g., median nerve in
carpal tunnel syndrome, ulnar nerve in cubital tunnel syndrome).
■ QST may be indicated when an entrapment neuropathy is suspected but
changes in nerve function are not detected by conventional neurological
examination. Further testing may include vibration thresholds for Aβ
fibres; as well as cold and warm detection for Aδ and C-fibres,
respectively.83
■ Upper motor neurone tests are added if spinal cord compromise is
suspected (cervical myelopathy). These include Hoffman, Babinski and
clonus tests, as well as an evaluation of balance and gait. Detection of
myelopathy should not depend on any single test because cord signal
changes may correlate poorly with upper limb reflexes and other
pathological reflexes.84 In a sample of patients with cervical myelopathy
and cord signal change on magnetic resonance imaging (MRI), 67% had a
 Hoffman sign, 16% had clonus, 44% had Romberg sign and 60% had a
gait abnormality.84
■ Evaluation of cranial nerve function85 may be indicated in clinical
presentations where patients report or display neurological symptoms such
as a change in balance or coordination, slurred or altered speech patterns,
changes in the senses, blurred vision, changes in behavior and/or fatigue.
Such symptoms could be suggestive of concussion when the patient has
had a traumatic head and neck injury or CAD when the patient presents
with an acute onset, moderate to severe, unusual headache.

Tests of nerve mechanosensitivity

Nerve tissue mechanosensitivity may be associated with antalgic postures, painful
restriction of active and passive movements including neurodynamic tests, tenderness on
nerve palpation, and relevant local signs (e.g., joint dysfunction).86–88 Active movements
and neurodynamic tests are positive for nerve tissue mechanosensitivity if they reproduce
symptoms, and symptoms can be altered by structural differentiation. Structural
differentiation delineates nerve tissue mechanosensitivity as a cause, by changing
symptoms when selectively loading or unloading the nervous system with manoeuvres at a
site remote to the symptoms.89–91 Examples include the following: when manual correction
of a depressed or downwardly rotated scapula reduces distal arm pain, it may indicate
postural based tensile strain on the brachial plexus in a relaxed upright posture; shoulder
and upper arm pain increases when shoulder abduction is repeated with the wrist in
extension compared with a neutral position; there is an increase in pain with cervical
flexion when it is performed in sitting with the knees straightened.

Neurodynamic tests
The four variants of the upper limb neurodynamic test87,90 (Fig. 9.6) and the slump test91
are relevant for the upper quadrant. As mentioned, a test is considered positive if it
reproduces symptoms that can be altered by structural differentiation.89–91 Neurodynamic
tests of the upper limb are reliable when these criteria for a positive test are used.75,81,87,92
The point of excursion of a test movement at which symptoms are reproduced (e.g., elbow
extension during the median nerve bias test) is a reliable measure93 and usually indicates a
positive test of nerve tissue mechanosensitivity. Yet this might not always be the case.
Range of motion is reflective of protective muscle responses that are elicited in both
symptomatic94 and asymptomatic states.95 A study in patients with chronic WAD showed
bilateral loss of elbow extension during neurodynamic testing irrespective of the presence
or not of arm pain.96 The reduction in mobility in these patients may have reflected a
hypersensitive flexor withdrawal response.
 FIG. 9.6 Neurodynamic tests include the conventional test, which biases the brachial
plexus and median nerve (pictured here) as well as tests that bias the median, radial
and ulnar nerves. In the conventional test, the movement sequence is gentle shoulder
girdle fixation in a neutral position, followed by shoulder abduction and lateral rotation,
elbow extension, forearm supination and wrist extension. The sequence of test
movements may be altered, and the test is often performed with wrist extension
preceding elbow extension, so that one angle, elbow extension, can be measured in
assessment. Sensitizing movements include contralateral cervical lateral flexion or
craniocervical flexion.

Nerve tissue mechanosensitivity may be a feature of cervicogenic headache where its

incidence is estimated as roughly 10% of cases.5,97 Here the provocative movement is
craniocervical flexion and the mechanosensitivity purportedly involves movement of the
dura. Described as a myodural bridge, the dura mater is attached to the foramen magnum
and to the body of the C2 vertebra. There are also fibrous connections between the rectus
capitis posterior minor and the ligamentum flavum in this region.98–100 The test for neural
tissue mechanosensitivity involves passive craniocervical flexion. A restriction in range
could reflect deficient dural movement in a cephalad direction, tightness in the
suboccipital extensors or hypomobility into flexion of the C0–1 and C1–2 joints. To
structurally differentiate a neural tissue origin of the restriction, craniocervical flexion is
repeated with the nerve tissue presensitized by placing the lower limb in a straight leg
raise and then the upper limb in the neurodynamic test position (Fig. 9.7A and B).101
Reproduction of neck or headache symptoms with the test is a positive neural tissue
response. This test is mandatory before the craniocervical flexion test to avoid any
exacerbation of symptoms of a neuropathic origin. There has been no formal evaluation of
the inter-examiner reliability of this test, but reliability has been established for a similar
test of neural tissue provocation using craniocervical flexion with added flexion.53
 FIG. 9.7 (A) The test for nerve tissue mechanosensitivity in the craniocervical region.
The clinician passively flexes the craniocervical region and notes the range, end feel
and pain response. Craniocervical flexion is repeated up to 4 times, (i.e., with each leg
in a straight leg raise position and with each arm in an upper limb neurodynamic
position). (B) The patient holds a straight leg raise position and the clinician again
performs craniocervical flexion and judges the range, end feel and pain response. A
slight change in available flexion range is not uncommon. Reproduction of neck or
head pain is a positive sign and is usually associated with a firm end feel and a definite
reduction in range of movement.

Nerve palpation
Nerve palpation is a further component of the assessment of nerve tissue
mechanosensitivity. Palpation of the trunks of the brachial plexus and peripheral nerves
has moderate to substantial measurement reliability.81 Nerves palpated include the median,
ulnar and radial nerves in cases of cervicobrachial pain, and the C2 nerve and greater and
lesser occipital nerves in cases of cervicogenic headache. In the presence of sensitized
peripheral nerve tissue, the nerves are tender to gentle palpation, that is, they exhibit
mechanical allodynia. Such findings reinforce the necessity for the physical examination
and physical treatments to be undertaken with care to avoid provoking the patient’s
symptoms.

Manual examination
The cervical segments from C0–1 to at least T3–4 or T4–5 are examined. A variety of
manual examination techniques can be used in a variety of positions and for a variety of
reasons. The reader is referred to relevant texts for detailed rationales and technique
descriptions.46,102–104 Techniques may be performed in sitting, supine or prone lying. They
may be performed purely as passive movements in single (Fig. 9.8) or combined (Fig. 9.9)
planes or with the addition of active movement (Fig. 9.10).105 Techniques may emphasize
the examination of physiological planes of motion (Fig. 9.11) or maybe regarded as more
“provocative” movement tests (Fig. 9.12). A number of techniques are usually used in
clinical decision making. Despite the variety of techniques, the desired outcomes of the
manual examination are similar, namely to determine the symptomatic segment(s) and to
further inform the management approach. No one method(s) is necessarily superior. One
commonality is that each method requires skilled application to deliver optimal outcomes.
Skill is gained through concentration and repetitive practice as required for acquisition of
any physical skill be it hitting a golf ball in an intended direction, performing arthroscopic
surgery or assessing cervical intersegmental motion. An important aspect of manual
handling skill is that the clinician can perform all techniques with no or negligible
clinician-induced local discomfort because this can lead to false positive interpretations.

FIG. 9.8 Test of left lateral flexion at the occipito-atlantal joint (C0–1) in supine lying.
The tip of the index finger is placed on the transverse process of C1 and the pad
palpates the mastoid process. Lateral flexion of the skull on C1 is performed and the
clinician feels for the approximation of mastoid process to the transverse process.

FIG. 9.9 Test of C3–4 right lateral flexion in extension as a component of a combined
movement examination. C4 is stabilized by gripping the lamina between the index
finger and thumb. The head to C3 is gripped by the opposite hand (hypothenar
eminence on C3) and the lateral flexion movement is produced by the arm and
shoulder girdle.
FIG. 9.10 Test of C4–5 left rotation using a sustained natural apophysial glide. The
medial border of the (R) thumb is placed on the lamina of C5 and the (L) thumb is
placed on C4 perpendicular to the (R) thumb in the facet plane. A passive glide is
applied as the patient actively rotates.

FIG. 9.11 An anteroposterior glide is performed in the facet plane to assess the
downward glide of the C2 on C3 (extension). Care must be taken to ensure that C2 is
well supported with a gentle lumbrical grip with the thumb on the anterior aspect of the
transverse process and the index and remaining fingers gripping the lamina. The
movement is produced by gentle elbow extension and flexion as direct force by the
thumb will be painful. The direction of the glide is in a cephalad direction and a medial
bias can be introduced which emphasizes a lateral flexion component.
 FIG. 9.12 A unilateral posteroanterior glide (PA) is performed on C3–4. The PA glide
can be regarded as a gentle provocation test that will elicit a reaction from the deep
segmental muscles overlying the joint (multifidus) in response to the manual
provocation. The extensor muscles overlying the facet joints are shifted medially so
that the clinician can locate the thumbs as close as possible to the lamina of C3. The
fingers and hands gently grip the side of C3 and the neck. The movement is produced
by gentle elbow extension and flexion as direct force by the thumb will be painful. Pain
produced by a clinician’s thumbs in performance of the technique could result in false
positive findings.

Manual examination of segmental motion is a qualitative assessment and not an

absolute measure. It has had an unsteady history from a scientific perspective. In the past,
it was treated as a semiquantitative measure of segmental motion and tissue compliance.
In these earlier times, there were enthusiastic beliefs about the accuracy of manual
examination techniques with respect to tissue compliance. This is evident in the design of
the inter-therapist reliability studies to test a clinician’s ability to rate segmental motion by
grading the displacement and stiffness of a segment to their applied manual force. Rating
scales varied, but in one study an 11 point scale was used.106 This means that clinicians
were asked to estimate which of 11 stress strain curves they perceived within a 2 to
2.8 mm sagittal translation displacement of a lumbar segment; a formidable and unrealistic
task. It is probably not surprising that a systematic review based on many of these earlier
studies found reliability of manual examination to be low107 and thus questioned the
continued use of manual examination in practice. In contrast, a more recent in vitro study
of three manual mobilization techniques of the atlanto-axial joint found that both inter-
observer and intra-observer reliability to produce similar motion with the techniques was
high.108 Thus more research asking different question, and using different designs and
measures might throw a different light on manual examination or manually induced
segmental movement.
It is often difficult to shape a clinical art into a quantifiable research question.
Importantly other relevant questions of manual examination have been asked. A crucial
question has been whether a patient’s neck pain is associated with painful segmental
dysfunction and whether clinicians can reliability detect this segmental dysfunction. In
these respects, manual examination is proving to be an accurate and valuable method of
examination.109–114 Most studies have validated its accuracy against the accepted gold
standard of diagnostic anaesthetic blocks. This judgement from manual examination
requires essentially a yes/no decision based on a simultaneous, multifaceted
(metacognitive) assessment of both the nature and amount of tissue resistance to the
manually applied force, the perceived displacement and the degree of pain provocation.
Palpation or manual examination is a fundamental test in health care practice, whether it
is to palpate an abdominal mass, to detect the tenderness and muscle guarding of acute
appendicitis or to elicit painful cervical segmental dysfunction. Thus the questioned use of
manual examination,107 on the basis of some poorly conceived tissue compliance studies
can in turn be questioned with the wisdom of hindsight. Nevertheless, claims of precision
with these tests with respect to motion and tissue resistance to motion also need to be
modified to be in line with the evidence. Manual examination is an important diagnostic
test that adds to the understanding of the patient’s neck pain condition.115 In perspective, x-
rays cannot reliably identify a symptomatic segment. This realizes the need and
importance of a skilled manual examination to identify the presence (or absence) and
location of symptomatic cervical segment(s) in a patient’s neck pain or headache disorder.
Judgement can also be made of the comparability of the joint signs to the level of reported
pain when reasoning the relative contributions of peripheral and/or central mechanisms in
a patient’s neck pain presentation.

Instability tests
Craniocervical instability and loss of ligamentous integrity must be considered in patients
who have either sustained head or neck trauma (motor vehicle crash, sporting injury, fall),
have an inflammatory arthritis (such as rheumatoid arthritis and ankylosing spondylitis),
an inherited condition such as Down syndrome or who have congenital anomalies in the
upper cervical region.116–118 Trauma from a motor vehicle crash may cause ligament
injury119,120 but the area of most controversy is the frequency of craniocervical ligament
ruptures in the absence of a concurrent fracture or dislocation. Diagnosis is difficult. There
is controversy about the relevance of MRI signal changes in alar and transverse ligaments
as they pertain to structural damage121 and reported pain and disability.122 Without a gold
standard radiological diagnosis, it is difficult to validate clinical tests. Thus it is not
surprising that the outcomes of a systematic review of the diagnostic accuracy of upper
cervical spine instability tests concluded that there was insufficient evidence to indicate
that craniocervical ligament tests could accurately identify ligamentous instability.123
More recent work has investigated the content validity of several craniocervical
ligaments tests on healthy young participants by determining if the tests displace relevant
anatomic points consistent with the proposed mechanisms of the test. Measurements have
been with MRI. These studies have confirmed the content validity of the clinical anterior
shear (transverse ligament) and distraction (tectorial membrane) tests124 as well as the
side-bending (Fig. 9.13) and rotation stress tests for the alar ligaments.125 The range of
craniocervical rotation in the rotation stress test, should typically not be greater than 21
degrees in the presence of intact alar ligaments.126 It is now necessary to determine if
measuring displacement will have clinical utility in patients following neck trauma. Here
in vivo variables such as muscle spasm may confound testing because these may occur,
for example, with tests of the anterior cruciate ligaments of the knee.

FIG. 9.13 The lateral stress test for the alar ligaments. C2 is fixed between the
clinician’s thumb and index finger. The occiput and C1 are laterally flexed. There
should be a solid end feel. The test is performed in neutral, slight flexion and extension
to account for variation in ligament orientation. The rotational stress test may also be
used for the alar ligaments. If the ligaments are partially or fully ruptured, some excess
movement would be expected, but often muscle guarding may confound the tests.
Nevertheless, there would be disturbed cervical afferentation and symptoms of pain
and dizziness may be reproduced.

Cervical segmental instability (C2–7) may be present as a result of trauma or it may be

part of a degenerative process. Segmental instability is tested with an anteroposterior glide
(Fig. 9.14). At this present time, it is unknown how much clinicians can rely on the
outcomes of the cervical segmental stability tests or craniocervical ligament tests. In the
clinical reasoning process, account is also taken of the history of onset and nature of
symptoms. In a Delphi study, clinicians nominated a variety of symptoms that might
arouse suspicion including a feeling of being unable to hold the head up, a desire for
support either by a collar or hands, a feeling of instability or lack of control.127 Protective
muscle spasm would be expected. Thus a pattern of symptoms and signs is sought, rather
than rely on any one test. Patients presenting with any neurological signs especially upper
motor neuron signs, should be referred immediately for further medical investigations.
 FIG. 9.14 Manual test of sagittal glide. The test is used for the segments from C2–3
to C7–T1. The clinician stabilizes the caudal segment through placement of the fingers
on either side of the spinous process. The head rests on the forearm and the
hypothenar eminence and little finger grip the cephalad vertebra of the segment. The
translation movement is performed by the arm and the clinician perceives any reduced
tissue resistance to the movement and compares with adjacent segments. Symptoms
may be reproduced.

Assessment of the neuromuscular system

In the initial assessment, attention is focused on testing the activation, coordination and
endurance capacity of muscle groups. Tests are conducted under low-load conditions so
that particular muscles can be targeted as much as possible. Tests against resistance
necessarily recruit many muscles to resist the force. Furthermore, low-load tests can be
performed without pain negating the effect of pain inhibition in the initial assessment.
Tests of strength and higher-level endurance are conducted in subsequent assessments.

Scapular muscle tests

Scapular holding test (lower trapezius)
This test might be delayed if upper trapezius guarding has been observed in the postural
assessment and the upper limb neurodynamic test has confirmed the presence of nerve
tissue mechanosensitivity. The scapular holding test is a modified grade 3 test of the lower
trapezius.128 The modifications are that the arm is positioned by the side and the clinician
places the scapula passively into a neutral position on the chest wall (Fig. 9.15). The
patient is requested to hold this scapular position. Two aspects are assessed.
 FIG. 9.15 Scapular holding test. The clinician passively lifts the scapula onto the
chest wall and requests the patient to hold the position. An analysis is made of the
muscle strategy used to hold the position.

■ The pattern of muscle activity used to hold the scapular position. The
clinician observes for activity in the lower trapezius together with
“balanced” activity of other scapular muscles. Actions masking weakness
of lower trapezius include dominant use of latissimus dorsi (arm and
scapular depression), rhomboids or levator scapulae (downward rotation
and elevation of the scapular border), infraspinatus/teres minor muscles
(lifting and/or externally rotating the arm). Winging of the scapula
indicates weakness of the serratus anterior.
■ The “holding capacity” of the lower trapezius (and serratus anterior).
The low-load nature of this endurance test is akin to the muscle’s
functional role in holding the scapular position in upright postures. The
patient is requested to hold the scapular position for approximately 5
seconds and the test is repeated up to 5 times or until the clinician has a
good appreciation of the pattern of muscle use. Impaired holding capacity
is observed when (1) the position cannot be held (i.e., the scapula slides
towards an outer range position); (2) a “fatigue” tremor develops; or (3)
the patient changes to another muscle strategy to hold the position (e.g.,
excessive use of latissimus dorsi).

Reassessment of cervical posteroanterior glides

Contraction of the scapular depressors in the scapular holding test induces reciprocal
relaxation of the scapular elevators (e.g., levator scapulae, upper trapezius) and thus
reduces muscle load on the cervical spine. This provides an opportunity to make a clinical
assessment of the possible effect of reduced axioscapular muscle activity on segmental
joint signs and pain. Following the manual examination of posteroanterior (PA) glides, the
patient is asked to rate the pain provoked on the symptomatic segment. Immediately after
the scapular holding test, the clinician again examines the PA glides on the same
symptomatic segment and reassesses the pain rating. The response is interpreted in a
similar way to the interpretation of posture correction.
The scapular holding test results in the following.

■ A marked reduction in pain on PA provocation

Interpretation: load from scapular elevator activity is a major
contributor to segmental joint pain.
Implication for management: train scapular muscles (trapezius,
serratus anterior) and scapular posture to relieve unnecessary
load. Training becomes a major feature of the intervention. The
pattern fits for the role of poor scapular muscle control if both
this test and the correction of scapular posture reduce pain. This
response makes a convincing link between relief of pain and
appropriate muscle control for patient motivation for exercise
and training of posture.
■ A slight reduction in pain on PA provocation
Interpretation: load from scapular elevator activity is a part
contributor to segmental joint pain.
Implication for management: train scapular muscles (trapezius,
serratus anterior) and scapular posture with the knowledge that
the painful joint dysfunction will need to be addressed with
other methods such as manipulative therapy and specific active
segmental exercise.
■ No reduction in pain on PA provocation
Interpretation: load from scapular elevator activity has little or no
direct role in the segmental joint pain.
Implication for management: depending on the findings from
other tests of scapular posture and movement control, findings
suggest that other management is needed to address the painful
joint dysfunction such as manipulative therapy and specific
active segmental exercise.

This postfacilitation assessment of the PA provocative test can also be conducted after
the craniocervical flexion test which reciprocally relaxes the cervical extensor muscles.
Changes in pressure pain thresholds over the neck have been demonstrated after the
muscle test.129,130 The aim is to demonstrate how much segmental muscle spasm is
potentially contributing to the joint pain and dysfunction.

Trapezius muscle tests

The scapular holding test emphasizes the lower portion of the trapezius muscle. The upper
trapezius muscle is often a site of tenderness and feelings of “tightness” yet when a
downwardly rotated scapular posture is observed, the upper trapezius is in a lengthened
state. The upper trapezius is commonly weak and it has also been shown to be more
fatigable in patients with neck pain.131
First impressions of trapezius muscle function were gained from the observation of
posture and scapular motion during forward arm elevation. A better determination of
trapezius function is gained from the control of the scapula in abduction. A test of resisted
abduction in 110 degrees has been proposed as a better test of the tripartite trapezius
muscle’s ability to control upward scapular rotation, than separate tests of its three parts.132
The upper trapezius can be formally tested with the classical test of a shoulder shrug. First
the patient’s capacity to shrug is determined by observing whether they can perform a
correct upward rotation strategy of the scapula (i.e., activating upper trapezius), rather
than a gross elevation of the scapula that encourages levator scapulae activity. The test is
progressed from non-resisted to resisted with the use of arm position and load as indicated.
Upper trapezius fatigability can be evaluated asking the patient to perform repeated
shoulder abduction or shoulder shrugs.131

Serratus anterior test

Initial assessment of serratus anterior function was made from the observation of scapular
posture and from the analysis of scapular control with light arm load and with arm
elevation. The serratus anterior can be further tested with a classical muscle test of
scapular protraction performed in lying or in sitting and in various positions of arm
elevation. A closed chain test may be conducted, such as a push up from the wall or the
more challenging position of four-point kneeling. Often the four-point kneeling or prone
on elbows position is used with people with neck pain (as opposed to those with
glenohumeral disorders). In these positions, the patient is encouraged to let their rib cage
sink between their scapulae and then push through their arms to raise their rib cage back
towards their scapulae, keeping the spine neutral (i.e., not flexing the thorax). This tests
the capacity of the axioscapular muscles to fix the scapula to the chest wall in a neutral
postural position under load. Substantial winging of the medial border of the scapula is an
indication of poor axioscapular muscle control particularly of the serratus anterior muscle.

Axioscapular muscle length tests

Muscles with a tendency for overactivity or tightness include levator scapulae,
suboccipital extensors, scalenes, pectoralis minor and major. Indications of overactivity
are revealed in neck and scapular postures as well as muscle bulk. Observations are
confirmed with formal muscle length tests.133,134 We do not prioritize muscle length tests
because our treatment philosophy is to train the impaired muscles or postures which
underlie increased use of some muscles. For example, rather than stretch levator scapulae,
we would prioritize training activity and control offered by the tripartite trapezius. Rather
than stretch the suboccipital extensors, we train the deep cervical flexors and cervical
posture. A notable exception is the pectoralis minor muscle where muscle stretching may
be required to train scapular posture. Our approach is not to suggest that it is “wrong” to
use muscle stretching in the management of a neck pain disorder, but often there is not a
lasting effect of treatment unless the underlying impaired motor control is addressed.
Muscle stretching is not indicated when muscle “shortness” is protective of nerve tissue
mechanosensitivity (scalenes and upper trapezius in cases of neck and arm pain and
suboccipital extensors muscles in cases of cervicogenic headache).

Craniocervical flexion test

The evidence indicates that poor activation and endurance of the deep cervical flexor
muscles (longus capitis and longus colli) is common in people with acute and chronic
neck pain regardless of the mechanisms of onset.135–140 The deep cervical flexor muscles
are tested in the craniocervical flexion test (CCFT).141 The CCFT has content validity54
and inter-therapist and intra-therapist reliability.142–145 The test is low load and is performed
in the initial assessment in patients with either acute or chronic neck pain conditions. The
exception is when patients have signs of neural tissue mechanosensitivity. Before testing,
the clinician screens for this occurrence (see Fig. 9.7A and B). The CCFT is delayed if
neural tissue mechanosensitivity is present and instead, priority is given to nerve tissue
management. In the screening test, the clinician also assesses the range of craniocervical
motion to gain a baseline for movement analysis during the CCFT.

Preparation for the test

The CCFT is performed in supine with the knees bent and the head and neck in a neutral
position (no pillow) such that the line of the face is horizontal. When the patient’s head is
in slight extension (often associated with a thoracic or cervicothoracic kyphosis), layers of
towel are placed under the head to gain a neutral position. Often layers of towel need to be
placed behind the neck as well because a distance of no more than 0.5 to 1 cm is desirable
between the supporting surface and the back of the neck. Too big a space encourages over
inflation of the biofeedback’s pressure pad which can force the neck into extension and
invalidate the test. If the patient rests with the head in flexion, they are taught a neutral
position by looking at a point on the ceiling slightly behind their head. They return to this
position between each stage of the CCFT. The folded pad of the pressure biofeedback
device (Stabilizer, Chattanooga, USA) is placed behind the neck so that it abuts the
occiput. Patients (and clinicians) are unable to see or palpate the deep cervical flexors to
know if they are contracting. This device guides the patient during the CCFT, by providing
feedback on the target pressures to be achieved with each stage of the test. The air-filled
pressure pad monitors the change in shape of the curve as it flattens with the contraction
of the deep cervical flexors.146 The pressure sensor is inflated to a baseline pressure of
20 mmHg, a standard pressure sufficient to fill the space between the testing surface and
the neck. The air must be distributed throughout the pad and the pressure stabilized before
testing commences (Fig. 9.16).

FIG. 9.16 The craniocervical flexion test position. Folded towels may be used to
position the head and neck in a neutral position. It is preferable to have no more than a
1-cm space between the back of the neck and the supporting surface. The pressure
sensor is positioned behind the neck so that its edge abuts the occiput. Note the
feedback is for the patient. The clinician must observe the pattern of movement and
any substitution strategies during the test.

Craniocervical flexion is taught as an active assisted movement with instructions to feel

the back of the head slide up the bed to nod the chin. Five, 2-mmHg progressive pressure
increases are sequentially targeted from the baseline of 20 mmHg to a maximum of
30 mmHg. The movement should be performed gently and slowly, allowing a 2 to 3
second rest between stages. There is a learning effect, so the patient should practice the
test once or twice before formal assessment.

Formal test procedure

The formal test is conducted in two stages.141
Stage 1: Analysis of the range and quality of the five progressive stages of the
craniocervical flexion.
Stage 2: Testing the isometric contraction of the deep cervical flexors.

Stage 1.
The patient is requested to slowly feel the back of their head slide up the bed to nod their
chin to reach the first target pressure of 22 mmHg. They hold the position for 2 or 3
seconds and then relax. This process is repeated through each of the four remaining stages
of the test. The clinician analyzes the pattern and range of craniocervical flexion motion,
observes the quality of the movement and observes or palpates for any excessive activity
in the superficial flexors (SCM and scalenes). The motion of the head should be a rotation
whose range increases proportionally through progressive stages of the test.147
Clinical measure: the stage of the test that the patient can achieve and momentarily hold
with the correct craniocervical flexion movement and without excess SCM and scalene
muscle activity is documented as the activation score. Expected scores in an asymptomatic
population vary, but most achieve a score between 26 and 30 mm Hg. Persons with neck
pain usually perform at the 22 to 24 mmHg levels.138,144
Several features indicate poor test performance.

■ There is not a progressive increase in craniocervical flexion range of

motion between stages. The patient attempts all stages of the test but uses
a subtle head retraction action (i.e., pushes back on the pressure sensor) to
attain the progressive pressure test increments.54
■ The patient cannot perform all test stages regardless of their movement
strategy.
■ Movement is performed quickly to mask weakness.
■ The clinician observes or palpates excessive activity in the SCM and
scalene muscles. Some SCM and scalene muscle activity is normal
especially in the latter stages of the CCFT but it is significantly less than
that measured in people with neck pain.54,137,138,140 Note there is an inverse
relationship between activity in the SCM and the deep cervical flexors
during the performance of the test, (i.e., the more activity in the SCM, the
less activity in the deep cervical flexors).148
■ If the patient is an upper costal breather, the test should be performed
during slow expiration to minimize overactivity in the anterior scalene
muscles.149
■ The patient clenches their jaw to use the hyoid muscles to augment the
contraction of the deep cervical flexor muscles. Correct the strategy by
requesting the patient to adopt a resting position of the mandible during
the test; ask them to lightly place their tongue on the roof of the mouth,
position their lips together with their teeth slightly apart.
■ On return from a test stage, the dial drops below 20 mmHg. (Check that
the pressure in the pressure sensor was stabilized before testing). A true
drop in pressure may indicate a deficit in proprioception, with the patient
overshooting the neutral head position on return from the movement.
■ On return to the starting position, the dial may read a pressure greater
than 20 mmHg. This usually reflects an inability to relax the muscles
 following a contraction. The muscles will relax, and the pressure will
return to the baseline when the patient is asked to look at a spot on the
ceiling behind their head.

Stage 2.
This stage tests the endurance (or the tonic holding) of the deep cervical flexors. It can be
conducted immediately after stage 1, but testing is delayed when substitution movements
(e.g., head retraction) were dominant in stage 1 of the test. There is no purpose in testing
the endurance of an incorrect muscle and movement strategy. In these cases, longus capitis
and colli activation is trained first with the correct movement, and endurance is tested in a
subsequent assessment.
In a research setting, the low-load endurance capacity of the deep cervical flexors is
tested by determining the pressure level that the patient can hold steady for 10 seconds,
with minimal activation of the SCM or anterior scalene muscles. The test is commenced at
the lowest level (22 mmHg) and, if 10 repetitions of 10-second holds are achieved, the test
is progressed to the next pressure target and so forth up to 30 mmHg or until the patient
fails. In the clinical setting, this approach can be very time consuming and a short cut is
used, which sacrifices a formal measure as might be required in research. The clinical
testing starts at the 22 mmHg target but contractions are held for approximately 5 seconds
and if after two to three repetitions, the patient is observed to be coping well, they relax
for a few seconds and then attempt the next pressure level. The test is continued until the
pressure level at which the patient fails is reached.
Clinical measure: the pressure level at which the patient fails. Training will begin at the
pressure level below (e.g., if failed on 24 mmHg, training commences on 22 mmHg).
Again, there is variability in performance between individuals, but most asymptomatic
individuals can successfully perform repetitions of the test to at least 26 mmHg (if not 28
and 30 mmHg stages), whereas neck pain patients often do not achieve more than the first
or the second levels of the test.5,144,150
Poor performance or failure is judged when the patient:

■ cannot maintain craniocervical flexion in the test stage and reverts to a

retraction strategy.
■ cannot hold the pressure steady at the designated test level (the needle
on the dial falls away even though the patient seems to be holding the
head in a flexed position).
■ cannot hold the position without overtly activating the superficial
flexors.
■ holds the position but with a jerky action, indicative of fatigue.

Cervical flexor strength and endurance

Tests of strength and endurance are performed as a progressive assessment in subsequent
treatments, once the patient can control the craniocervical region in a head lift assessment.
Early strength testing without adequate control may aggravate symptoms or conversely,
pain inhibition may flaw test outcomes.
Neck flexor strength and endurance may be tested using dynamometry151,152 but the
most common test is a head lift test. This test has mainly been investigated as a strength
test for the deep cervical flexors where an individual’s ability to hold their head 2 cm off a
supporting surface while controlling the chin position is timed. In this respect, the test has
proven reliable.153–156 Nevertheless, the SCM is the major flexor of the neck and the
antigravity head lift is a test of the strength of all cervical flexors.
When considering endurance, the neck flexors have impaired capacity over a spectrum
of contraction intensities. Poor endurance and fatigability occur at 50% and 20% to 25%
of maximum voluntary capacity.157,158 Thus endurance should not be tested in antigravity
head lift tests only, but in positions where the effect of gravity and head load are reduced
(e.g., various angles of reclined sitting).

Cervical extensor muscle tests

The cervical extensors weaken and may become more fatigable in association with neck
pain (see Chapter 5). Factors that guide clinical testing is the emerging evidence that
impairment is relatively more pronounced in the deeper extensor muscles of the cervical
spine, such as semispinalis cervicis and multifidus159–161 and that the suboccipital muscles
frequently display atrophy or substantial fatty infiltrate in some people with WAD and
older persons with headache.159,162–165 Therefore assessment aims to bias these muscle
groups.
The patient is positioned, as they personally tolerate initially, in one of three positions
of decreasing gravitational load; either four-point kneeling (or alternatively prone with the
head over the edge of the bed), prone on elbows or forward lean sitting propped on
elbows. All cervical extensor muscles contribute to supporting the weight of the head
against gravity. Tests are not specific to one muscle group but rather aim to target
particular muscle groups.

Suboccipital muscles
Tests are conducted for the suboccipital extensors (rectus capitis major and minor) and for
suboccipital rotators (obliquus capitis superior and inferior). The clinician gently stabilizes
the C2 vertebra to assist in the localization of the movement to the upper cervical region.
For the rectus capitis major and minor muscles, the patient is asked raise and lower their
chin to perform alternating small ranges of craniocervical extension and flexion (nodding
action to say yes) while maintaining the cervical spine (C2–T1) in a neutral position (Fig.
9.17A). This is a familiar movement and usually the patient has no difficulty with it.
Nevertheless, the movement is tested (and exercised) routinely based on the evidence of
the morphological changes in the muscles in persons with neck pain disorders coupled
with the knowledge of their major contribution to sensorimotor control (see Chapter 6).

FIG. 9.17 Tests of the neck extensor muscles. (A) Craniocervical extension. The
cervical region remains in neutral. (B) Craniocervical rotation. Ensure that it is head
rotation on the cervical spine (C1–2 rotation). Observe if movement is occurring in the
mid cervical region which is an incorrect action. (C) C1–2 rotation is facilitated by
stabilizing C1–2 and rotating the patient’s head in an assisted active movement.

The obliquus capitis superior and inferior are tested by asking the patient to perform
small ranges of head rotation as if saying no (Fig. 9.17B). What is expected is a pure spin
of the head on the neck (C1–2 rotation) with a range of no more than 30 to 40 degrees.
The clinician must observe where motion is occurring. Often the motion occurs in the mid
to lower cervical region rather than at C1–2, particularly in patients with upper cervical
disorders. If this is the observation, then it is necessary to determine the origin of this
altered movement pattern. To do this, the clinician now stabilizes C2 more firmly and asks
the patient to again turn the head as if saying no. The patient may now be able to perform
the C1–2 movement aided by the localizing input of the hand grip. Alternately, they
cannot rotate their head to the desired ranges, and often they can barely achieve any
rotation. This may reflect C1–2 joint hypomobility or it may reflect poor proprioception
and an inability to dissociate head from neck movement. This is easily differentiated by
the clinician facilitating C1–2 rotation (Fig. 9.17C). There will be one of three results.

■ Rotation range immediately begins to improve and approaches normal

excursion. The reasoning is that joint hypomobility is not the issue, rather
the patient has poor movement sense.
■ Rotation range is blocked. This is often more movement to one side that
the other and suggests C1–2 hypomobility. The finding should be
consistent with the result of the cervical flexion rotation test.
■ Facilitation improves the range of rotation but there is still less than
acceptable range. There is a combination of problems; the patient has poor
movement sense coupled with hypomobility at C1–2.
Cervical extensors
All cervical extensors will be recruited to support the weight of the head against gravity.
The test nevertheless aims to bias the deeper cervical extensors (semispinalis cervicis and
multifidus). The patient is requested to perform cervical extension while keeping the
craniocervical region in a neutral position to place head extensor muscles such as splenius
capitis and semispinalis capitis at a mechanical disadvantage. The axis of rotation passes
through the C7 vertebra.
The craniocervical region is maintained in neutral during cervical extension by
facilitating the position with an eye focus task. A pen or book is placed between the hands
in the four-point kneeling position (or equivalent in other positions). The patient is asked
to curl their neck down to look at their knees and then to curl it back as far as possible
while keeping their eyes on the book/pen. In relation to instructions, the word “curl” is
important to discourage a backward translation or retraction action (Fig. 9.18). Normally,
the patient should be able to extend the neck to approximately 20 to 30 degrees. Poor
performance in the test is indicated by the following.

FIG. 9.18 Cervical extension: the patient curls their head into extension while keeping
their eyes on the book/pen (i.e., in a craniocervical neutral position). It is important to
check that the patient can dissociate craniocervical extension from cervical extension
and not allow the head extensors, such as splenius and semispinalis capitis, to
contribute significantly to the extension movement.

■ An inability to extend to 20 degrees; many neck pain patients cannot

extend past the neutral position (also differentiate hypomobility in the
cervicothoracic region limiting motion).
■ The patient cannot dissociate head extension from neck extension,
 subtle extension of the cranium is observed, often in association with a
visual outline of overactive splenius capitis and semispinalis capitis
muscles.
■ Fatigue. The patient reports they are tiring after a few repetitions.
Alternately, the clinical observes an increasing lordosis develop in the
upper cervical region as the cranial extensors begin to dominate the
movement.

When active cervical extension is painful and limited, there can be a reluctance to test
the cervical extensors in the initial assessment. Painful active extension should not deter
testing because the loads and muscle actions are very different between the two tests. In
testing positions for the cervical extensors, the compressive forces of head load and
gravity are eliminated, and the movement is controlled by the extensor muscles. Patients
usually find the test comfortable and they can stop short of pain if relevant.

Cervical extensor strength and endurance

Tests of strength and endurance are performed as a progressive assessment in subsequent
treatments, once the patient can perform full range cervical extension with the
craniocervical region maintained in a neutral position.
Neck extension strength may be tested with a dynamometer if available, or use may be
made of a handheld dynamometer, which is a reliable method of measurement.166
Endurance can be assessed using the modified Biering-Sorensen test,167 and light weights
may be added to the head to test endurance at different contraction intensities.

Assessment of disturbances in sensorimotor control

Assessments for impaired sensorimotor control are indicated when patients report
dizziness, light headedness or feelings of unsteadiness in association with their neck pain.
A legitimate argument could be raised to incorporate these tests routinely in all patients
with neck pain because deficits in sensorimotor control have been found in those not
complaining of these symptoms (see Chapter 6). However, these tests should be conducted
routinely in patients with symptoms of dizziness/light headedness and in patients where
the onset of neck pain is related to trauma. Sensorimotor testing should also be considered
in patients not responding to management as expected.
Four sets of measures are undertaken; tests of cervical proprioception (joint position
and movement sense), balance, oculomotor control and coordination. Differentiating
whether an impairment is arising from a cervical or vestibular origin is always a challenge
especially in patients with balance and eye movement control disturbances (see Chapter
10). Likewise, challenging is identifying the role of the cervical spine in altered
sensorimotor control in patients who have sustained neck or head trauma such as a
concussion or whiplash injury (see Chapter 10).
Cervical proprioception
Cervical position sense
Cervical position sense is commonly assessed in the clinical setting by measuring a
person’s ability to relocate their natural head posture while vision is occluded.168 Joint
position error is the angular difference between the starting natural head posture and that
assumed following a neck movement. Errors are commonly measured following return
from cervical extension, and rotation to the left and right, although return from flexion and
lateral flexion can be assessed if time allows. As an extension of the test, cervical joint
position sense can be assessed by measuring the accuracy in relocating selected points in
range.169
Moderate deficits can be judged visually in the clinical situation, but joint position
errors as little as 4 to 5 degrees170,171 indicate a deficit in cervical joint position sense and
are difficult to judge visually. A simple quantitative measure is preferable, and it becomes
an outcome measure on which to reassess effects of management. A simple, reliable and
valid measure involves the use of a target and a laser pointer mounted onto a lightweight
headband.168,172 Alternate measuring instruments include a gravity dependent
goniometer,173 or the use of a standard computer, webcam and free head tracking
software.174
When the test is implemented using a laser and target, the patient sits comfortably such
that the laser pointer is 90 cm away from a wall and the starting position is projected by
the laser onto the wall (Fig. 9.19). The target is positioned so that the laser is in the centre
of the target. The patient concentrates on the starting position, then closes their eyes. They
actively move their head in a specified direction ([L] or [R] rotation or extension), then
return to the starting position as accurately as possible. Six trials are optimal for research
purposes,175 but at least three consistent trials are considered satisfactory for clinical use.
The participant’s head is manually repositioned to the starting position between trials. No
verbal feedback is provided, and the patient keeps the eyes closed between repetitions.
Each return position is marked on the target. The difference between the starting and
return points is measured in centimetres which can be converted to degrees.172 In addition
to the quantitative measure of cervical position sense, other signs of impaired cervical
position sense may be observed including jerky movements, uncertainty or searching for
the initial position, overshooting the initial position, reproduction of dizziness or there is a
noticeable difference between movement patterns when performed with the eyes closed
compared with eyes open.
 FIG. 9.19 Head relocation accuracy: the laser pointer is placed on the head and the
patient attempts to relocate the head as accurately as possible after performing a
specific neck movement with the eyes closed.

An alternate test might be considered especially when aiming to differentiate vestibular

and cervical causes of dizziness or light headedness. The laser is now attached to the
sternum (Fig. 9.20), the head is held still (to neutralize a vestibular cause) and the patient
rotates the trunk. Accuracy in trunk repositioning is used to measure joint position
sense.176,177

FIG. 9.20 Trunk relocation accuracy: the laser is positioned on the sternum and the
patient is asked to relocate the trunk back to the neutral position with the eyes closed.
The examiner gently stabilizes the head throughout the test to prevent head motion.

Cervical movement sense

Cervical movement sense is tested by assessing the accuracy with which a patient can
perform fine head and neck movements to trace intricate patterns such as a diagonal
zigzag pattern. A pattern is placed on the wall 90 cm in front of the patient and it is traced
using the laser method (Fig. 9.21). At present, a qualitative assessment is used to judge the
accuracy of the motion, deviation from the target and the speed-accuracy trade-off. Work
is currently underway to develop a quantitative method for this test. “The Fly” is a more
sophisticated computerized method to measure accuracy of head and neck movement
during unpredictable movements.178 Applications using a smart phone to detect and
compare neck motion will be a helpful clinical tool. A virtual reality device is also being
researched for assessment of accuracy of head motion.51

FIG. 9.21 Movement sense: assessment of the quality of movement when the patient
attempts to accurately move the laser on their head to trace the pattern ahead.

Standing balance
The clinical examination of standing balance takes the patient through tasks that
progressively challenge postural stability by altering foot position, visual input and the
supporting surface. Balance in comfortable (Fig. 9.22) and subsequently narrow stance is
assessed with the patient standing on a firm and then a soft surface such as a piece of
10 cm dense foam. The tests are performed with the eyes open and then closed. It is
reasonable to expect that a person under the age of 60 years can maintain stability for up
to 30 seconds in comfortable and narrow stance tests. Abnormal responses include large
increases in sway, slower responses to correct sway or rigidity to prevent excessive sway
as well as an inability to maintain balance. The test level and response are recorded.
Research is continuing to develop ways to bias cervical proprioception in tests of
balance.179,180 Performance in normal stance is compared with stance when the head still
faces forward but the trunk is rotated under the stationary head. Test results are
encouraging for using torsion as a method to distinguish balance disturbances attributed to
alterations of cervical afferent information from those of a vestibular cause.179
 FIG. 9.22 Balance in comfortable stance: balance with eyes closed is assessed with
the head in neutral. Simple inexpensive devices such as the Wii board can be used to
gain an objective measure of sway. A worsening of balance in the torsion (head still
trunk rotated 45 degrees) compared with neutral head position may indicate a cervical
cause of balance disturbances.

Patients aged under 45 years may require more challenging tasks to display balance
deficits. To increase the challenge, balance can be tested in tandem and then single leg
stance on a firm surface with eyes open and closed.181 Patients with neck pain of either
insidious or traumatic origin, and especially those complaining of dizziness or
unsteadiness, have greater difficulty in completing the tandem stance tasks on a firm
surface than asymptomatic persons.181,182
Consideration is also given to including dynamic tests such as the step test, timed 10
metre walk with head turns and tandem walk as required, for example, if the patient
complains of dizziness when walking, loss of balance or falls (Fig. 9.23).183,184 The
Dynamic Gait Index185 can be conducted in the clinical setting to provide measures of
functional dynamic balance especially in elders, where an increased risk of falls might be
suspected.186,187
 FIG. 9.23 Walking with head turns: the quality and time to walk 10 metres when
keeping the head still is compared with walking while moving the head in large range
side-to-side or up-and-down movements.

Oculomotor assessment
Oculomotor assessment incorporates qualitative assessment of the ability to (1) maintain
gaze while moving the head and (2) eye follow while keeping the head still. These tests
are not exclusive to, nor can they specifically differentiate, individuals with neck pain.
They are often used in assessment of vestibular or central nervous system disorders.
Nevertheless, some tests have been modified to bias a cervical component in attempts to
determine the influence of the cervical region on the visual system. The routine tests are
gaze stability and the smooth pursuit neck torsion test. They are performed with the
patient sitting. Abnormal test responses include difficulty or inability to perform the task,
reproduction of symptoms, jerky or non-fluent head or eye movements. In general,
patients with neck related oculomotor disturbances do not present with nystagmus at rest
or during these tests. Its presence is more indicative of vestibular pathology.

Gaze stability
Gaze stability is assessed by asking the patient to keep their eyes focused on a target while
they actively move their head into flexion, extension and rotation to the left and right (Fig.
9.24). Pertinent findings are an inability to maintain focus on the target, awkward or
reduced cervical motion (< 45 degrees despite having available movement without eye
fixation) or reproduction of symptoms such as dizziness, blurring of vision or nausea. This
test is performed relatively slowly rather than quickly to bias the cervical rather than
vestibular afferents.
 FIG. 9.24 Gaze stability: the patient is asked to fixate on a point (e.g., pen) in front of
them as they move their head as far as possible in each direction.

Eye follow: smooth pursuit neck torsion test

Eye follow is tested using the smooth pursuit neck torsion test.188 In the test, eye follow is
compared between the neutral head position and when the trunk is rotated on the head
(neck torsion) so that input to the vestibular system is avoided. The patient is asked to
keep the head still and follow, as closely as possible, a moving target (e.g. the clinician’s
index finger or a pen) with the eyes. The target is moved slowly side to side (20 degrees
per second through a visual angle of 40 degrees). The test is first performed with the head
and trunk in neutral and then repeated with the neck torsioned to the left (left torsion) by
rotating the trunk and shoulders 45 degrees to the right, keeping the head still. It is
repeated with the trunk and shoulders rotated 45 degrees to the left (right torsion) again
keeping the head still (Fig. 9.25A and B). Any difference is noted in smooth eye follow or
symptom reproduction between the neutral and torsioned positions. Patients with neck
pain are often unable to keep up with the target and display quick catch up eye movements
(saccades) when the neck is in torsion, particularly when the target is crossing the midline.
Table 9.2 lists possible outcomes of the test. Two points to note are that it can be normal to
have saccadic eye movements at the extremes of the visual angle and with the change of
movement direction.189 An alternate cause is suspected when performance is poor when
the head is in neutral and it is unchanged by adding neck torsion. Qualitative assessment
of eye movement has acceptable validity and reliability,190,191 but further accuracy is likely
when patient symptoms are added to eye movement assessment.
 FIG. 9.25 The smooth pursuit neck torsion test. (A) The patient follows a moving pen
(40-degree angle, 20 degrees per second) with their eyes while keeping their head still.
The clinician observes the pursuit of the eyes. (B) The pursuit of the eyes in neutral is
compared with when the head is still and trunk turned to the left 45 degrees (right
torsion). It is repeated on the other side. Increased catch up saccades in the torsion
positions especially as they cross the midline and/or reproduction of symptoms in the
torsion positions compared with the neutral position is a positive test.

TABLE 9.2

Rating scale smooth pursuit neck torsion test eye movements in neutral head
position compared with torsion
Score Rating definition
Negative 0 Smooth, precise eye movements in all positions

Negative 00 Catch up saccadic eye movements in the midline in all positions, but no change in eye movement in torsion versus
neutral
Positive 1 Moderately positive, slight catch up saccades in the midline compared with neutral, can occur on either side
Positive 2 Strongly positive, many catch up saccadic eye movements in the midline when compared with neutral, can occur on
either side

Adapted from Casa ED, Helbling JA, Meichtry A, et al. Head-eye movement control tests in patients with
chronic neck pain; inter-observer reliability and discriminative validity. BMC Musculoskelet Disord 2014;15:16.

Eye-head coordination; trunk-head coordination

Eye-head coordination is depicted in Fig. 9.26. The patient first moves the eyes to look at
a target and then moves the head ensuring the eyes keep focused on the target. The eyes
are then moved back to the centre, followed by the head. The test can be performed to left,
right and up and down directions. Patients with neck pain are often unable to keep the
head still while the eyes move or they lose focus during the head movements.192,193 Eye
and head movements can also be assessed by following a trunk or a hand movement.
 FIG. 9.26 Eye-head coordination: the patient moves the eyes first to focus on a target
30 degrees away and then the head to the target ensuring the eyes keep focused on
the target. This can be performed to the left, right and up and down.

Trunk-head coordination is assessed in standing. The patient holds the head still, eyes
open looking straight ahead while rotating their trunk to the left and right (Fig. 9.27).
Patients with neck pain often have difficulty keeping the head still while the trunk is
moving or are unable to dissociate head and trunk movement. A positive test is an inability
to fix the head and/or a decreased range of trunk movement. A laser mounted on the head
can monitor any head motion.194

FIG. 9.27 Trunk head coordination: the patient tries to hold the head still with the
eyes open while rotating their trunk to the left and right.

Other causes of disturbances to the sensorimotor

control system
Primary vestibular pathology may result from a whiplash injury, especially when it is
associated with head trauma. Symptoms could be of vestibular origin in such patients or
conversely, there is some evidence that the neck may influence vestibular function (see
Chapter 6).195 Disturbances of cervical sensory input may give rise to a mismatch of
sensory input from the cervical and vestibular systems, which may contribute to
asymmetry of the vestibulo-ocular reflex (VOR).196 Some patients with neck pain who had
previously normal vestibular function, could feasibly have an asymmetry of the VOR of a
cervical origin.197 Secondary vestibular influences on sensorimotor control may need to be
considered in people with neck pain.
There is an overlap in responses between the vestibular and cervical musculoskeletal
systems in a number of tests. In some patients, additional tests may be necessary to further
examine vestibular function. A simple screening test, the vestibular oculomotor screening
test (see Chapter 10) might be suitable in musculoskeletal practice.198 It includes tests of
saccadic and smooth pursuit eye movement, near point convergence (Fig. 9.28), gaze
stability with fast head movements (180 beats per minute) and vision motion sensitivity
(Fig. 9.29). An increase in symptoms of more than 2 points on an 11-point numerical
rating scale is considered a positive response to either central or vestibular causes.

FIG. 9.28 Near point convergence: the participant focuses on a small target at arm’s
length and slowly brings it toward the tip of their nose until they see two distinct
images. The distance between the target and the tip of nose is measured and recorded
(≥ 6 cm from the tip of the nose is considered abnormal).
 FIG. 9.29 Visual motion sensitivity: the participant stands with feet shoulder width
apart with the arm outstretched and focuses on their thumb while performing 5
repetitions of rotating the whole body (eyes, head and trunk) together through an 80-
degree excursion to the right and left.

More specific tests of the VOR may be required such as head shaking nystagmus183 or
the head impulse test.199 In cases where benign paroxysmal positional vertigo in the
posterior canal is suspected, the Hallpike-Dix manoeuvre is the screening test.183 For a
more detailed review of vestibular evaluation, the clinician should consult texts designed
specifically for that purpose.183 Referral for a more thorough investigation of the vestibular
or central nervous systems may be warranted where cervical causes of dizziness or
disturbances in the sensorimotor system cannot be substantiated.
There are other causes of disturbances to sensorimotor control that could be
concomitant with neck pain. These include medical conditions such as diabetes and
merely the factor of ageing. Vestibular function deteriorates as a consequence of age.200 In
older patients, neck pain may magnify the degree of disturbances in sensorimotor
control.201 Such co-occurrences should not detract from the rehabilitation program but may
influence speed of recovery or outcomes.

Conclusion
This chapter has provided a comprehensive set of tests for use in the clinical setting to
detect impaired processes and function in patients presenting with neck pain disorders.
Certainly not all tests are relevant for every patient and clinicians will need to prioritize
examination procedures according to the patient’s presentation. The physical examination
provides a wealth of information. The clinician should be constantly reflecting on the
patient’s presenting complaint, testing if the pattern fits between complaints and physical
findings and most importantly, using the examination findings to develop with the patient,
a relevant management approach. The management planning should address both the
patient’s current complaint and prevention of further episodes of neck pain, that is, restore
function and not just provide pain relief. Likewise, a set of outcome measures informs on
the effectiveness of the intervention as well as provides a set of incentives for the patient
and clinician to achieve.

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associated disorders- Relationship to self reports of neck pain and disability,
 dizziness and anxiety. J Rehab Med. 2005;37:219–223.
190. Daley L, Giffard P, Thomas L, et al. Validity of clinical measures of smooth
pursuit eye movement control in patients with idiopathic neck pain. Musculoskel
Sci Prac. 2018;33:18–23.
191. Casa ED, Helbling JA, Meichtry A, et al. Head-eye movement control tests in
patients with chronic neck pain; inter-observer reliability and discriminative
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192. Grip H, Jull G, Treleaven J. Head eye co-ordination and gaze stability using
simultaneous measurement of eye in head and head in space movements -
potential for use in subjects with a whiplash injury. J Clin Monit Comput.
2009;23:31–40.
193. Treleaven J, Jull G, Grip H. Head eye co-ordination and gaze stability in subjects
with persistent whiplash associated disorders. Man Ther. 2011;16:252–257.
194. Treleaven J, Takasaki H, Grip H. Trunk head co-ordination in neck pain. 2012
[IFOMPT; Quebec Canada].
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interaction with vestibulo-ocular reflex. Exp Brain Res. 1973;18:512–1530.
196. Fischer A, Verhagen W, Huygen P. Whiplash injury. A clinical review with
emphasis on neurootological aspects. Clin Otolaryngol. 1997;22:192–201.
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induces asymmetric gain of the vestibulo-ocular reflex in healthy subjects. Acta
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199. Halmagyi G, Curthoys I. Clinical testing of otolith function. Ann NY Acad Sci.
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200. Speers R, Ashton-Miller J, Schultz A, et al. Age differences in abilities to perform
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parameters in community-dwelling elders. Man Ther. 2008;13:317–324.
10

The Differential Diagnosis of Symptoms

and Signs of Sensorimotor Control
Disturbances
The proprioceptive, visual and vestibular systems together provide input into the
sensorimotor system for control of head and eye movement and postural stability. They
interact closely in function and dysfunction. Cervical proprioceptors have reflex
connections to both the vestibular and visual systems. They can influence the function of
these systems and can also partially compensate for any deficits. Changes in cervical
somatosensory information (Chapter 6) can influence the control, interaction and tuning of
afferent input. This, in turn, may cause secondary adaptive responses in the visual or
vestibular systems.1–4 Likewise, both visual and vestibular deficits can impact on the
cervical spine and cause altered head and neck positioning or increased muscle activity. A
primary vestibular problem is often associated with a neck complaint5,6 and altered vision
can directly influence cervical musculature.7,8 Thus there are many interactions and
variables to appreciate to effectively clinically reason in differential diagnosis.
Signs and symptoms of altered sensorimotor control may be caused by a primary
cervical, visual or vestibular problem, which may or may not cause secondary changes in
the other systems. Further, increased reliance on the cervical spine may be required in
circumstances where visual or vestibular input is impaired. If the cervical system
subsequently becomes unreliable, this could lead to further amplification of symptoms
stemming from visual or vestibular dysfunction. A mixed presentation may occur with
coexisting visual, vestibular and cervical causes of sensorimotor disturbances (e.g., a
postconcussion syndrome; age changes in the elderly). Certain medications and emotions
such as anxiety can perpetuate or cause disturbances via several mechanisms.9,10
Postconcussion, altered autonomic nervous system function and its control of cerebral
blood flow can also exacerbate symptoms.11 Consequently, it can be difficult to determine
the precise causes of sensorimotor control disturbances. Nevertheless, it is essential to be
aware of all possible common causes of dizziness, visual disturbances, tinnitus, altered
head and eye movement control and postural instability, and be able to determine; (1)
when a cervical cause or component is present or not; (2) when treatment directed towards
the cervical spine is indicated; and (3) when referral is required for specialist assessment
and investigations.

Differential diagnosis of dizziness

Cervical dizziness attributed to altered cervical afferent input is often described as
unsteadiness or light headedness. It is common in neck disorders especially in persons
with persistent whiplash-associated disorders (WAD)12 and cervicogenic headache.13 Yet
altered cervical afferent input is not the only possible cause of dizziness or light-
headedness. The relationship between the cervical spine and dizziness has, and still is, a
source of controversy. There are few reliable clinical tests to differentiate cervical from
other causes of dizziness and some neurologists reject a possible cervical aetiology of
symptoms.14–16 Nevertheless, there is sufficient experimental and clinical evidence to
support a cervical cause.12,17–20 For instance, a cervical cause is supported when people
with neck pain and dizziness have greater deficits in specific tests of cervical sensorimotor
control compared with people without dizziness.12,21–23 A cervical cause is also supported
when symptoms improve with treatments directed specifically towards the cervical
spine.18,24–27
A cervical disorder is more readily accepted as the cause of dizziness when neck pain is
of an idiopathic origin. This is in contrast with dizziness associated with trauma such as a
whiplash injury where other causes of dizziness are possible (e.g., an associated vestibular
injury). It has also been proposed that dizziness and unsteadiness associated with WAD
are side effects of medication or anxiety caused by either ongoing pain or financial gain.28
Our research counters this view. We have found no difference between patients with
chronic WAD with and without dizziness in medication intake, anxiety levels or
compensation status. Neither do these features influence measures of sensorimotor
control.12,21,22,29 Other causes of dizziness must always be considered, but in the absence of
traumatic brain injury following a whiplash injury, dizziness is most commonly caused by
altered cervical afferent input.12,30–35
Conditions that must be considered in the differential diagnosis of dizziness include:
central vestibular causes (vertebrobasilar insufficiency, cervical arterial dissection,
vestibular migraine and mild brain injury/concussion) and peripheral vestibular disorders
(e.g., benign paroxysmal positional vertigo [BPPV], labyrinthine concussion, or otolith
disorders). The clinician should be cognizant of all causes to facilitate differentiation of
dizziness in the patient presenting with neck pain.

Central vestibular disorders

Central vestibular disorders relate to any central nervous system (CNS) cause of vertigo.
The most likely central vestibular causes to present to a musculoskeletal clinician are
those secondary to cervical vascular disorders (vertebrobasilar insufficiency [VBI], or
cervical artery dissection [CAD]), mild brain injury/concussion or vestibular migraine.

Cervical vascular disorders

Vascular supply to the vestibular system depends on arteries that originate from the basilar
artery, which has supply from the vertebral arteries. Central vertigo and other neurological
symptoms, arising from vascular compromise, are common to both VBI and CAD because
the arteries also supply other cerebral structures including the vestibular system.36 The
reader is directed to a review by Thomas37 on cervical arterial dysfunction.
 VBI is more common in elderly patients who have degenerative musculoskeletal and
peripheral or cardiovascular changes that may impact on blood flow in the cervical
arteries. Abnormal vertebral artery blood flow and subsequent dizziness can also occur
following a whiplash injury.38,39 Although VBI can cause dizziness, its importance and
frequency as a cause of dizziness in neck pain disorders has probably been overestimated
because of concerns with the use of high velocity manipulative thrust procedures.
Nevertheless due care is needed even with the use of low velocity manipulative therapy
techniques in the management of older patients.40,41 Patients with VBI may report transient
vertigo and neurological symptoms that can be reproduced with sustained neck positioning
and do not abate when the position is held. There may be a latent effect where symptoms
are experienced soon after the head is returned to the neutral position.42–44 However, other
studies have found that dizziness is uncommon even in the presence of vertebral artery
blood flow abnormalities. Nevertheless, caution is always warranted, especially in patients
who develop symptoms with VBI testing because of a potential risk of a cerebrovascular
incident.
CAD is a tear or haematoma in the wall of the artery. CAD accounts for 10% to 25% of
ischaemic stroke in the young to middle-aged population. It can occur spontaneously, but
commonly follows minor neck or head trauma.45 The most common initial symptoms are
unilateral neck pain or headache. Thus a person with impending CAD could inadvertently
present to a musculoskeletal clinician for treatment.37 Those in early stage CAD must be
identified so that they can be referred for vital medical management, avoiding unnecessary
and potentially harmful treatment. CAD can be confirmed with medical imaging such as
magnetic resonance angiography or computed tomography angiography.37,46 Risk factors
for CAD include: genetic predisposition or history of migraine;47 recent infection and even
very minor head or neck trauma such as jerky head movements or heavy lifting.48
Although rare, an ischaemic event and CAD soon after a whiplash injury has been
reported in a few isolated cases.42 However, generally damage to the vertebral artery is
thought to be rare in the absence of a fracture or dislocation,49,50 and if it occurs, it may be
asymptomatic owing to collateral artery compensation.
Thomas et al.51,52 suggests that CAD be suspected particularly in persons under the age
of 55 years, who present with moderate to severe, new or unusual unilateral neck pain
and/or headache associated with any unexplained transient or ongoing specific
neurological dysfunction including dizziness within the last five weeks. Neurological
signs and symptoms relevant to the area of the brain supplied by the cervical vertebral
arteries, such as Horner syndrome, tinnitus, facial pain, vertigo and/or ataxia, should be
considered but may not present initially.53 Other risk factors, such as recent minor neck or
head trauma and infection, must be noted. Work is currently underway to develop and test
a clinical prediction tool to assist primary care providers in early diagnosis of CAD.

Minor brain injury

Dizziness from central vestibular dysfunction can result from a minor brain injury
sustained from a direct blow to the head in a motor vehicle crash or a blunt injury trauma
to the head or neck from a sports injury or other causes. Brain injury should be considered
especially with reports of amnesia or head trauma.54,55 Minor brain injury or concussion is
an occasional cause of dizziness postwhiplash, but is a more common cause in contact
sports injuries. However, a cervical cause of dizziness is also relatively common after
blunt head trauma20 and the role of cervical trauma in concussion incidents is being
investigated as a primary cause of dizziness and other symptoms.56–61

Vestibular migraine
Vestibular migraine is a common cause of central vestibular vertigo with a population
incidence of 1%. It occurs predominantly in middle-aged females.62 It is characterized by
episodic vertigo lasting several minutes to days. It can be associated with migraine
headaches and, during an attack, clinical signs of central vestibular dysfunction may be
apparent. There are usually no signs of abnormal vestibular function between attacks.63
Preattack auras (reversible neurological symptoms) and postdromal fatigue can occur.64,65
The precise cause is unknown, but there are suggestions that in some cases it is triggered
by neck injury and pain.62,66

Peripheral vestibular lesions

In cases of neck trauma, injurious forces can shear the delicate structures of the peripheral
vestibular system which can result in vertigo attributable to either benign BPPV,
labyrinthine concussion or otolith disorders.20 Trauma can also rupture the otic capsule
window resulting in a perilymph fistula.67 In cases of nontraumatic neck pain, the main
considerations in differential diagnosis are Ménière disease, labyrinth infections,
vestibular neuronitis, acoustic neuromas and BPPV.36
There is considerable controversy regarding the frequency of peripheral vestibular
versus cervical causes of dizziness in the whiplash injured patient, although there is a
greater likelihood of a vestibular cause (35%) when there has been a mild head
injury.20,67,68 At one extreme, many consider vestibular disorders to be the primary cause of
dizziness, although these reports are based largely on clinical patterns rather than tests of
the vestibular system.32,69,70 Other studies, which have screened with vestibular tests, report
variable proportions.20 Hinoki et al.71 and Fischer et al.1 reported normal vestibular test
results in most of their whiplash cohorts, although many participants had some vestibular
hyperactivity reasoned to result from limited neck movement and pain, with subsequent
vestibulo-ocular reflex enhancement. Injuries induced by axial rotation as against linear
acceleration in the crash may result in different types of neuro-otological injury.72 The
clinician should seek details of the injuring mechanism in the patient interview and choose
tests accordingly to differentiate possible causes of the disturbances.

Benign paroxysmal positional vertigo

BPPV is the most common cause of peripheral vestibular vertigo. Symptoms are usually
sudden-onset, short-duration vertigo, often accompanied by nausea and vomiting.
Symptoms follow movements such as rolling over in bed and tilting the head back and are
the result of otolith debris moving into the semicircular canal. The posterior canal is most
commonly involved, but it can occur in the other canals.68 Symptoms and signs of BPPV
can cease either spontaneously or after otolith repositioning manoeuvers, but they can
reappear.73 Possible causes are trauma, infection, degeneration or idiopathic.

Perilymph fistula
A perilymph fistula is an abnormal opening in the inner ear. Symptoms such as dizziness,
vertigo, imbalance, nausea, tinnitus or fullness of the ear are reproduced with changes in
ear pressure that occur with for instance, coughing, sneezing and loud noises.74,75

Ménière disease
Ménière disease is a disorder of the inner ear that can cause episodes of vertigo. The
symptoms are variable but the most common are severe attacks of spontaneous rotational
vertigo, that last from 20 minutes to several hours. They can be accompanied by tinnitus
and hearing loss.76

Labyrinthitis and vestibular neuronitis

Labyrinthitis and vestibular neuronitis are characterized by acute, sustained vertigo with
associated nausea and vomiting, which is aggravated with any position change. The
patient may be forced to stay in bed for several days.36 Patients may present to
musculoskeletal clinicians in the subacute phase with dizziness, neck pain and stiffness
resulting from attempts to limit head movement to avoid symptom exacerbation.

Acoustic neuroma
An acoustic neuroma is a slow growing benign tumour on the eighth (vestibulocochlear)
cranial nerve and thus can cause both hearing and balance deficits. Symptoms such as
tinnitus, true hearing loss, vertigo, imbalance and fullness in the ear are common.36

Differential diagnosis of other symptoms

After dizziness, the most common sensorimotor symptoms associated with neck pain are
visual disturbances77 and tinnitus78,79 but other symptoms such as subjective hearing loss
and fullness in the ear can also occur. Similar to dizziness, there can be several causes of
these symptoms. They can have peripheral and central vestibular causes and can also be
caused by altered cervical input. Differential diagnosis of these symptoms takes on a
similar process to that used for dizziness. Specific unique aspects to consider for both
visual symptoms and tinnitus will now be explored.

Visual system disturbances

After neck or head trauma, any dysfunctions in functionally related structures in the visual
pathway can cause a variety of visual symptoms such as blurred or double vision,
photophobia, difficulty with focusing, reading and tracking objects. Deficits can include
strabismus (crossed eyes), convergence and/or accommodation insufficiency and
oculomotor, binocular or visual spatial dysfunction. Collectively, these signs and
symptoms are termed posttrauma vision syndrome.80,81 Disturbance to the optokinetic
reflex can also occur and has been noted as a specific finding after concussion.82
The role of the visual system should be considered in development or persistence of
neck pain or discomfort. Unfavourable, challenging or demanding visual tasks or visual
dysfunction may influence cervical posture, movement and muscle activity. Some direct
relationships have been observed between unfavourable visual conditions and neck muscle
activity which were independent of postural changes. This is thought to reflect a possible
interaction between the visual system, sympathetic nervous system and the head-
stabilizing muscles.83 Visual ergonomics may be a potential driver of symptoms in some
patients.7,83–85

Tinnitus
Tinnitus is associated with peripheral vestibular disorders such as Ménière disease,
perilymph fistula74 or labyrinthine concussion86 or central vestibular disorders such as
vestibular migraine.62 Tinnitus can also result from abnormal cervical afferent input
known as cervicogenic somatic tinnitus (CST). Specifically CST is characterized by
severe subjective tinnitus with associated neck complaints in the absence of objective
hearing deficits.87 There is a high prevalence of tinnitus in temporomandibular
dysfunction, which too may be associated with neck, head and face pain.88

Clinical examination
The diagnosis should establish a correlation between symptoms such as dizziness, visual
disturbances and tinnitus and signs of cervical spine dysfunction. Diagnosis is based on
the patient’s history, the clinical assessment of cervical musculoskeletal and sensorimotor
impairments and, if required, the use of oculomotor, vestibular functional tests and a
neurological examination to exclude vestibular and or visual disorders.89 At present the
primary criterion to confirm cervicogenic dizziness is exclusion of other pathologies.
Nevertheless, a cluster of tests is emerging that may be useful for diagnosing cervical-
related causes to assist differential diagnosis. This is especially important for patients with
coexisting pathology.

History and interview

The clinician seeks a pattern to link symptoms to likely causes. The type of symptoms
(dizziness or unsteadiness, tinnitus or visual complaints), the temporal relationship with
neck pain, their frequency and duration and triggering factors help to distinguish cervical
sensorimotor disturbances from other causes. However, the picture can be clouded in
subacute vestibular conditions when compensatory adaptations have already been made
and reports of unsteadiness or imbalance rather than vertigo become the main complaint.90
Some patients report neck pain or stiffness as a consequence of adaptations to limit head
movements to minimize dizziness or vertigo symptoms.6 In this latter case, the dizziness is
caused by a primary vestibular pathology and a cervical musculoskeletal problem is a
secondary comorbidity.

Symptom differentiation
Table 10.1 presents a summary of the characteristic features of dizziness of various origins
to consider in differential diagnosis.
TABLE 10.1

Characteristic features of dizziness of different origins

Vertebral Perilymph Peripheral Central
Type Cervical BPPV
artery fistula vestibular vestibular
Description Unsteady Faint Vertigo Vertigo Vertigo Imbalance
Light-headed Vertigo Imbalance Unsteady Motion
Dizziness Motion intolerant
Motion
intolerant
intolerant

Frequency Episodic Episodic Discreet attacks Episodic Episodic Varies

vertigo
Constant
Constant
unsteady

Duration Mins-hours Several secs Secs Constant Secs to minutes Varies

Aggravate Neck pain/ Sustained neck Rolling in Visual Head positions or Spontaneous or
movement extension or bed challenges movement provoked
rotation
Looking up Increased ICC
Lying down Loud noises

Relieve Decreased neck pain Neck back to neutral Subsides if stay Head/body still Varies
in provoking
position
Associated Blurred vision Dizziness Nausea Unilateral Nausea Nausea
symptoms Dysarthria tinnitus
Photosensitive Vomiting Vomiting Imbalance
Dysphagia
Aural
Visual fatigue Diplopia Hearing loss CNS signs
pressure
Nausea Drop attacks Tinnitus Double vision
Hearing loss
Tinnitus Nystagmus Ear fullness Visual field shift
Numbness
Nausea

Suggested Abnormal cervical Vertebral artery Debris in Leak of perilymph Vascular Brain stem
cause afferent input dissection/ endolymph fluid injuries
insufficiency Cerebellum
Fractures
Trauma
Acoustic
neuroma
 Main signs Cervical MsK VBI tests? Positive Positive pressure Head impulse Spontaneous or
Hallpike gaze evoked
JPE >4.5 ? Positive Head shake
Dix or nystagmus
degrees selected DVA
head a
CECNT cranial Oculomotor
roll En-bloc
nerve tests deficits or
SPNT coordination movements exacerbation
Cervical torsion tests of
symptoms
Trunk head (VOMS)
coordination
Ataxia
Absence other
findings

a
Oculomotor- smooth pursuit, saccades, skew deviation, near point convergence.
CECNT, Comfortable stance eyes closed neck torsion; CNS, central nervous system; DVA, dynamic visual
acuity; H, hours; ICC, inter-cranial pressure; JPE, joint position error; Mins, minutes; MsK, musculoskeletal;
NPC, near point convergence; SPNT, smooth pursuit neck torsion; VBI, vertebrobasilar insufficiency; VOMS,
vestibular oculomotor screening.

Cervical dizziness is usually described as episodic unsteadiness or light headedness91,92

but not true vertigo (environment and self-spinning), which is more characteristic of
vestibular pathology.93 Peripheral vestibular causes, apart from vestibular neuritis and
Ménière disease, are often of short duration. They can be accompanied by hearing loss and
tinnitus, but do not present with neurological signs. This is different to central vestibular
complaints where vertigo duration can be longer and is usually associated with
neurological signs such as cranial nerve impairments, ataxia and coordination
difficulties.94
Visual complaints such as blurred vision, sensitivity to light, visual fatigue and
difficulty judging distances are common in cervical disorders.77,95 They probably reflect
disturbances in the cervico-ocular reflexes and the close links between the eye and neck
musculature.33 Complaints of double vision or spots and words moving are common in
visual system disorders but are uncommon in cervical disorders. Tinnitus, fullness in the
ear and subjective hearing complaints may be associated with cervical disorders79,87 but are
more common in peripheral vestibular disorders.
The behaviour of symptoms assists differential diagnosis. Symptoms of cervical
sensorimotor origin are usually exacerbated by specific neck movements or positions
rather than whole body movement (vestibular), coughing (increased intracranial pressure)
or anxiety.96 Symptoms should co-vary with neck pain and there should be a close
temporal relationship with onset of pain or injury. Accordingly, relief of symptoms should
occur with relief of neck pain.89,91 Thus symptom description, temporal pattern and
aggravating factors are the foundation for differential diagnosis.12,90,97–99 Recently, the
combination of three questions on the dizziness handicap inventory (i.e., the combination
of answering yes to: “Does looking up or does moving your head quickly increase your
symptoms?” and answering no to: “Are you afraid to leave your house because of
symptoms?”) were shown to be useful to diagnose cervicogenic dizziness.96 However,
symptoms alone cannot be used to determine the diagnosis. This is illustrated in studies of
dizziness postconcussion, where symptoms could not confirm or dismiss a cervical
component. Rather, physical signs of musculoskeletal impairment, particularly the
identification of upper cervical joint signs with manual examination, were most useful to
indicate cervical involvement.100–103

Physical assessment
Cervical musculoskeletal examination
The clinician seeks a pattern of cervical musculoskeletal dysfunction (e.g., reduced range
of motion, painful cervical joint dysfunction plus altered neuromuscular control) in
conjunction with cervical related sensorimotor signs and symptoms to confirm a cervical
origin of symptoms.104,105 The presence of these cervical musculoskeletal impairments,
especially involving the upper cervical spine, were central to patients whose main
complaint was cervicogenic dizziness26,103 and in patients with concussion who responded
positively to treatment of the cervical region.101

Cervical sensorimotor examination

At present, the consensus is that tests to identify vestibular or CNS dysfunction have
stronger clinical utility than tests for cervical causes of dizziness and sensorimotor control
disturbances.106 Nevertheless, some tests designed to support a cervical aetiology may help
differential diagnosis, recognizing that a cluster of tests is more likely to be discriminatory
than individual tests.103 For example, in a study comparing patients with cervicogenic
dizziness and BPPV, the combination of a cervical joint position error of greater than 4.5
degrees in at least one movement direction, abnormal responses to the cervical torsion test
and the smooth pursuit neck torsion test collectively, were specific to cervicogenic
dizziness.103
Not one sensorimotor test alone can confirm the diagnosis. Rather clinical reasoning
towards differential diagnosis is based on findings of a cluster of sensorimotor tests,
together with the patient’s symptomatic reports and the presence of cervical
musculoskeletal impairments. Sensorimotor tests with most discriminating potential,
based on both laboratory and clinical studies, include cervical joint position tests and tests
where neck torsion is incorporated.103

Neck torsion versus en-bloc trunk torsion

Neck torsion refers to movement of the neck via rotation of the trunk on a stable head. Its
purpose is to selectively stimulate the cervical rather than the vestibular afferents. This is
different to en-bloc tests, where there is simultaneous trunk and head rotation (no relative
neck rotation) such that the vestibular rather than the cervical afferents are stimulated.
When symptoms are reproduced with en-bloc rather than neck torsion movements, it
suggests a vestibular rather than a cervical cause and vice versa.36 Several studies
investigating smooth eye pursuit,21,33 balance107 and joint position error (JPE) have
incorporated neck torsion into tests to support a cervical cause of sensorimotor deficits.
The difference in performance when the head is in neutral compared with the torsion
position is used to make decisions in tests of smooth pursuit eye movement and balance.
Impaired cervical afferentation is indicated when there is a decrease in the ability to eye
follow smoothly or an increase in postural sway occurs when the tests are performed in
neck torsion compared with neutral positions. These changes observed with neck torsion
in patients with neck pain disorders are not seen in healthy controls or in patients with
brain injury or peripheral vestibular pathology.21,33,108 A recent study also demonstrated
that near point visual convergence was altered in persons with idiopathic neck pain when
tested in torsion compared with the neutral position supporting its potential use in
differential diagnosis.109
In researching the test of JPE, we developed a modified test where the head was held
still and the patient repositioned the trunk to neutral (the laser pointer was attached to the
chest rather than the head).110 Patients with neck pain had significantly greater errors in
almost all the “JPE torsion tests” when compared with healthy controls. The JPE torsion
test may be more appropriate than the conventional JPE test when trying to differentiate
altered cervical afferentation from vestibular dysfunction in people with chronic neck pain
and dizziness, but this hypothesis needs further exploration.111
Another test using similar methodology is the cervical torsion test. In this test, similar to
the torsion tests above, the head is held still, and the patient rotates the trunk to the left,
then returns to neutral, then rotates the trunk to the right, and finally returns to neutral.
This test was found to be one of a cluster of useful discriminating tests for cervicogenic
dizziness.103 Each position is sustained for 30 seconds and nystagmus of greater than 2
degrees in any of the end range or neutral positions is considered a positive test.103
L’Heureux-Lebeau and colleagues103 demonstrated a positive test in 52% of patients with
cervicogenic dizziness compared with 8% in patients with diagnosed BPPV. In similar
tests, where observation rather than measurement of nystagmus was used, 64% of
whiplash patients demonstrated nystagmus.112 However, up to 50% of subjects with no
cervical pathology showed some observable nystagmus with this test113 possibly from
elicitation of the normal cervico-ocular reflex.89 Thus more research is required to
determine the real value of this test.

Vestibular and visual tests

More specific tests are required when vestibular or visual deficits are suspected in patients
with neck trauma or when complaints are more indicative of these pathologies. The reader
is again referred to Table 10.1 for a potential schema for differential diagnosis, possible
symptom and physical test findings.
Recently a clinical vestibular oculomotor screening test (VOMS) was developed as a
postconcussion test.114 It uses exacerbation of symptoms (headache, fogginess, dizziness
and nausea) following each of the clinical tests of saccades, smooth pursuit, gaze stability,
near point convergence and vision motion sensitivity, to screen for both peripheral and
central vestibular signs and visual system impairment. Another study used a similar
approach with the addition of the response to an optokinetic reflex (OKR) stimulus.82
VOMS, OKR and positional BPPV tests are relatively quick and easy for clinicians to
institute and can be good screening tests to assist differential diagnosis and direct
management. Nevertheless, in patients in whom symptoms cannot be explained using
these measures, referral to a vestibular physiotherapist or a behavioural optometrist or
vision therapist may be warranted for a more thorough investigation of the vestibular,
CNS, or visual systems using specialized equipment. Appropriate medical referral for
further diagnostic workup and management may be required in some cases.
In benign cases where a cervical component is suspected, even in the presence of
vestibular pathology, a closely monitored trial of treatment directed towards the cervical
spine is warranted. Vestibular rehabilitation is often compromized when there is a cervical
component and thus treatment directed towards the cervical spine in the first instance is
recommended. In contrast, in circumstances where the visual system is the main driver of
the patient’s complaints, visual problems may need to be addressed first to allow gains to
be maintained with cervical management.

Conclusion
Diagnosis of a cervical cause of symptoms of sensorimotor control disturbances is based
on a combination of tests rather than any single test. The clinical reasoning considers the
patient’s symptomatic reports and history in combination with results from the physical
examination of the cervical musculoskeletal system and tests for cervical sensorimotor
control. Tests of vestibular and visual function may also be required as directed by the
examination findings.

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11

Headache

The Differential Diagnosis of Cervical

Musculoskeletal Causes or Contributors
Headache is a common disorder that does not discriminate on the basis of age, gender or
sociodemographic parameters.1 Headache comes at high personal, social and financial
costs.1–3 Historically, physiotherapists have long had an interest in cervicogenic headache,
a headache secondary to a cervical musculoskeletal disorder.4 In recent years, there has
been increasing interest in the primary headaches, migraine and tension-type headache
(TTH) because neck pain is frequent in these headaches with as many as 60% to 80% of
people with migraine and TTH reporting neck pain with their headache.5–8 Neck pain is so
frequent that some suggest that future Global Burden of Disease studies group neck pain
with headache rather than with low-back pain1 because aetiologically, the thought is that
much neck pain is secondary to headache.3 Furthermore, manual therapy to the cervical
spine (manipulation, mobilization, massage) appears to be the most common non-medical
treatment used for the management of common recurrent headaches such as migraine,
TTH and cervicogenic headache either on a practitioner-prescribed or self-prescribed
basis.9 Thus there appears to be an assumption that headache-associated neck pain and
cervical musculoskeletal dysfunction are automatically related.
It goes without saying that treatment should match the condition, for example, triptans
are indicated for migraine but not for cervicogenic headache. Likewise, treating the neck
with methods such as cervical manipulation and mobilization is indicated for cervicogenic
headache. Yet are these methods always indicated when neck pain accompanies primary
headaches such as migraine and TTH? This chapter focuses on the critical question of
differential diagnosis of cervical musculoskeletal causes or contributors to various
headache forms that underpins the relevance or not of local neck treatments such as
manipulative therapy and specific therapeutic exercise in the management of various
headache types.

Neck pain and headache

Neck pain is a frequent symptom of headache. The critical question is: “Does the presence
of neck pain with headache implicate a cervical musculoskeletal cause?” It is invalid to
assume that the site of pain always overlies its source, for example, intense forearm pain
may be a symptom of a centrally located cervical radiculopathy, anterior knee pain may
have its origin in the hip. Similarly, headache-related neck pain may have a local or
remote source.
The mechanism underlying the relationship between head and neck pain involves
convergence between cervical and trigeminal afferents in the trigeminocervical nucleus in
the brainstem. Nociceptive afferents from the upper three cervical nerves (C1, C2, C3)
converge onto common second-order neurons that also receive afferents from the
trigeminal nerve.10 The pathway is bidirectional. It not only explains how nociception
from the upper three cervical segments can refer pain into the frontal region of the head,
but also in the presence of central sensitization and increased excitability to converging
synaptic inputs, how nociception from trigeminal afferents can refer pain into the neck.11–13
Migraine is a primary headache. It is a neurobiological disorder that is not fully
understood, but the role of the trigeminovascular system, sensitization of pain pathways,
the central nervous system (CNS) and neurotransmission are all considered in possible
mechanisms. Neck pain is common and palpation of the neck may produce headache.14
There are reports of findings of cervical musculoskeletal dysfunction in persons with
migraine,15,16 but equally, there is evidence that the neck pain is part of migraine
symptomology and not a symptom of local neck dysfunction. When the neck pain
associated with the migraine responds to acute triptan therapy,17 it implies that the pains
share an underlying pathophysiology rather than having separate causes. There is a body
of research suggesting that migraine-associated neck pain is a biomarker for central
sensitization18 because neck pain and migraine are often tightly linked. For example, neck
pain intensity is related to migraine severity, neck pain and nausea increase with the
increasing migraine severity,6 neck pain is predictive of migraine-related disability and the
higher the neck pain, the more treatment resistant is the migraine.19 Migraineurs may not
automatically relate neck pain to the beginning of a headache attack,20 which often delays
them taking medication.21 It was shown that migraines were better managed when
medications were taken at the first sign of neck pain.18
Thus neck pain may be part of the migraine symptom complex, without any necessary
contribution from local cervical musculoskeletal disorders. Certainly this would fit with
the results of several studies, which have not found cervical musculoskeletal impairment
in persons with migraine.22–29 It would also fit with the evidence that manipulative therapy
and other local treatments directed towards the neck do not make substantive changes to
headache frequency or intensity or to the course of migraine.30–32
Nevertheless, the prevalence of neck pain and disability appears to increase with
migraine chronicity.6,33 The classification of chronic migraine in the current International
Headache Classification (ICHD III)34 may also present confusion in terms of the
relationship between cervical musculoskeletal dysfunction and migraine. Chronic
migraine is defined as “headache occurring on 15 or more days per month for more than 3
months, which has the features of migraine headache on at least 8 days per month” (ICHD
III p650). This means that a person diagnosed with chronic migraine could have eight
migraines and seven or more cervicogenic headaches per month, which could account for
any cervical musculoskeletal signs associated with chronic migraine. There is already
well-recognized symptomatic overlap between migraine and cervicogenic headache,
which could add to diagnostic confusion.35 Thus there needs to be care in history taking to
tease out potentially different headache types, otherwise there could be flawed conclusions
about the role of cervical musculoskeletal dysfunction in migraine.
The same questions present about the role of neck pain and cervical musculoskeletal
dysfunction in TTH. The pathogenesis of TTH is still uncertain. Even though TTH is
classified as a primary headache in the ICHD III, both central and peripheral mechanisms
may be at play, suggesting that it may be a primary or secondary headache or both.34 TTH,
with the potential diversity in causes or contributors, presents the greatest challenge in
differential diagnosis. Some associate TTH with the same cervical musculoskeletal
dysfunction that classifies cervicogenic headache,36 others regard the presence of trigger
points in neck muscles as an indication of cervical musculoskeletal dysfunction,37 whereas
others find no association between cervical musculoskeletal dysfunction and TTH.26,29
Similar to migraine, TTH when classified as chronic (> 15 headache days per month)
requires that only eight headaches fulfil the TTH criteria,34 meaning that chronic TTH can
potentially be a mix of headaches. There is some evidence that manipulative therapy and
other physical therapies may be helpful for TTH,38,39 but in many studies, it is difficult to
know if the headaches, albeit named TTH, were clearly TTH when responding to therapies
that have proven efficacious for cervicogenic headache. The potential heterogeneity in
causes and contributors to TTH indicate the need for a skilled clinical examination of the
cervical region to determine the role or not of cervical musculoskeletal dysfunction in an
individual’s TTH presentation.
Neck pain is a critical feature of cervicogenic headache and is a classification
criterion.34,40 In contrast to most other headache forms, neck pain is a main feature of
cervicogenic headache. Characteristically, pain begins in the neck and once it builds up,
the headache begins.41 The neck pain is directly associated with cervical musculoskeletal
dysfunction. Restricted neck motion and symptomatic upper cervical joint dysfunction
(relief of pain by anaesthetic joint blocks or blocks of the medial branch of the dorsal
ramus) are classification criteria. Cervicogenic headache is classified as a secondary
headache, directly attributable to cervical musculoskeletal dysfunction where traditional
treatments for cervical musculoskeletal dysfunction have proven helpful.39,42–45
It would be simple if cervical musculoskeletal dysfunction was related to one headache
type, cervicogenic headache, but it is far from straightforward. The role of cervical
musculoskeletal dysfunction in migraine and TTH as a causative, contributing or
comorbid factor is still to be determined. Cervical musculoskeletal dysfunction may also
contribute to other headache types, such as headaches associated with craniomandibular
dysfunction and concussion46–48 and is a frequent comorbid feature of headache in older
persons.8 Mixed headaches are common. Patients may suffer two different headache types
concurrently as indicated in the definitions of chronic migraine and TTH. The role of neck
pain is probably more complex than a simple neck-headache relationship. The Norwegian
longitudinal population-based cohort study found a bidirectional relationship between the
development of chronic musculoskeletal complaints (cervical, lumbar, extremity pain) and
the development of chronic daily headache. Persons who developed chronic
musculoskeletal complaints were almost twice as likely to develop chronic headaches and
vice versa.49 The authors summarized that either shared underlying mechanisms via CNS
sensitization, psychological predisposition, reduced pain coping skills or shared genetic
susceptibility could underlie these relationships.
Neck pain associated with headache may have a local or remote source. This behoves
the clinician to undertake an effective clinical examination of the headache patient. It is
important to listen to the description of the history, onset, temporal pattern and behaviour
of headache and determine whether the story matches the classification criteria for a
particular headache type or has aberrant features which might suggest mixed or other
headache types. From the perspective of any associated neck pain, a skilled physical
examination of the cervical region is necessary to determine the presence or not and
comparability of any cervical musculoskeletal dysfunction.

What defines cervical musculoskeletal dysfunction?

There is little consistency in the headache literature as to which cervical musculoskeletal
impairments are measured and which need to be present to conclude that cervical
musculoskeletal dysfunction has a causative, contributory or comorbid role in a particular
headache type.
The history of cervicogenic headache has witnessed several proposed causes. Early
candidates were: irritation of the cervical sympathetic nerve running along the vertebral
artery or cervical migraine (since disproven);50 cervical discal disorders; and disorders of
the cervical nerve roots.51–54 Work from the 1960s onwards confirmed that the most
common source is referred pain from the upper cervical joints (C0–3) with C1–2 and C2–
3 articulations probably the more common sites.55–58 Other segments are not excluded.
Reports of headache relief with surgery to lower segments are not uncommon.59
Radiological imaging of painful upper cervical joints, especially in younger to middle age
usually does not demonstrate any relevant pathological change. However, osteoarthritis
was evident radiologically in late middle-aged to older-aged persons with cervicogenic
headache using bone single-photon emission computed tomography/computed
tomography.60 In advanced osteoarthritis, C2 spondylitic radiculopathy was reported as the
lesion causing cervicogenic headache.61
Any structure innervated by the upper three cervical nerves is capable of referring pain
into the head via common neurons in the trigeminocervical nucleus. Nevertheless as per
the classification criteria for cervicogenic headache,34,40 articular dysfunction and
movement impairments are fundamental to defining cervicogenic headache or a cervical
role in headache. Painful joint dysfunction does not occur in isolation and will always be
associated with changes in the neuromuscular system. The nervous system and
sensorimotor system may also contribute to the pain syndrome. The question is: “Which
impairments are fundamental to define a cervical musculoskeletal cause or contributor to
headache?”

Articular system
Reduced cervical motion and relief of headache with anaesthetic cervical joint or nerve
blocks are classification criteria for cervicogenic headache,34,40 and most studies
investigating cervical musculoskeletal impairments in headache include measures of
cervical range of movement.15,23,26,29,62,63 Reduced motion is consistently found in
cervicogenic headache cohorts of all ages and the cervical flexion rotation test has proven
validity to identify headaches associated with C1–2 dysfunction.8,26,28,29,63–66
The second criterion for diagnosis of cervicogenic headache is the presence of upper
cervical joint dysfunction. Radiological imaging is often not informative but manual
examination is a safe clinical alternative. Manual examination has not been without its
controversies, but when the question and clinical decision is simply to nominate whether
or not a person has symptomatic upper cervical joint dysfunction, it is proving to be a
valid and valuable examination technique.26,28,66–71 It is worthy of note that reproduction of
headache by palpating a cervical structure whether bone or muscle is not necessarily a
positive sign of a cervical cause.14 The CNS is sensitized in both migraine and TTH, and a
peripheral nociceptive stimulus into a sensitized system can be expected to aggravate
headache. Neck tenderness alone is non-discriminative and cannot be regarded as a
positive joint sign for cervicogenic headache. Rather joint dysfunction is present when the
clinician detects with manual examination, altered segmental motion, altered resistance to
the induced motion and pain is reproduced. Manual handling must be skilful. Thumb and
finger contact must never elicit discomfort or pain, it will confound interpretation. Poor
manual skills can result in false positive findings.

Neuromuscular system
Changes in muscle function occur in reaction to painful joint dysfunction and include
changes in motor control and reduced strength and endurance. Changes documented to
date specifically in cervicogenic headache include: an altered pattern of flexor muscle
activity (reduced activation of the deep cervical flexors and heightened activity in the
superficial flexors) as measured in the craniocervical flexion test (CCFT); and reduced
strength and endurance of the craniocervical flexors, the cervical flexors and cervical
extensors.22,24,26,28,72 Migraine cohorts have not demonstrated the altered pattern of muscle
activity in the CCFT,26,28,73 or demonstrated reduced strength in the craniocervical
flexors,24 cervical flexors and extensors.26,74 One study reported differences in the CCFT in
migraine patients compared with controls, but the mean value recorded for the CCFT
(26 mmHg) was within values for pain-free individuals.16 Changes in muscle function
have, in the main, not been demonstrated in TTH.22,26,73 One small study of TTH revealed
that 4 out of 10 subjects had poor performance in the CCFT.75 Reduced neck extensor
strength but not flexor strength was demonstrated in one study of migraine76 and one of
TTH.77 Reduced extensor strength, without any deficit strength or endurance in the
flexors, is not a typical finding of a cervical musculoskeletal disorder. These findings
might reflect pain inhibition with the application of resistance during the test procedure
because both headaches are associated with considerable pericranial tenderness.
Muscle trigger points have been regarded by some as primary cervical musculoskeletal
dysfunction.37,78,79 However, trigger points can be present in migraine and TTH as well as
in non-musculoskeletal conditions such as cancer pain, visceral pain and chronic
prostatitis.62,78,80–85 Perhaps they are better considered as a secondary reaction in muscles to
a pain state of various origins. The presence of trigger points does not determine or
differentiate a cervicogenic headache. In relation to headache, most research into trigger
points has been conducted with TTH.
It is not surprising that changes in neck muscle activity are observed in migraine
cohorts.76,82,86 This is likely to be a reaction to pain rather than a reaction to primary
cervical musculoskeletal dysfunction, given the evidence, on balance, of the lack of
cervical musculoskeletal dysfunction in migraine. It is possible that these instances of
general muscle tension underlie feelings of neck stiffness that may accompany headache,
although a biomechanical study of stiffness characteristics of the upper cervical spine in
rotation revealed no differences between persons with migraine, TTH and controls.87

Posture
Static postures, in particular, angles representing a forward head posture (FHP) have been
measured as an indication of the presence of cervical musculoskeletal dysfunction. The
literature is divided on the relevance of this measure to neck pain disorders because
studies are divided on a relationship between the static FHP and neck pain disorders,
including cervicogenic headache.28,72,88 The FHP is not a feature of migraine15,28,79 but has
been found in some groups of chronic TTH, and lesser so in episodic TTH, yet the FHP
has not related to headache frequency, intensity or duration.62,75,78,89 As a static FHP is not
always associated with a cervical musculoskeletal disorder, it is not a measure to define a
cervical musculoskeletal cause or contributor to headache. Nevertheless, evidence is
mounting for a relationship between assuming a FHP while working and neck pain,90–92
but this functional posture has not been examined in migraine, TTH or indeed
cervicogenic headache.

Neural system
There are anatomic links between the deep cervical muscles and spinal dura mater93 and
movements of the upper cervical spine and suboccipital muscles can move the spinal dura
mater in this region. The spinal dura in this region is innervated by the upper three cervical
nerves. If it becomes irritated and sensitive to movement (e.g., from neighbouring joint
inflammation) or has reduced extensibility, it is capable of contributing to, or causing
headache as a “cervicogenic source”. There has been little research into nerve tissue
mechanosensitivity in cervicogenic headache or indeed in other headache types.28,44,94,95
Preliminary evidence suggests that nerve tissue mechanosensitivity may contribute to a
cervicogenic headache in, at most, 8% to 10% of cases.28,44 Although important to
recognize in those cases, the low incidence of nerve tissue mechanosensitivity cannot
serve as a feature to define a cervical cause or contributor to headache.

Sensorimotor dysfunction
Sensorimotor control and differentiation of sensorimotor disturbances such as
proprioception and balance deficits are considered in detail in Chapters 6 and 10.
Sensorimotor dysfunction is certainly not uncommon in cervical spine disorders,
especially when the symptoms of dizziness and unsteadiness are present. In one trial of
cervicogenic headache, about 30% of participants reported light headedness/dizziness.44
However, sensorimotor disturbances are not unique to cervical musculoskeletal causes.
They can be a feature of postconcussion headache96 and migraine, particularly vestibular
migraine where a recent study estimated that 21% of a migraine cohort had vestibular
migraine.97,98 Findings of sensorimotor disturbances are disparate in TTH,99–101 but there is
very little research in this field. Symptoms and disturbances in sensorimotor control are
not unique to cervicogenic headache and therefore cannot serve as a feature to
differentiate a cervical cause. Nevertheless, there is every possibility that measures to
differentiate cervical-related sensorimotor control disturbances may emerge in the future.

Cervical musculoskeletal dysfunction defined

We return to the question of which cervical musculoskeletal impairments need to be
present to indicate a cervical musculoskeletal cause or role in headache. Population-based
findings of reduced cervical motion or muscle strength are characteristic of cervicogenic
headache but are not helpful in differential diagnosis of the individual patient. Each
measure has age and gender effects and with the exception of the flexion rotation test,25
there are no cut-off values for ranges of cervical movement or strength to suggest what is
“normal” or dysfunctional. In practice, the clinician does not make a decision based on
one feature. Rather clinical reasoning decisions are based on a pattern of dysfunction.
Musculoskeletal features consistently present in cervicogenic headache populations are
reduced range of movement, upper cervical joint dysfunction and impaired neuromuscular
function, both in the CCFT as well as cervical flexor and extensor muscle strength.
Indeed, it is these features in combination that have been shown to be highly specific and
sensitive to differentiate a cervical musculoskeletal source of headache, (i.e., distinguish
cervicogenic headache from migraine and TTH).22,26
The presence collectively of reduced cervical motion (either in single planes, or specific
test movement combinations e.g., the flexion rotation test,25,63 the extension rotation test11),
upper cervical joint dysfunction and poor cervical muscle function is a fundamental
signature of cervical musculoskeletal dysfunction. This pattern should be present if the
neck pain associated with headache is to be attributed to a cervical musculoskeletal cause.

Cervical musculoskeletal dysfunction in headache:

clinical decisions
Cervical musculoskeletal disorders are the primary cause of cervicogenic headache. Yet
cervical musculoskeletal dysfunction may be present in other headache types: headaches
associated with craniomandibular dysfunction, headaches associated with concussion,
mixed headaches and chronic migraine or TTH which, by definition, can include a second
headache type which could be cervicogenic.
 The clinical examination, headache history and behaviour as well as the physical
examination assumes considerable importance in differential diagnosis. The decisions
required from a cervical musculoskeletal perspective are first, whether or not there is a
pattern of cervical musculoskeletal dysfunction (reduced motion, painful upper cervical
joint dysfunction, and impaired neuromuscular function). When the pattern is not present,
any neck pain is more probably part of the headache symptom complex. If the pattern of
cervical musculoskeletal dysfunction is present, then the decisions are whether (1) it has a
primary causative role (the pattern of headache history, symptoms and magnitude of
dysfunction match a cervicogenic headache classification); (2) a contributing role (e.g.,
the magnitude of cervical musculoskeletal dysfunction does not match the history of
headache intensity and frequency); or (3) a comorbid role (i.e., the behaviour of neck pain
and associated cervical musculoskeletal dysfunction is not consistently related to the
headache) (Fig. 11.1). Treatment decisions and expectations of outcomes are based on
these decisions.

FIG. 11.1 Clinical reasoning on the role of cervical musculoskeletal dysfunction in a

patient’s headache to inform treatment planning. MSK, Musculoskeletal.

Conclusion
Neck pain commonly accompanies headache. It is fundamental to know whether such
neck pain is related to a local cervical musculoskeletal cause or whether it is part of the
headache symptom complex, if understanding is to be progressed of the role of cervical
musculoskeletal disorders in cervicogenic and other headache types and to offer patients
appropriate treatment.
Cervical musculoskeletal disorders are clearly linked to cervicogenic headache (or a
neck-related headache as an alternate term) but the literature is divided about any link
between cervical musculoskeletal dysfunction and migraine and TTH in a causative role.
Several aspects probably underlie this uncertainty, including the relevance of single signs.
Another problem in today’s literature is that inclusion criteria for headache cohorts are
often described as “according to the ICHD III classification criteria” or “as diagnosed by a
neurologist”, but no detail of the headache characteristics are provided to ensure
“pureness” of the classification in the population studied.102 Thus when a study reports
reduced cervical motion in migraine or TTH, there is uncertainty about the result knowing
that there can be confusion in diagnosis between migraine without aura and cervicogenic
headache20,35 and that chronic migraine or TTH can include seven or more headache days
per month of a second headache type.34 Thus two important criteria for future studies
investigating cervical musculoskeletal dysfunction in different headache types are
confirmation of the population studied and whether all of the key determinants of cervical
musculoskeletal function were present, (i.e., the pattern of reduced range of movement,
upper cervical joint dysfunction and impaired neuromuscular function).
These recommendations also apply to inclusion criteria for clinical trials. Management
methods of cervical manipulative therapy and specific exercise have been used
successfully to treat cervicogenic headache. These methods can also be helpful when
cervical musculoskeletal dysfunction is an apparent “contributor” to headache.103 Yet to
use these methods to treat headache-associated neck pain that is not related to a local joint
and neuromuscular dysfunction lacks rationale and potentially detracts from evidence of
their effectiveness. This is not to suggest that persons with migraine and TTH without any
cervical joint or neuromuscular dysfunction cannot gain some benefit from some forms of
hands on treatment to the neck, instruction in relaxation, pain coping skills and lifestyle
advice as part of multiprofessional management, but this management approach has a
different rationale.
More research and critical thinking in clinical practice is required to better understand
the role of cervical musculoskeletal dysfunction in various headache types. Future clinical
trials are required to evaluate the benefits of management methods for the cervical spine
when they are knowingly directed towards a proposed causative, contributing or comorbid
role of cervical musculoskeletal dysfunction if the true benefits of treating the neck in
headache are to be understood.

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92. Szeto G, Straker L, Raine S. A field comparison of neck and shoulder postures in
symptomatic and asymptomatic office workers. Appl Erg. 2002;33:75–84.
93. Palomeque-Del-Cerro L, Arráez-Aybar L, Rodríguez-Blanco C, et al. A systematic
review of the soft-tissue connections between neck muscles and dura mater: the
myodural bridge. Spine. 2017;42:49–54.
94. Piekartz Hv, Schouten S, Aufdemkampe G. Neurodynamic responses in children
with migraine or cervicogenic headache versus a control group. A comparative
study. Man Ther. 2007;12:153–160.
95. Rumore AJ. Slump examination and treatment in a patient suffering headache.
Aust J Physiother. 1989;35:262–263.
96. Schneider K, Meeuwisse W, Nettel-Aguirre A, et al. Cervicovestibular
rehabilitation in sport-related concussion: a randomised controlled trial. Br J
Sports Med. 2014;48:1294–1298.
97. Carvalho G, Bonato P, Florencio L, et al. Balance impairments in different
subgroups of patients with migraine. Headache. 2017;57:363–374.
98. Yollu U, Uluduz D, Yilmaz M, et al. Vestibular migraine screening in a migraine-
diagnosed patient population, and assessment of vestibulocochlear function. Clin
Otolaryngol. 2017;42:225–233.
99. Giacomini P, Alessandrini M, Evangelista M, et al. Impaired postural control in
patients affected by tension-type headache. Eur J Pain. 2004;8:579–583.
100. Ishizaki K, Mori N, Takeshima T, et al. Static stabilometry in patients with
migraine and tension-type headache during a headache-free period. Psychiatry
Clin Neurosci. 2002;56:85–90.
101. Marchand A, Cantin V, Murphy B, et al. Is performance in goal oriented head
movements altered in patients with tension type headache? BMC Musculoskelet
Disord. 2014;15:179.
102. Aguila M, Rebbeck T, Mendoza K, et al. Definitions and participant
characteristics of frequent recurrent headache types in clinical trials: a systematic
review. Cephalalgia. 2018;38:786–793.
103. Uthaikhup S, Assapun J, Watcharasaksilp K, et al. Effectiveness of physiotherapy
for seniors with recurrent headaches associated with neck pain and dysfunction: a
randomized controlled trial. Spine J. 2017;17:46–55.
SECTION 4

Clinical Management
OUTLINE

Introduction
12 Principles of Management
13 Communication, Education and Self-Management
14 Management of Joint and Movement Dysfunction
15 Management of Neuromuscular Dysfunction
16 Management of Sensorimotor Control Disturbances
17 Management of Nerve Tissue
18 Case Presentations Clinical Reasoning and Clinical Decision
Making
19 Concluding Remarks Focusing on Prevention
Introduction
12 PRINCIPLES OF MANAGEMENT 173
13 COMMUNICATION, EDUCATION AND SELF-MANAGEMENT 181
14 MANAGEMENT OF JOINT AND MOVEMENT DYSFUNCTION 189
15 MANAGEMENT OF NEUROMUSCULAR DYSFUNCTION 201
16 MANAGEMENT OF SENSORIMOTOR CONTROL DISTURBANCES 221
17 MANAGEMENT OF NERVE TISSUE 231
18 CASE PRESENTATIONS: CLINICAL REASONING AND CLINICAL
DECISION MAKING 241
19 CONCLUDING REMARKS: FOCUSING ON PREVENTION 257

This section discusses the management of patients with neck pain disorders. The
various components of an intervention are discussed in separate chapters but all features
are considered concurrently in clinical practice. Communication and education occur
continually throughout treatment. Physical treatments for pain management and relief of
other associated symptoms are applied in an integrated manner together with exercise
programs to rehabilitate the various impairments in neuromuscular and sensorimotor
function. The importance of self-management strategies is highlighted and comprehensive
programs are developed and progressed throughout the management period.
As mentioned, topics have been considered separately in sequential chapters, for ease
and clarity of presentation of information. Therefore Chapter 18 presents a series of case
examples to demonstrate the clinical reasoning process and the necessary multimodal
management approach for patients with cervical spine disorders.
12

Principles of Management
Management programs are based on a comprehensive clinical reasoning process to
interpret and apply the detailed information gained about the patient and their neck pain
disorder in the patient interview and physical examination. The principles of management
revolve around patient-centred care in which the patient receives relevant information and
contributes to decisions about their care.1 Good management relies on an effective
therapeutic relationship between the patient and clinician, which is based on good
communication where the patient is assured that their concerns are being heard and
understood.
Management programs are developed within the framework of the biopsychosocial
model. The model itself does not provide any specific guidance as to which interventions
should be implemented. Rather it encourages consideration of biological,
behavioural/psychological and social aspects of a patient’s presentation both in
management and in evaluating outcomes. The relative contributions of the three domains
of the model are very fluid, and they will not stay constant. They vary between patients
and within a patient as they progress through their rehabilitation.
Pain is commonly the primary reason that a patient seeks help for a neck disorder. As is
well appreciated, pain is a multidimensional sensory and emotional experience, and the
management of pain is a major multidisciplinary field of practice and research. Pain can
be managed with pharmacotherapies, physical therapies as well as various psychological
and cognitively based behavioural therapies. In a patient-centred approach to managing
people with neck pain, often some components of many of these therapies will be used,
albeit in differing proportions depending on the individual patient’s needs. We focus in
this text on the management of pain with physical therapies with attendant education, self-
management programs and patient empowerment. Yet management programs must not
focus on pain relief only. Pain relief is very important to the patient, but the real burden for
the person and society in general, lies not in a single episode of neck pain but in its
recurrent or persistent nature and consequent years lived with a disability.2 Management
programs must change as treatment goals change from pain relief, to restoration of full
function, to prevention of recurrent episodes. All management programs must have a
focus on rehabilitation.
The principles of management incorporate:

■ A patient-centred approach featuring clear communication, the

provision of relevant information and a diagnosis, and inclusion of the
patient in decision making.
 ■ The development of collaborative intervention strategies from a
physiotherapy perspective, which will help the patient reduce neck pain
and disability and promote optimal function and participation.
■ The use of a combination of approaches which may include education
on a variety of topics, manual therapies, various exercise strategies, self-
management strategies and work and lifestyle advice.
■ Strategies to enhance coping or other personal skills to assist patients to
(1) manage their neck in both pain and nonpainful states and (2) comply
with home exercise and self-management programs, which support and
enhance treatment gains.
■ Strategies to fulfil aims of preventing further recurrent episodes of and
slowing disease progression: (1) provision of a simple long-term
preventative regime for patients to continue; (2) help patients to problem
solve to adjust leisure or work practices to care for their neck.
■ A self-management program for the patient to use if, in the future, the
neck pain disorder appears to be returning.

Selection of management strategies

Selection of management strategies is guided by the clinical reasoning process throughout
the patient interview and physical examination. The clinical reasoning process around
selection of management strategies is guided by the principles of evidence-based practice
(EBP), integration of best available research evidence, clinical expertise, and patient
values and circumstances.3 Clinical practice guidelines (CPGs) are a primary tool of EBP.
Other tools that might inform the clinical reasoning process are subordinate to CPGs.
These include clinical prediction rules and subgrouping, which are tools that attempt to
match specific interventions or management approaches to particular patient presentations.

Clinical practice guidelines

CPGs are built on the outcomes of systematic reviews and where possible, meta-analyses
of the research evidence. They are developed by a panel of multidisciplinary experts who
produce recommendations that aim to optimize patient care. Recommendations are
variously provided on: assessment, particularly to identify “red flags” or risks of harm,
contraindications to particular treatments; prognostic indicators for a good, fair, poor or
delayed recovery; treatment methods with evidence of effectiveness for different stages of
various neck pain disorders; recommendations on actions that should be taken if the
patient is not responding to treatment; and recommendations for outcome measures.4,5
Contemporary guideline development may also include aspects that patients have
nominated as important from their experiences and needs.6 This fulfils the ideology of
EBP.3 In one CPG for the management of whiplash-associated disorders (WAD),6 patient
input was sought and their recommendations were that guidelines be mindful of
terminology used both for the persons who sustained the injury and in describing the
injury (e.g., calling whiplash a minor injury was distressing). They also recommended that
an emphasis be placed on partnerships and shared decision making between patient and
health care provider; that the emotional distress of being in a car crash be recognized and
actively managed when necessary, and that the injured persons be repeatedly oriented to
the health care system and insurance industry about which many were nonfamiliar. Such
recommendations provide sound advice to clinicians.
One set of CPGs have been developed for specific categories of neck pain disorders
namely; WAD, cervical radiculopathy and insidious onset neck pain.4,5,7,8 Within these
disorder categories, treatment guidelines are provided for subclassifications of whiplash—
WAD grades I–III,9 and neck-associated disorders—NAD I-III.10 Differentiation is also
made for the acute/subacute or persistent stages of neck pain disorders for management
recommendations. Another recently updated CPG classified neck pain disorders on the
basis of categories within the International Classification of Diseases (ICD) together with
the relevant impairment-based category for neck pain according to the International
Classification of Functioning, Disability, and Health (ICF).11 Four classifications were
derived and treatment recommendations were provided for: neck pain with mobility
deficits; neck pain with headaches; neck pain with movement coordination impairments;
and neck pain with radiating pain.
CPGs direct the use of treatments that have evidence of effectiveness and discourage
use of treatments with no evidence of effect or evidence of harm based on the available
evidence. For example, for neck pain of 3 months or less, based on the evidence, a
multimodal program inclusive of structured patient education in combination with range
of motion exercises and mobilization or manipulation is recommended. Clinicians are
advised not to use structured education alone, strain-counterstrain techniques, collars or
electrotherapy modalities because there is no evidence of effectiveness for these methods.4
CPGs, as the name implies, are guidelines to the prescription of best evidence-based
treatment. They do not inform on the precise technique of treatment, combination of
techniques or dosage that may be best for the individual patient. This relies on the
clinician’s reasoning based on the findings of the patient interview and physical
examination. CPGs have other limitations. For example, as explored in Chapter 5,
evidence indicates that neck pain is associated with considerable change in neuromuscular
function, yet a guideline for neck pain of 3months or less did not include any
recommendation for exercise to address this muscle dysfunction.4 This runs counter to any
principles of rehabilitation for musculoskeletal disorders. Although there is evidence of
effectiveness of exercise in the management of neck pain disorders,12 randomized
controlled trials (RCT) of exercise are yet to be conducted in this acute/subacute group
with idiopathic neck pain. Thus there is no evidence for exercise for this neck pain
category that the guideline can use in recommendations. Recommendations are made on
the available evidence. This deficit not only points out the urgent need for clinical trials of
exercise in this specific patient group but also highlights the limitations of evidence-based
guidelines. CPGs point the way, but patient management must still be informed by the
clinician’s reasoning and a research informed physical examination and management
approach.

Clinical prediction rules

Clinical prediction rules (CPRs) are developed for diagnostic, prognostic and prescriptive
purposes. For interventions, a CPR guides prescription of a certain treatment technique.
There is considerable heterogeneity in the presentation of patients with neck pain
disorders. Likewise, there is no universal response to any one treatment. Thus CPRs
attempt to better match patients to treatments. They are based on historical and physical
characteristics that predict patients’ responses to that treatment and are usually derived
from an RCT. Several prescriptive CPRs have been developed to direct treatments for
neck disorders. As examples, CPRs have been developed to identify patients with neck
pain who may respond to neck manipulation,13,14 to thoracic spine manipulation,15 to
traction and exercise,16 and for patients with neck and arm pain, to neural tissue
mobilization.17
Although in principle a valuable prescriptive tool, CPRs are failing in the validation
process. In other words, the technique or treatment designated by the CPR is not
producing a superior effect against a comparison treatment when tested prospectively in a
new clinical trial using a new group of patients. This failure is not limited to techniques
for neck pain but is occurring for CPRs for the lumbar spine and other regions.18–22
Reasons proposed for the apparent failure of many prescriptive CPRs include, for
instance, vastly inadequate sample sizes and considerable statistical methodological
limitations in the original derivations of the rules.23,24 Thus at present, the use of CPRs
does not have strong scientific support, but further research with stringent scientific
methodology might change this state. Therefore CPRs could be used to direct a certain
management technique(s), but at present there is no evidence that the technique(s) would
result in a superior outcome to another treatment method.
CPRs in principle may assist in the initial prescription of a treatment or treatment
technique, but they cannot act as a stand-alone tool. CPRs offer no guidance on the
progression of the technique/treatment nor on any other treatment that might be required
for rehabilitation of the patient’s neck pain disorder. Furthermore, they provide no
alternative for the neck pain patient whose presentation does not fit the rule, nor any
alternative if the prescribed treatment technique proves not to be efficacious. Thus even if
valid CPRs become available, they will always be a secondary supplementary tool to the
primary tool of the clinical reasoning process in patient assessment and management.

Subgrouping
Subgrouping is another method to try to deal with the heterogeneity in neck pain disorders
to better match treatments to individuals. Subgrouping has gained greater attention for
low-back pain. For cervical spine disorders, there are essentially two physiotherapy-based
subgrouping systems to guide management. One subgroups patients on ICD and ICF
criteria based on the patient’s clinical presentation, that is, neck pain with mobility
deficits; neck pain with headaches; neck pain with movement coordination impairments;
and neck pain with radiating pain.11,25 A treatment approach is proposed for each
classification derived from available evidence. The other system subgroups patients based
on a particular management approach—Mechanical Diagnosis and Therapy (MDT). In
this system, the pain response to repeated movement is assessed and patients are classified
into one of four basic syndromes: posture, dysfunction, reducible derangement, irreducible
derangement or “other” category.26,27 The category directs which movement or postural
strategy will be used in management.
Subgrouping can assist in selecting a treatment technique or proposing a management
regime that might be suitable for a particular patient but they have limitations. For
example, the four subgroups based on ICD and ICF criteria11 describe four different, very
legitimate symptom sets, but it is easy to think of numerous patient presentations outside
these four descriptions. Similarly, the MDT classification provides no guidance if patient’s
fall into the “other” category. It is easy to be critical, but it is probably an impossible task
to create subgroups that could cover all possible presentations of neck pain disorders.28 In
addition, current subgrouping schemes are quite narrow in their focus and do not consider,
for example, pain mechanisms that may influence management approaches. There is an
emphasis on dealing with the presenting complaint but not on a full rehabilitation
program, which aims to reduce recurrence of the disorder. The schemes do not position
themselves in the biopsychosocial context of neck pain disorders. These limitations do not
dismiss the usefulness of these classifications systems in contributing to management
decisions, but as with CPRs, they best operate as a secondary supplementary tool to the
primary tool of the clinical reasoning process in patient assessment and management.

Selection of interventions
It is now well appreciated that there is no single modality “magic bullet” that has the
answer for the management of patients with neck pain disorders. No one modality or
approach can improve all dimensions of a neck disorder. Evidence from systematic
reviews and uptake in CPGs supports the prescription of multimodal management.4,5,29
Selection of specific interventions as a manual/manipulative therapy, exercise or
sensorimotor training will be discussed in the relevant chapters. Here broader issues
behind recommendations for selection of interventions are considered.
Recommendations for an intervention or management approach in a CPG are guided by
the cumulative evidence of effectiveness from a number of RCTs. A factor governing the
strength of the recommendation for an intervention is the quality of the RCTs. The quality
of the RCTs is assessed in terms of methodological excellence, for example, concealed
randomization; blinding of assessors, patients’ therapists; intention-to treat statistical
analysis. However, there is not a formal evaluation of the suitability of the many clinical
aspects of the RCT, such as the population studied, the intervention chosen or the primary
outcome measure. Quality in these aspects could be argued to be equally as important as
methodological excellence in gauging the strength of the evidence for a particular
intervention.
 The problem of heterogeneity in presentations within populations with neck pain
disorders is well appreciated as is the false expectation that all patients will respond in a
similar manner to an intervention. Inclusion criteria in RCTs, such as individuals with
non-specific neck pain of 3 months’ duration or more and between the ages of 18 and 65
years stand to recruit many different presentations of neck pain disorders. An intervention
may have excellent results for one patient but is ineffective in another patient. The
washout consequence of diverse results from a heterogeneous population is agreed to be
one of the possible reasons for small to, at best, moderate effect sizes gained by most if
not all potentially beneficial treatments for neck pain. Thus it is essential that as
homogeneous a population as possible is recruited into future RCTs. Nevertheless, even
though they continue to be the mainstay to produce evidence, RCTs cannot replicate the
varying characteristics of individual patient encounters in clinical practice. With the
current situation, clinicians must be aware that an overall small effect size in an RCT does
not mean that an intervention might not have a large effect for a particular patient
presentation.
It is not only necessary to recruit a homogeneous population into an RCT, but the
population needs to have “the condition” for which the intervention is suitable, if a
judgement of the efficacy of an intervention is to be made. For example, cervical
manipulative therapy added to medication was shown to add no substantive benefit on
migraine frequency over medication alone in patient management.30 This finding cannot
reflect adversely on the effectiveness of manipulative therapy. Rather it could be argued
that it is an expected finding because there is no substantive evidence that migraine is
associated with cervical musculoskeletal dysfunction (see Chapter 11). Similarly, a study
tested a contention that psychological and social factors play a major role in the transition
from acute to chronic neck pain. The researchers proposed that a behavioural graded
activity program would be at least as effective as a program of advice, manipulative
therapy and exercise.31 The behavioural program was found to have no superior effect on
future pain and disability at 12 months and it afforded no significant change in
psychological variables. However, most participants recruited into the RCT in this
transition phase did not have abnormal psychological features. Initial baseline scores for
psychological features for the majority of participants were very low, so the possibility for
change was marginal at best. Thus possessing “the condition” for which the intervention is
suited is critical if any judgement is to be made about an intervention. As an example,
there is growing interest in the contribution to neck pain of adverse scapular posture
associated with poor muscle control. There is very preliminary evidence (case study) of
effectiveness of a scapular retraining program.32 The next step is to test the training
program in an RCT. Considering participant selection, a major inclusion criteria (i.e.,
those potentially suited to the intervention) would be individuals who firstly, demonstrated
altered scapular posture and secondly, whose pain and neck movement improved
markedly when the scapula was positioned into a neutral posture (see Chapter 9). If this
response was not achieved in a screening process for the trial, then training scapular
posture is unlikely to be a successful intervention and such participants should not be
included in this first RCT. An intervention can only be appraised when it is used for
patients for whom it is indicated.
 Another aspect to consider in judging the effectiveness of an intervention, is the
“suitability” of the primary outcome measure on which it was judged. The primary
outcome of most RCTs for the management of neck pain disorders is a pain rating, a score
from a pain and disability questionnaire, or a patient’s global perceived effect of treatment.
This reflects an outcome relevant to the patient, which is correct, but it can be questioned
if pain relief is the only expectation of an intervention and the only criterion on which an
intervention is to be judged. Considering exercise, if an exercise intervention is prescribed
for relief of neck pain, then it does not appear to matter what exercise mode (e.g., motor
relearning or strengthening) is prescribed.33,34 However pain is not the appropriate
outcome measure if the intent of the exercise program is to optimize the function of the
neck muscles for activities of daily living, work or sport. Muscle function measures are
required as the primary outcomes. Of interest, when return of normal muscle control is the
outcome, then it does matter what exercises are prescribed. As discussed in Chapter 5,
exercise modes to train muscle coordination and restore direction specificity are different
to those required to improve endurance or muscle strength. The primary outcome should
also direct the dosage or training period required. Should there be an assumption that the
training period will be the same when the intent is to modulate pain versus strengthening
muscles? The effect of an intervention must be judged on an outcome relevant to its
primary intent, not as currently, principally on pain relief.

Conclusion
The principles of management incorporate a patient-centred approach and development of
collaborative intervention strategies for neck pain disorders. Multimodal management
based on the individual patient’s presentation and needs is the key in rehabilitation. A
rehabilitation program should address the problems associated with the immediate episode
of neck pain as well as establish a self-management regime towards prevention of
recurrent episodes. The patient must have the knowledge and understanding to empower
them to self-manage their neck pain. Selection of management strategies is guided by the
principles of EBP. Nevertheless, clinical reasoning throughout the patient examination is
the overarching process. The clinical reasoning process encourages and has the necessary
flexibility in thought for interpretation of all information about the patient to guide the
selection of appropriate individualized management strategies.

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manipulation, exercise, and patient education. Phys Ther. 2007;87:9–23.
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17. Nee R, Vicenzino B, Jull GA, et al. Baseline characteristics of patients with nerve-
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13

Communication, Education and Self-

Management
This chapter considers three interrelated topics all of which are integral to good patient
management. There has long been interest in the art and science of communication. A
growing body of research points to the positive impacts of good communication and the
negative impacts of poor communication on patient outcomes.1,2 Good communication is
central to patient-centred practice and intimately linked to effective education. Good
communication and effective education can facilitate patient empowerment, which stands
to enhance compliance in self-management strategies both throughout the treatment period
as well as in efforts towards secondary or tertiary prevention.

Communication
Communication in health care covers a wide field3 including interpersonal skills, written
skills for reports and, in today’s world, professional social media skills. Interpersonal
skills for effective communication encompasses many different elements. These include
among many, active listening, use of individualized language, empathy, patient respect,
hearing their concerns, understanding their beliefs, expectations and desired outcomes of
management, providing information, encouraging questions and discussion to confirm
understanding. Developing trust and rapport is the basis for a positive therapeutic
relationship, ensuring the patient is an active participant in a genuine patient-clinician
partnership. All elements of communication are important and effective communication is
central to the entire management period. In this section, comments are offered on practical
aspects of some communication skills in the context of the initial assessment of patients
with neck pain disorders.

Listening
Considerable information is required from a patient presenting with neck pain, or indeed
any musculoskeletal disorder. Following the initial patient interview, the clinician wants to
be assured that the patient has no “red flags”. As well, information is required for the
clinician to reason intelligently about pain mechanisms, possible underlying causes and
pathophysiology, influences on functional activities, participation in work, recreational
and daily activities, psychological or social moderators, influences of any health
comorbidities and prognosis (see Chapter 8). Thus it is tempting to ask a series of
questions supplemented by various questionnaires to “cover all bases”. Although this may
be an understandable approach for the novice clinician, it is one which risks missing
important information and one that does not assure an optimal patient-clinician
relationship.4
Information that is required can be better gained by inviting and encouraging the patient
to tell the story of their neck pain disorder. The clinician should listen without distraction,
responding to any concerns that the patient raises and requesting clarification when
required.5 The benefits of listening cannot be overestimated in relation to the quality of
information gained. Listening to how the patient describes their symptoms, how the
disorder is affecting their function and participation and how the patient is dealing with the
neck disorder will provide information not only on the biological components of the neck
pain disorder but it provides insight into any concerns or anxieties that the patient has as
well as any helpful or unhelpful beliefs or expectations. Being responsive to the patient
with a comment or question, displays to them that the clinician has a genuine
understanding of the condition from the patient’s perspective. This is a skill that develops
with experience,5 but one to which all clinicians should aspire. Displaying empathy
increases trust, assures the patient they are being understood and begins to validate the
patient’s complaint.
In the physical examination, the clinician can provide an appropriate commentary on
what they are testing, for what reason, explaining the outcomes as relevant at that stage of
the examination and respond to any questions the patient may have. Providing the patient
with information will help them to understand and contribute to initial decisions about
their care.

Language
Language should be individualized to the patient. In the initial examination, it begins by
keying into terminology that the patient is using to describe their condition and using that
terminology. For example, if the patient describes the symptom of light headedness with
the word fuzziness, the clinician should adopt the term “fuzziness” when asking the patient
for a response in any assessment of this symptom. Likewise, if pain is described as an
ache, the term “ache” should be used. If the patient refers to their anxiety as
“apprehension”, this is the term that should be used from that point. Using the language of
the patient contributes to assuring them of the clinician’s understanding of their condition.
It is important to have consistent language or terminology between health care
providers. Patients find it disturbing to receive differences of opinion about their neck pain
disorder from different health care providers.6 Thus even though a clinician might disagree
with a previous diagnosis, it is better for the patient if the current clinician acknowledges
that diagnosis rather than be dismissive or make derogatory statements about it. Unless the
previous diagnosis is harmfully incorrect, the artful clinician can weave it into the
explanation that they wish to provide about the patient’s disorder to limit perceptions of
differences of opinion.
Language is very important in explaining the patient’s disorder. The “disadvantage” of
having a neck disorder is that usually there is nothing readily visible to validate it. The
“advantage” of having an extremity disorder is that it can often be seen (swelling,
bruising, muscle wasting, painful to weight bear). Use of a simple analogy as an ankle
sprain or overuse injury is often a good start to providing a basic explanation of what
might be underlying a patient’s neck pain. Alarmist explanations must be avoided, for
example, “the x-rays show advanced degenerative changes at all levels, your neck is a real
mess!” Such explanations sadly transfer a negative expectation of outcome to the patient,
which may adversely shape their future attitudes and coping skills. When explaining the
nature of the neck pain disorder to the patient, clinicians should avoid the use of
professional jargon. As an example, telling a patient that their “C2 is rotated” and is the
reason for their pain, is at best unhelpful and at worst mitigates against a good outcome.
Patients often focus on the “rotated C2” and once the seed is planted by this explanation,
they cannot get better until they are convinced it is “un-rotated”. This is difficult if C2 was
not rotated in the first instance, or the rotation is merely an epiphenomenon of head
position.7 This type of language can often lead to clinician induced, patient maladaptive
beliefs!

Communication through touch

The power of touch is well recognized and there is continuing research investigating its
physiological and therapeutic effects.8,9 Touch is also a powerful nonverbal
communication tool and can contribute substantially towards building a positive
therapeutic relationship. Patients want to be assured that the clinician understands their
neck pain and believes them.10 Nothing can be more validating for the patient than when
the clinician, without requesting patient feedback, can identify the painful cervical
segment(s) during a skilled manual examination. This is very assuring to patients and they
can gain considerable confidence in the clinician through this physical contact.
Furthermore, patients can judge a clinician’s mastery through such touch. As any educator
could attest, patients can differentiate the lack of confidence in a novice compared with an
expert’s manual examination. The better the clinician’s manual skills, the more confident
the patient will become in the clinician.

Education
Systematic reviews have found that education as a stand-alone treatment is not efficacious
for relieving neck pain,11 whether the education is about advice to stay active, or advice on
stress-coping skills, workplace ergonomics or self-care strategies. This is hardly surprising
and is an unrealistic expectation of any monotherapy. Education has other outcomes.
Ensuring patients have sufficient information and understanding of their neck pain
disorder is critical if the patient is to contribute informed decisions about their own care,
have positive expectations of management, see clear reasons to adhere to exercise
programs as well as make any changes to lifestyle, i.e., have greater self-efficacy.
Education forms part of a multimodal management approach for a patient with a neck pain
disorder.
Information required is varied and patient specific. Patients’ health literacy and learning
styles need to be explored for effective education. The learning experience for the patient
and their engagement in treatment and self-management is often a reflection of the
communication and teaching skills of the clinician. Because the effectiveness of these
skills has a powerful influence on patient uptake, it is salient for clinicians to reflect
frequently, on their own skills and abilities as an educator.

Education on the neck pain disorder

Providing information and helping patients understand their neck pain condition is a vital
first step in the education process and several topics are covered.

(1) The patient needs an understanding and validation of their neck pain disorder.
Validation comes when the clinician acknowledges the patient’s symptoms and the
impact on their lives and offers a provisional pathoanatomical mechanism
possibly using an analogy, such as a sprained ankle, an overuse injury or a flare up
of an osteoarthritic knee. The clinical can provide a clear physical diagnosis based
on the examination findings and explanation should encourage positive
expectations of outcomes. It is important that conventional anatomical and
medical terms are used and mystical, jargonish explanations are avoided.
(2) Pain education is an important aspect in the acute, subacute as well as persistent
pain states.12 Education should reflect the multidimensionality of pain
incorporating sensory, emotional, cognitive and behavioural components. The
educational content is best tailored to the patient’s presentation. Information is
provided on the sensory components or pain mechanisms in both the peripheral
system and central nervous system (CNS). Where relevant, augmented CNS
processing or central sensitization can be discussed, again avoiding alarmist
terminology. Explanations of how emotions can influence the experience of pain
through both CNS and hormonal processes can underpin treatment strategies to
decrease stress or anxiety as relevant to the patient. Explanations of endogenous
ascending and descending pain inhibitory mechanisms can likewise underpin
discussions on management strategies. There is increasing interest in education in
pain neurosciences and it makes a very important contribution to patient care.
Pain education is relevant across all stages of musculoskeletal disorders although
most research to date into its effectiveness is in chronic pain where it is proving
helpful.13 Similar to any intervention, some patients are more responsive than
others.14 Pain education’s role in preventing the transition of acute to persistent
back pain is currently being investigated.15
(3) The course of neck pain, prognosis and patient’s expectations of recovery should
be discussed. This may seem to be an eclectic group of topics but it is important to
understand patient expectations of recovery to best contextualize explanations of
the course of neck pain and prognosis. Patients may define their expectations of
recovery in many different terms,16,17 for example, complete pain relief versus
relief until symptoms are manageable. Recovery may mean a return to normal
everyday activities or it may mean being able to undertake basic activities without
hesitation. Expectations will also be guided by personal beliefs and past
 experiences.

The epidemiology of neck pain, regardless of aetiology, indicates that its course is
typically of recurrences with variable degrees of recovery between episodes.18–21 This
relatively pessimistic message can be expressed in a positive and motivating way to
support the need for self-management and maintenance programs in efforts to prevent or
lessen recurrences.
Discussing “how long to get better” can be more challenging. Walton and colleagues22
conducted a preliminary longitudinal study of patients presenting for treatment of
mechanical neck pain and found that a mean linear trajectory for the population actually
represented three different trajectories over a 1-month period. The majority (66%) had
gradual improvement, some improved rapidly (20%) and some regressed (14%). People
with more recent onset (< 6 months), and higher levels of pain were likely to improve
more rapidly. Leaver et al.23 made similar observations in patient cohort with an acute
episode of neck pain. Those who reported recovery did so in a median of 6.4 weeks (75%
recovered in 4 weeks). Thus it is difficult to estimate how long it will take for symptoms
to ease for an individual, although the shorter duration of pain is a positive sign for a more
rapid recovery.
There is some knowledge of prognostic indicators for recovery from a whiplash injury
with which there can be strong confidence, but few for mechanical neck pain.24,25 Risk
factors for a poor prognosis after a whiplash injury include high pain intensity and high
disability ratings at the initial presentation (strong confidence) and the presence of
abnormal cold thresholds, posttraumatic stress symptoms and catastrophization (moderate
confidence). Discussing outcomes with patients with poor prognostic indicators can be
difficult. Not all patients presenting with initially high pain levels fail to recover.
Informing a person that they will not recover would not be viewed well in a third-party
insurance environment. However not informing a person of the poor prognosis could be
another case of clinician-induced “catastrophic thoughts” as the patient worries that they
are not getting better as the clinician advised them that they should. These are areas of
professional communication and care that need to be discussed and resolved. At present, it
is probably reasonable to inform the patient that there are some symptoms of concern to
alert them, but not automatically align them with a poor prognosis.

Education in anatomy and biomechanics

Education in basic cervical anatomy and biomechanics is not an intervention for neck
pain. However, when considering self-management strategies and neck care, patients
benefit from some anatomical and biomechanical knowledge of the cervical spine and
shoulder girdle on which to problem solve so that they can self-manage effectively. It is
important that patients understand the relationship between the loads induced by
functional activities and pain so that they have the capability to develop appropriate
strategies for their daily functional activities and develop an understanding of the value of
undertaking exercise to improve physical support of their neck.
Education and use of behavioural strategies
Cognitive behaviour therapy (CBT) is a type of psychotherapy delivered by psychologists,
which aims to help a person identify and challenge unhelpful thoughts and to learn
practical self-help strategies to help improve quality of life. CBT has many forms. On
current evidence, the benefits of CBT for neck pain disorders is marginal at best when its
effectiveness is evaluated with pain as the primary outcome, although it can assist patients
with chronic neck pain overcome fear of movement.26 This marginal effect of CBT may
not be a reflection of the potential benefit of CBT, but again may reflect the potential
limitations of monotherapies, the lack of recognition of the heterogeneity of neck pain
disorders and disregard of patient preferences. For example, Keefe et al.27 advise that the
patients most suitable for Pain Coping Skills training are those who accept that their pain
is likely to persist and who are open to learn new skills for pain management. A CBT
graded activity program may be suitable for some patients with persistent neck pain but
may not be suitable for those patients with whiplash-associated disorders who display
repetition-induced summation of activity-related pain.28,29 Likewise a clinical trial is
underway to test the efficacy of a CBT stress inoculation training program but for only
those patients who exhibit early stress responses following an acute whiplash injury.30
CBT is a treatment method offered by trained health psychologists. This does not
necessarily preclude physiotherapists or others from delivering a full CBT program, but it
does take considerable training to meet psychologists’ competency levels.31,32
Nevertheless, physiotherapists do and should use psychologically informed practices.33
Listening to the patient, acknowledging their pain, discussing and often normalizing a
patient’s anxieties and fears is central to a good patient/clinician relationship. In addition,
physiotherapists have the skills to incorporate several of the CBT “lessons” into their
management. These include (as relevant to the patient) progressive muscle relaxation,
activity-rest cycling, pleasant activity scheduling and, importantly, problem solving.34 An
equally important lesson is helping the patient to recognize the signs of a potential relapse
and providing them with strategies to abort or manage an acute episode of neck pain.

Self-Management
Self-management is a vital component of management, especially considering the
recurrent nature of neck pain and in some cases, the persistence of neck pain. Patients
ideally become involved in their own management from the beginning and the clinician
may have to work to change patient behaviours. Their participation in treatment and
compliance with home management programs is the foundation upon which to build an
effective self-management program for use into the future. Patient compliance is essential
to the success of any home or self-management program, and the skills and clinical
attributes of the clinician influence this compliance.
From a content viewpoint, the patient requires knowledge and skills to manage their
work practices and activities of daily living in ways that will not adversely overload the
neck and cause unnecessary strain and pain. These will be very patient specific but may
include best methods for working at a computer or other devices, best methods for driving,
lifting and carrying, sleeping positions and pillows and gym and exercise, as examples.
From a process point of view, some information will be delivered didactically, for
example, data indicating that compared with a neutral head posture, using a device in a
neck flexion position will increase the mechanical demand on extensor muscles by 3 to 5
times (and increase the resulting load on the cervical spine).35 However, there is deeper
learning when, after the patient identifies which are the aggravating activities or postures,
they are helped to problem solve and find solutions or ways to perform the activity in a
way that will not adversely load the neck and cause pain.
Self-management also includes an exercise component, which in the first instance will
focus on rehabilitation strategies to ensure as optimal function as possible. Positive patient
traits for self-management and exercise include greater self-efficacy for exercise and
positive exercise outcome expectations.36 A program usually consists of a manageable
regime of exercises to help ease pain, restore movement and rehabilitate the
neuromuscular and sensorimotor systems. The program should be patient specific and
constantly modified and progressed throughout the management period. At all times,
patients must have ready access to a description of the program. From a process
viewpoint, determine the patient preference for receipt of this information. For example,
one patient might be very happy to access exercise descriptions and demonstrations
through an App downloaded onto a phone or tablet, another patient may prefer a hard
copy of exercises.
Self-management should also include a simple and “do-able” maintenance program that
a patient can continue after discharge from treatment to redress the recurrent nature of
neck pain disorders. As well, the patient should have treatment strategies to implement if
they recognize signs of a potential relapse and return of neck pain. Education should also
address issue of general activity and fitness within the total management plan of patient
care. The nature of these self-management strategies will be explored throughout the
chapters on management.

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16. Carroll L, Jones D, Ozegovic D, et al. How well are you recovering? The
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skills program? An examination of training processes and outcomes. Phys Ther.
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disorders: the role of coping skills training and exercise interventions. J Orthop
Sports Phys Ther. 1996;24:279–290.
35. Vasavada A, Nevins D, Monda S, et al. Gravitational demand on the neck
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14

Management of Joint and Movement

Dysfunction
Painful cervical joint and movement dysfunction is managed in various ways depending
on the underlying causes and contributors to the dysfunction. Information is sought
throughout the patient interview and the physical examination to understand the relative
contributions of external factors, for instance postures, poor muscle control and intrinsic
factors such as articular changes, to the presenting joint and movement dysfunction. This
information can direct initial management. Fig. 14.1 presents an example of clinical
reasoning for a patient presenting with limited and painful cervical movement with
associated cervical joint signs. It illustrates how the relative contributions of manipulative
therapy, active mobilizing exercise and neuromuscular training may be apportioned in
initial patient management on the basis of the examination findings. Nevertheless,
regardless of their proportional contribution, the roles of manipulative therapy and
neuromuscular training are synergistic.

FIG. 14.1 Example of clinical reasoning to inform on proportionate roles of

manipulative therapy and muscle training in initial interventions. C/Th, cervicothoracic,
MT, manipulative therapy, ROM, range of motion.

This chapter discusses manipulative (or manual) therapy and exercise. The exercises in
this context focus on active or assisted movement at a segmental or regional level to
improve range and quality of movement. The patient must be an active participant. Any
improvement gained in range and quality of motion in a treatment session must be
supplemented by a home program of specific exercise because the immediate effects of
manipulative therapy management, if not reinforced, will reduce.1

Manipulative therapy
Manipulative therapy (mobilization and manipulation) makes an important contribution to
the management of patients with neck pain disorders, which are associated with painful
segmental dysfunction. The evidence from systematic reviews indicates that manipulative
therapy (manipulation and mobilization) is effective in reducing neck pain as a single
modality2,3 or as part of a multimodal program.4 Furthermore evidence is emerging of its
cost effectiveness when compared with exercise alone, advice or general practitioner
care.5–8 Manipulative therapy has shown benefit for acute, subacute and persistent or
chronic neck pain disorders, for various age groups, including older patient groups with
long-standing or chronic neck pain.6,9 Yet manipulative therapy is not a panacea. It is not
best practice when it is used as a sole treatment. Rather it is best positioned as part of a
multimodal management approach. As with any intervention whether pharmacological,
physical or psychological, patient suitability for and responsiveness to manipulative
therapy will vary and the intervention should be abandoned if it is not producing the
desired outcomes after a reasonable trial of treatment.

Benefits of manipulative therapy

The benefits of manipulative therapy are in relief of symptoms, be the symptoms of neck
pain, neck-related arm pain, neck-related headache or dizziness.2,9–12 Studies have
indicated that manipulative therapy elicits hypoalgesia both locally and remote to the neck
and induces excitation of the sympathetic nervous system suggestive of systemic pain
modulation effects.13 Studies conducted on spinal and peripheral joints suggest the effects
of manipulative therapy may be attributed to peripheral, spinal and supraspinal
mechanisms.13 For example, at the peripheral level, spinal manipulative therapy has been
shown to significantly downregulate or reduce the production of inflammation-associated
chemokines14,15 which may be elevated in people with low-back and neck pain,15,16 a
change not observed following sham manipulation.15 Similarly, manipulative therapy can
promote changes in β-endorphin, anandamide, N-palmitoylethanolamide and serotonin
levels.17 Spinal mechanisms may include decreased activation of the dorsal horn of the
spinal cord,18 and changes in spinal reflex excitability19,20 including a reduction of the H-
reflex21 and an increase in nociceptive flexion reflex threshold.22 Finally, supraspinal
responses with manipulative therapy shown at this time include decreased activation of
areas in the brain associated with pain including the anterior cingulate (bilateral), frontal
cortex (bilateral) and sensory motor cortex (contralateral).18
Manipulative therapy increases pressure pain thresholds both locally23–25 and at remote
distal sites,23,26 but in contrast, thermal sensitivity seems to be unaffected.22,24,25,27
Manipulative therapy also affects an immediate excitatory response in the sympathetic
nervous system24,26,28 as demonstrated by, for example, significant increases in skin
conduction, breathing rate and heart rate.24,28 Other mechanisms contributing to symptom
relief could include the effects of placebo and patient expectations.29,30 The physiological
and therapeutic effects of hands on treatment also contribute to patient assurance and,
indirectly, pain relief.
There is less certainty about the mechanical mechanisms of effect of manipulative
therapy procedures.27 For example, the technique of central posteroanterior (PA) glides, as
its nomenclature suggests, should theoretically induce segmental translation at the target
segment. In a magnetic resonance imaging study, cervical segmental motion was measured
when a PA mobilization was performed centrally on C5 at a grade III technique (clinical
definition—large amplitude of movement moving to the end of available range).31 Not
surprisingly with this large amplitude technique (over a segmental translation excursion of
1–1.5 mm), it was found that the mobilization induced extension in the levels above C5
and flexion in the levels below. In an earlier study of a grade IV PA technique, negligible
to no intervertebral translation was observed.32 In a similar vein, a cadaveric analysis of a
localized high velocity, low amplitude C1–2 rotary thrust revealed that the displacement
induced during the technique was unintentional, unpredictable and not reproducible.33
Thus to base explanations of mechanism on a movement directional basis is not relevant
for some techniques.
Several studies have investigated the effect of mobilization on tissue stiffness in the
cervical spine (i.e., the resistance to deformation induced by the manual force or in clinical
terms, the through range resistance and end feel). Stiffness tested segmentally in vivo is
increased in patients with neck pain disorders, although there is no direct relationship
between degree of stiffness and reported pain and disability.34 The latter is understandable
because stiffness is quite variable between individuals depending on collagen make up,
age and gender. Cervical mobilization can reduce spinal stiffness and pain, although one
study determined that this was not measurable until the short-term follow-up (4 days later)
and was not related to any increase in range of movement.35 In contrast, a study of
unilateral PAs applied over the zygapophysial joints demonstrated an immediate,
posttreatment reduction in segmental stiffness and an increase in range of movement.36
Notably, the change was only determined when treatment was applied locally to the
symptomatic and hypomobile segment, suggesting the need for localized application of
treatment.
There is increasing clarity about potential neurophysiological mechanisms underpinning
the symptomatic relief that can be afforded with manipulative therapy. However, more
research is needed to better understand the importance of mechanical factors. This is both
in relation to mechanisms of effect and also guidance for selection of manipulative therapy
techniques.

What manipulative therapy cannot achieve

Manipulative therapy can modulate and help relieve symptoms such as pain, dizziness or
light headedness or unsteadiness. Yet rehabilitation is also concerned with addressing
impaired functions in the neuromuscular and sensorimotor systems to assist the return of
normal safe function and in efforts to prevent recurrent episodes of neck pain. Thus the
important question is whether manipulative therapy can address the impaired function as
well as symptoms.
The immediate effect of cervical PA mobilization on muscle activity has been assessed
by measuring sternocleidomastoid or longus colli muscle activity in the craniocervical
flexion test (CCFT). There is evidence both for and against an immediate posttreatment
change in muscle activity.24,37,38 The change in muscle activity might relate to reduced pain
following the PA technique. However, there is evidence from a randomized controlled trial
that this immediate change is not sustained. No improvement in performance of the CCFT
occurred in the short, medium or long term, despite the relief of neck pain and headache
afforded by manipulative therapy.10
Dizziness and unsteadiness are not uncommon symptoms of cervical musculoskeletal
disorders. They are associated with impairments in proprioception and balance.
Manipulative therapy can efficiently alleviate these symptoms.39 However this relief of
symptoms was not accompanied by any substantive changes in measures of joint position
sense in the short or long term. As found in other studies, neither techniques of
mobilization or manipulation have been able to change balance sway measures.12,40,41
Thus manipulative therapy can successfully relieve symptoms, but symptom relief does
not guarantee any improvement in impairments in neuromuscular and sensorimotor
systems. Pain relief from manipulative therapy is the example used here, but it applies to
pain relief by any modality and even pain relief over time.42 This reinforces the need for
multimodal management in a rehabilitation program for patients with neck pain disorders
because aims are not just to address the episode of neck pain but to lessen future recurrent
episodes.

Patients suitable for manipulative therapy

A systematic review of clinical trials, in which the intervention tested was cervical
manipulative therapy, studied the inclusion criteria to reveal those patients who were
deemed suitable for this therapy. The data from 30 trials revealed inclusion criteria of the
broad categories of mechanical or idiopathic neck pain, cervical spondylitis, whiplash-
associated disorders (WAD) and cervicogenic headache. The “manipulable lesion”, if
defined, was usually described as a positive response to a clinical test identifying
abnormal segmental movement.43 It is certainly not the ideal criteria especially when
clinical tests based on identifying abnormal segmental movement are of themselves not
highly reliable.43,44
Nevertheless, despite limitations, the basic framework to identify patients potentially
suitable for manipulative therapy management remains: those with neck pain associated
with impaired neck movement (usually painful), which is associated with symptomatic
segmental joint dysfunction; and for whom there are no conditions or patient features
which contraindicate the use of this therapy. Definitions are modified depending on the
manipulative therapy approach followed, for example, detection of abnormal segmental
motion and reproduction of pain during manual examination,45 versus the reduction of
pain and improvement of segmental/regional movement during manual examination.46
Thus at this time, indications for manipulative therapy are in many ways, a definition
essentially of exclusion of those unsuitable.
Another way to identify patients suitable for manipulative therapy is to recognize
patients who are likely responders to manipulative therapy based on their clinical
presentation. In this respect, most attention has been paid to developing classification
schemes/subgrouping patients or developing clinical prediction rules.44 Although of some
assistance, these methods too have inherent limitations (see Chapter 1). An alternate
method is to identify which clinical features indicate that patients are likely non-
responders to manipulative therapy.47 Discussion here has focussed on manipulative
therapy, but the same challenge is still present for selecting patients who are suitable and
will respond to most approaches or modalities used to treat neck pain.
Clinical reasoning throughout the entire clinical examination will inform selection of
management strategies including manipulative therapy. The basic framework of impaired
neck movement and associated symptomatic segmental joint dysfunction might be the
appropriate guide. These indications for suitability for manipulative therapy treatment
would be strengthened with evidence that relief of pain afforded by manipulative therapy
is associated with resolution of the clinical signs that were used to detect the manipulable
lesion.43 This process of assessment and reassessment of the change in clinical signs in
response to the intervention is used in clinical practice to guide the continuation or
abandonment of the technique or approach. Suitable measures can and need to be included
in clinical trials to provide the evidence of the validity of this guide.

Contraindications and cautions to manipulative

therapy
Much attention has rightly been afforded to safety in practice. Texts have been devoted to
nominating and clinically identifying serious spinal pathologies48,49 as well as identifying
conditions that might masquerade as spinal conditions50 and would contraindicate the use
of spinal manipulative therapy and indeed other physical therapies. The reader is referred
to these sources for a comprehensive coverage of these conditions and their recognition. In
the cervical spine, greatest concerns are vascular disorders (cervical arterial dissection,
vertebrobasilar insufficiency, anticoagulant therapy) (see Chapter 10); any state which
might reduce the integrity of cervical structures, such as acute trauma, metastases;
inflammatory arthritides; traumatic or degenerative instability; connective tissue disease;
congenital anomalies (Down syndrome); osteoporosis; infection and advanced
degenerative disease with lateral and/or spinal canal stenosis with or without neurological
signs.51
Fortunately, catastrophic adverse events associated with cervical manipulative therapy
such as stroke or even death are rare. However, accurate estimates are not available as the
quality of the literature on which estimates are based is still quite poor and all cases are
not recorded in the literature. Best estimates vary widely from 1 in 20,000 to 1 in
250,000,000 manipulations.52 To enhance accuracy, clinical trials that follow Consolidated
Standards of Reporting Trials (CONSORT) guidelines now are required to report adverse
events.53 This might allow better analysis of practitioner, patient and technique
characteristics associated with serious adverse events.54 In perspective, a systematic
review of adverse events with manipulative therapy (for either neck pain or low-back
pain) confirmed that the risk of major adverse events was very low.55 Nevertheless about
one-half of the patients experienced minor to moderate adverse events, (often
posttreatment pain) which lasted for a few to 72 hours. Of note, the incidence was similar
for manipulative therapy and exercise. All clinicians should aim to eliminate these minor
adverse events from practice, and this should be achievable with better understanding of
the patient’s pain state and skilled manual handling and exercise prescription.

Which manipulative therapy approach?

Manipulative therapy within physiotherapy incorporates several different approaches,
which although not radically different, do have some unique philosophies and
practices.45,46,56–59 Each has an examination approach which underpins technique selection.
This means that a patient’s neck disorder or joint dysfunction could be treated with
different techniques based on the clinicians’ background training. Nevertheless, the
evidence indicates that, when tested head to head, symptomatic outcomes are essentially
the same between different manipulative therapy approaches.2,39,60,61 Similarly, there is no
consistent evidence that manipulation has superior outcomes to mobilization.2,60,62–64 This
encourages thought on mechanisms of effect, and the commonalities rather than
differences between techniques. The commonalties would be neurophysiological effects
and probably the changes the techniques afford in tissue stiffness. This then raises the
question of the nature of tissue stiffness or altered tissue compliance underlying the
segmental hypomobility. It could be reasoned that it is probably, in large part, muscle
activity in response to a symptomatic joint when different techniques/movement directions
all cause a similar change in tissue stiffness, and the change is achieved quite rapidly.

Selection and application of technique

The decision to use manipulative therapy and the selection of a particular technique is the
culmination of clinical reasoning throughout the patient interview and physical
examination. The process in different approaches varies slightly but is common,
consideration is usually given to the nature and intensity of pain, functionally impaired
movement or posture, the direction(s) of impaired and painful cervical motion and the
local segmental test results.45,46,56–59 The selection of a technique will usually relate to the
pain response and direction of movement loss, noting that there are always different
options (Figs 14.2A–C to 14.3A–C). The clinician must always test the response to the
technique and, if it is not achieving the desired effect within a treatment, an alternate
technique should be tried. Changes within a session can predict changes in subsequent
treatments.1 Nevertheless changes in impairments do not necessarily relate to changes in
activity limitations,65 which again emphasizes the need for multimodal treatment.
 FIG. 14.2 Techniques which can address a restriction in (R) C1–2 segmental motion.
(A) Unilateral posteroanterior glide on C2 with the head and C1 positioned in slight (R)
rotation. (B) A sustained natural apophysial glide on C1 with active (L) cervical rotation.
(C) (R) lateral flexion mobilization of C0–1. (L) C1–2 rotation can be limited if there are
restrictions in contralateral lateral flexion.

FIG. 14.3 Techniques which can address a restriction in C3–4 lateral flexion. (A) An
anteroposterior glide of C3 on C4 with a medial bias. The pad of the thumb is placed
on the anterior surface of the transverse process of C3 and the thumb position is
supported by the fingers gripping the lamina posteriorly. The grip around the segment
remains constant and the movement is produced at the elbows. The thumb is the
transmitter not the producer of the movement/force. If the movement is produced
through thumb pressure, the technique will be painful. (B) A lateral flexion technique.
The hands cradle the head and the index or middle finger is placed on the lamina of
C3. The movement is a combination of a lateral flexion and medial glide to move the
facet into lateral flexion. (C) Lateral flexion is performed in sitting. The spinous process
and lamina of C4 is stabilised by a pincer grip of the (R) hand. The thenar eminence of
the (L) hand grips C3 and the lateral flexion movement is produced by an arm/shoulder
girdle movement.

There has been discussion of whether it is necessary to be precise in treating the most
dysfunctional cervical level.44 A few studies have addressed this issue using a one-session,
pre-post design in both the cervical and lumbar regions with some diverse outcomes.36,66,67
Such pre-post single application studies have major limitations, but a systematic review
found evidence to favour specific mobilization of the dysfunction cervical segment for
pain relief.68 Further research is required to evaluate whether treating the most
symptomatic level produces superior treatment effects. Stronger questions and designs are
necessary, for example, investigating effects of treating the most symptomatic cervical
segment versus a random segment after three or four treatment sessions over, for instance,
a 2-week period. Certainly, intuitively, treating the most symptomatic segment is logical
clinical practice.
Nevertheless, upper thoracic spine mobilization and manipulation may also relieve neck
pain.69,70 However various trials have shown that although treatment of the upper thoracic
region can relieve neck pain, this remote treatment is not as effective as local cervical
treatment.71–73 There are strong indications for including treatment to the upper thoracic
region of patients with neck pain disorders because of the interdependent nature of
cervical and upper thoracic motion and the need for upper thoracic movement to allow full
head excursion. It is reasonable that both areas receive attention as required in
management as is currently occurring.62,63
Various manipulative therapy approaches offer recommendations for the dosage of
techniques, but it is an area that is not well researched. Various approaches have guides
relevant to their approach, such as the grade of technique that might be used,45 the position
in range it might be performed58 or the appropriate force to improve the impaired
movement without causing pain.46 Many factors influence “dosage” or how much
mobilization or manipulation is delivered. These include the nature and severity of the
patient’s pain, the acuteness of the condition, the irritability of the condition and patient
preferences.
Preliminary research is providing some initial guidelines. For example, a study of the
delivery of one to five sets of PA mobilizations, albeit on the lumbar spine of healthy
individuals, found that at least 4 sets of 60 seconds mobilizations were required to elicit
the best hypoalgesic response.74 Another study investigated the effects of high (90 N mean
peak force) versus low (30 N mean peak force) mobilization forces when delivering a PA
mobilization to the most symptomatic segment of patients with chronic neck pain.35 Better
effects (reduced segmental stiffness and pain) were found with the higher force
mobilization. However, these effects were not determined immediately posttreatment but
at the follow-up up to 4 days later. Immediately posttreatment, pain levels were increased
in the high force group, which may not be an optimal outcome. Dosage is a priority area
for further research.
Application of techniques should at all times be comfortable for the patient (Fig. 14.4).
Preferably, all treatment should cause nil or minimal pain. This is especially true when
pain levels are high and/or when central sensitization is present as occurs in patients with
cervicogenic headache, cervical radiculopathy and in some cases of whiplash.75–77
Treatments that aggravate pain in these patients are counterproductive. Nevertheless, the
presence of central sensitization does not mitigate against the use of manipulative therapy.
It was thought that patients with WAD who displayed central sensitization would not
respond as well to manipulative therapy,78 but subsequent studies have not shown that this
is the case.79,80
 FIG. 14.4 Unilateral posteroanterior (PA) glides C3–4. Unilateral PA glides should be
performed painlessly and this can be achieved if the hands grip the side of C3 to
support the position of the thumbs on the lamina to perform a unilateral PA. The
movement is generated by the elbows/forearm and the thumbs are the transmission
point, not the generator of force.

Treatment of the cervical spine for pain in adjacent

areas
There has been much study into potential neurophysiological and biomechanical links
between the cervical spine and disorders of the craniomandibular complex and upper
limb.81–85 Clinical trials have evaluated the effect of treating the neck for a
craniomandibular or an upper-limb pain syndrome or conversely treating the
craniomandibular disorder to ease neck pain.28,82,84–87 Outcomes have been variable. In
clinical practice, patients can present with apparent “signs” in both the cervical spine and
temporomandibular joint (TMJ). Clinicians need to undertake a disciplined
assessment/reassessment process to determine the primary source of pain and dysfunction.
Treatment of one region (e.g., the neck) might result in an immediate change in pain and
range of motion in the TMJ. However, the critical issue is whether the treatment effect is
maintained at the second treatment session. A basic guide is that at least 50% of any
change gained in TMJ pain and motion in the previous treatment must be maintained to
justify repeated treatments or a focus on the neck. Often the initial gains are from pain
modulation, not true changes in the local dysfunction. Persisting with treatment that does
not result in lasting changes is poor practice.

Active exercise
Active exercise is a vital component of the management of joint and movement
dysfunction. In this context, active exercise is used to regain active range of motion and to
train movement velocity as indicated.

Range of motion
Active exercise is used to gently load the tissues during the healing process following
acute trauma such as a whiplash or sporting injury. Active movement is used in idiopathic
neck pain with movement and segmental dysfunction, to mobilize neck hypomobility at
both segmental and regional levels. Active range of movement exercises as a sole
treatment for neck pain is not optimal88 but active exercises are an important part of a
multimodal program.
In an acute phase of a neck disorder, patients may find it painful to perform range-of-
motion exercises in the sitting position. Exercises are often easier to perform and less
painful when head load and gravity are reduced. This is achieved by positioning the
patient in four-point kneeling, prone on elbows or forward inclined sitting position as
tolerated.
Active exercise should be prescribed to complement and supplement the manipulative
therapy treatment to address the local segmental hypomobility. Fig. 14.5A–C illustrates
examples of segmentally biased exercises. Early radiological studies demonstrated that an
active regional movement does not mean that all segments are contributing.89 Thus the
segmental bias to the regional exercise aims to ensure that the segments of interest are
contributing to the motion. The segmental exercises are best taught and practised in
conjunction with the manipulative therapy component of management. This helps the
patient to understand and “feel” the movement that the treatment is trying to achieve.
Patients replicate it with the active exercise. Teaching the active exercise at this time in
treatment involves the patient immediately in management and does not divorce the active
segmental mobilising exercise from the manipulative therapy treatment. Patients
immediately understand the relevance of the exercise which might help compliance. This
opportunity can be lost when teaching active exercise is relegated to the end of treatment
and to a home program only.
 FIG. 14.5 Segmentally biased active movement. (A) Lateral flexion C3–4. The patient
places their index or middle finger on C4 and focusses lateral flexion at the C3–4 level.
(B) A mobilization with movement technique to encourage C1–2 rotation. (C) The
“archery exercise’ ”. This exercise compliments the passive mobilization of the
cervicothoracic region with the lateral glide + active rotation technique (see Fig. 9.5).
The patient keeps their eyes fixed on an imaginary target and draws the string back on
an imaginary bow. They focus on producing and feeling the movement in the upper
thoracic region. The action is performed on alternating sides.

Exercises for training movement velocity and

accuracy
Recent research has investigated the use of both a customized neck virtual reality system
and a laser and target for feedback during cervical kinematic training for impairments in
range, velocity and accuracy of motion.90,91 The applications are highly suitable for use in
a home program of exercises. Training for range of motion, movement velocity and
accuracy includes exercises such as quick active head movements, fine head movement
control and stability in several movement directions (Fig. 14.6A and B). In the clinical
trial, patients had non-acute, persistent neck pain and performed exercises at home for 20
minutes, 4 times per week. Both forms of training (virtual reality and the laser and target
system) improved patients cervical kinematics as well as their neck pain and disability in
both the short and intermediate terms.90,91 Because training with both the virtual reality and
the laser and target system produced similar outcomes, the choice of training mode could
depend on availability. Perhaps a more important consideration is the patient’s preference,
and in this technological age, a virtual reality device might be more appealing to some.
Obliging with the patient’s preference may facilitate exercise compliance.
 FIG. 14.6 Exercises to train movement velocity, accuracy and range. (A) Kinematic
training with a head mounted laser directed towards lines on a poster. Tasks include:
moving as far as possible in all directions, moving quickly from the centre point to the
circles placed in different directions and then stabilizing the laser before quickly
returning to the centre and tracing the vertical and horizontal lines and then the curved
pattern lines as accurately as possible with the laser using head motion. These
exercises can be commenced in sitting and progressed to comfortable standing or
more challenging stance conditions. (B) Kinematic home training using the virtual
reality head mounted display, and customized software. Here, head motion controls a
virtual airplane. Range of movement is challenged by gradually increasing the range of
movement required to hit targets in flexion, extension, rotation left and right. Velocity of
head motion is encouraged by motivating the participant to move quickly towards the
target in random directions before it disappears. Finally, the player is directed to keep
the head of the virtual pilot on a moving target up, down, right and left as accurately as
they can.

Self-management
A home exercise program is a very necessary component of the management program.
The small dosage of movement delivered and practised within a treatment session is
insufficient. Dosage of either active segmentally biased exercise or exercises to address
movement velocity will depend on the acuteness of the condition but low repetitions (e.g.,
5–10 repetitions) performed several times during the day (e.g., 3–5 times) is a reasonable
approach to commence the self-management program. Exercises will be progressed in
nature and repetitions in line with the patient’s and treatment progression.
The patient should be encouraged to think about how they can incorporate the exercise
into their daily routines. The clinician needs to follow this up with the patient to
demonstrate the importance of self-management to treatment outcome. Equally important
is to determine how patients would like the exercises presented to them for home practice.
Some patients, for instance, may prefer a hard copy description of the exercises, others
may prefer a video of themselves performing the exercise to refer to at home.
Patient involvement with the development of the exercise program, which will evolve
with the addition of other strategies into the self-management program, is a positive step
towards compliance.

Conclusion
The treatment of painful cervical joint and movement dysfunction is an important element
of the multimodal management program for patients with neck pain disorders.
Manipulative therapy has effective and beneficial analgesic effects. Active movement
exercises both segmentally directed and regional are vital and necessary compliments to
manipulative therapy to address the joint and movement dysfunction. All aspects of
movement dysfunction need to be considered including the quality and range of
movement, poor movement sense and velocity. Effective exercises need to be devised for
the patient to practise efficiently and successfully.

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57. Kaltenborn F, Evjenth O, Kaltenborn TB, et al. Manual mobilization of the joints:
the spine. 4th ed. 2003. Oslo: Norli. vol. 2.
58. McCarthy C. Combined movement theory. Churchill Livingstone, Elsevier: UK;
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59. Mulligan B. Manual therapy ‘NAGS’, ‘SNAGS’, ‘MWMS’. 5th ed. Wellington:
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60. Lopez-Lopez A, Perez JA, Gutierez JG, et al. Mobilization versus manipulations
versus sustain apophyseal natural glide techniques and interaction with
psychological factors for patients with chronic neck pain: randomized controlled
trial. Eur J Phys Rehabil Med. 2015;51:121–132.
61. Pérez H, Perez J, Martinez AG, et al. Is one better than another? A randomized
clinical trial of manual therapy for patients with chronic neck pain. Man Ther.
2014;19:215–228.
62. Dunning J, Butts R, Mourad F, et al. Upper cervical and upper thoracic
manipulation versus mobilization and exercise in patients with cervicogenic
headache: a multi-center randomized clinical trial. BMC Musculoskelet Disord.
2016;17:64.
63. Griswold D, Learman K, O’Halloran B, et al. A preliminary study comparing the
use of cervical/upper thoracic mobilization and manipulation for individuals with
mechanical neck pain. J Man Manip Ther. 2015;23:75–83.
64. Leaver A, Maher C, Herbert R, et al. A randomized controlled trial comparing
manipulation with mobilization for recent onset neck pain. Arch Phys Med
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65. Tuttle N, Laasko L, Barrett R. Change in impairments in the first two treatments
predicts outcome in impairments, but not in activity limitations, in subacute neck
pain: an observational study. Aust J Physiother. 2006;52:281–285.
66. Aquino R, Caires P, Furtado F, et al. Applying joint mobilization at different
cervical vertebral levels does not influence immediate pain reduction in patients
with chronic neck pain: a randomized clinical trial. J Man Manip Ther.
2009;17:95–100.
67. Chiradejnant A, Maher C, Latimer J, et al. Efficacy of “therapist-selected” versus
“randomly selected” mobilisation techniques for the treatment of low back pain: a
randomised controlled trial. Aust J Physiother. 2003;49:233–241.
68. Slaven E, Goode A, Coronado R, et al. The relative effectiveness of segment
specific level and non-specific level spinal joint mobilization on pain and range
of motion: results of a systematic review and meta-analysis. J Man Manip Ther.
2013;21:7–17.
69. Cleland J, Childs J, McRae M, et al. Immediate effects of thoracic manipulation in
patients with neck pain: a randomized clinical trial. Man Ther. 2005;10:127–135.
70. González-Iglesias J, Fernández-de-las-Peñas C, Cleland J, et al. Thoracic spine
manipulation for the management of patients with neck pain: a randomized
clinical trial. J Orthop Sports Phys Ther. 2009;39:20–27.
71. Cleland J, Childs J, Fritz J, et al. Development of a clinical prediction rule for
guiding treatment of a subgroup of patients with neck pain: use of thoracic spine
manipulation, exercise, and patient education. Phys Ther. 2007;87:9–23.
72. Puentedura E, Cleland J, Landers M, et al. Development of a clinical prediction
rule to identify patients with neck pain likely to benefit from thrust joint
manipulation to the cervical spine. J Orthop Sports Phys Ther. 2012;42:577–592.
73. Puentedura E, Landers M, Cleland J, et al. Thoracic spine thrust manipulation
versus cervical spine thrust manipulation in patients with acute neck pain: a
randomized clinical trial. J Orthop Sports Phys Ther. 2011;41:208–220.
74. Pentelka L, Hebron C, Shapleski R, et al. The effect of increasing sets (within one
treatment session) and different set durations (between treatment sessions) of
lumbar spine posteroanterior mobilisations on pressure pain thresholds. Man
Ther. 2012;17:526–530.
75. Chien A, Eliav E, Sterling M. Whiplash (grade II) and cervical radiculopathy
share a similar sensory presentation: an investigation using quantitative sensory
testing. Clin J Pain. 2008;24:595–603.
76. Chua N, Suijlekom HV, Vissers K, et al. Differences in sensory processing
between chronic cervical zygapophysial joint pain patients with and without
cervicogenic headache. Cephalalgia. 2011;31:953–963.
77. Sterling M, Jull G, Vicenzino B, et al. Sensory hypersensitivity occurs soon after
 whiplash injury and is associated with poor recovery. Pain. 2003;104:509–517.
78. Jull G, Sterling M, Kenardy J, et al. Does the presence of sensory hypersensitivity
influence outcomes of physical rehabilitation for chronic whiplash? - a
preliminary RCT. Pain. 2007;129:28–34.
79. Castaldo M, Catena A, Chiarotto A, et al. Do subjects with whiplash-associated
disorders respond differently in the short-term to manual therapy and exercise
than those with mechanical neck pain? Pain Med. 2017;18:791–803.
80. Michaleff Z, Maher C, Lin C, et al. Comprehensive physiotherapy exercise
programme or advice for chronic whiplash (PROMISE): a pragmatic randomised
controlled trial. Lancet. 2014;384:133–141.
81. Coombes B, Bisset L, Vicenzino B. Cervical dysfunction is evident in individuals
with LE without obvious neck pain and may reflect central sensitization
mechanisms. Further study of the nature of the relationship between cervical
dysfunction and LE is required. J Manipulative Physiol Ther. 2014;37:79–86.
82. Fernández-de-Las-Peñas C, Cleland J, Palacios-Ceña M, et al. The effectiveness
of manual therapy versus surgery on self-reported function, cervical range of
motion, and pinch grip force in carpal tunnel syndrome: a randomized clinical
trial. J Orthop Sports Phys Ther. 2017;47:151–161.
83. Grondin F, Hall T, Laurentjoye M, et al. Upper cervical range of motion is
impaired in patients with temporomandibular disorders. Cranio. 2015;33:91–99.
84. Mintken P, Cleland J, Carpenter K, et al. Some factors predict successful short-
term outcomes in individuals with shoulder pain receiving cervicothoracic
manipulation: a single-arm trial. Phys Ther. 2010;90:26–42.
85. Piekartz H, Pudelko A, Danzeisen M, et al. Do subjects with acute/subacute
temporomandibular disorder have associated cervical impairments: a cross-
sectional study. Man Ther. 2016;26:208–215.
86. Grondin F, Hall T. Changes in cervical movement impairment and pain following
orofacial treatment in patients with chronic arthralgic temporomandibular
disorder with pain: a prospective case series. Physiother Theory Pract.
2017;33:52–61.
87. Piekartz H, Lüdtke K. Effect of treatment of temporomandibular disorders (TMD)
in patients with cervicogenic headache: a single-blind, randomized controlled
study. Cranio. 2011;29:43–56.
88. O’Leary S, Jull G, Kim M, et al. Training mode-dependent changes in motor
performance in neck pain. Arch Phys Med Rehabil. 2012;93:1225–1233.
89. Dvorak J, Froehlich D, Penning L, et al. Functional radiographic diagnosis of the
cervical spine: flexion/extension. Spine. 1988;13:748–755.
90. Bahat HS, Takasaki H, Chen X, et al. Cervical kinematic training with and without
interactive VR training for chronic neck pain - a randomized clinical trial. Man
 Ther. 2015;20:68–78.
91. Sarig-Bahat H, Croft K, Carter C, et al. Remote kinematic training for patients
with chronic neck pain- a randomised controlled trial. Eur Spine J.
2018;27:1309–1323.
15

Management of Neuromuscular
Dysfunction
Exercise in the broader context is being discovered to have many and diverse benefits for
physical and mental health. One of its valuable benefits in the musculoskeletal context is
its hypoalgesic effect. This effect has been measured immediately after various exercise
modes including aerobic,1,2 dynamic resistance3 and isometric exercise.4,5 The mechanism
is considered to involve a systemic analgesic process6 with activation of central inhibitory
pathways7 as well as peripheral mechanisms.8 However, specific research into immediate
hypoalgesic effects following local neck or general exercise in people with neck pain is as
yet quite sparse.9–11 Nevertheless, in accord with patient centeredness and their desire for
pain relief, current clinical trials and systematic reviews of interventions for neck pain all
evaluate the effectiveness of exercise on the criterion of its pain relieving effect.12–14
Evaluation is based on patient-centred outcomes of self-reported pain intensity and/or
perceived disability immediately following the intervention and at intermediate and longer
terms following intervention.
The benefits of exercise on pain are important but exercise that is also specially
prescribed to address the neuromuscular dysfunction, a known feature of musculoskeletal
disorders, is a key component of rehabilitation. It seems that with the emphasis on pain
outcomes, there has been a recent loss of focus on exercise prescription for
“rehabilitation”. For instance, participant inclusion criteria in clinical trials usually do not
include measures of muscle function that link to the intervention (e.g., presence of a
muscle strength deficit for a strengthening program intervention). There appears no major
interest in whether or not exercise has addressed the neuromuscular deficits associated
with neck pain (see Chapter 5) because measures of impairment are rarely included as
primary (and often not even as secondary) outcomes. Exercise for pain relief is a very
different construct to exercise for rehabilitating the neuromuscular system and
neuromuscular impairments. We argue here for a reemphasis on the benefits of exercise
for restoration of neuromuscular function in addition to its pain-relieving benefits.
An acute episode of neck pain usually resolves in a timely manner with appropriate
management, although it can be incomplete.15,16 The message that must be repeatedly
emphasized is that for the majority of people neck pain is a recurrent or persistent
disorder.15,17 Together with low-back pain, neck pain accounts for more years lived with a
disability than any other chronic disease.18 The true personal and immense fiscal cost of
neck pain is not in a single episode, but in the cost of repeated episodes, i.e., the repeated
healthcare costs, the potential costs of harm from repeated use of medications such as
nonsteroidal antiinflammatory drugs (NSAIDs), the personal cost of loss of quality of life
as well as costs of lost work productivity. Managing an episode of pain is important but a
pressing aim is to decrease recurrence rate. There are multiple features from biological,
social and psychological perspectives that potentially contribute to the recurrent or
persistent nature of neck pain. There will never be a perfect correlation between physical
impairments and pain levels or states. Nevertheless, impaired neuromuscular function
does not necessarily automatically resolve when pain resolves, which cannot be good for
neck health.19–21 Although not the sole solution, rehabilitation of neuromuscular and
sensorimotor impairments stands to make a positive contribution to both recovery and
decreasing recurrence rate.
Exercise can relieve pain, but when a reduction in pain is the primary outcome, it does
not appear to matter what exercise is prescribed, at least for those with chronic pain. Both
low-load and high-load exercises can similarly reduce chronic neck pain.19,22 Nevertheless,
it does matter what exercises are prescribed if the aim is to restore the impaired elements
of neuromuscular function. The evidence clearly indicates that changes in motor
behaviour are best addressed through a low-load motor relearning approach in the first
instance. Yet this exercise mode is clearly inadequate and inappropriate when the aim is to
increase muscle strength and higher-level endurance where exercise against load is
required.23–27
The exercise protocol presented in this chapter is informed by research into the changes
in neuromuscular function that are induced by neck pain and injury, as well as research
which has informed the need for specificity of exercise to address each impaired function
(see Chapter 5). Muscle facilitation and training in the clinical setting is always
accompanied by a home program of exercises, which will change as the patient progresses
through the program. We will recommend certain exercises, but this is not to suggest that
they are the only exercises that can be used or necessarily the best exercise for a certain
patient. The final choice of an exercise is at the clinician’s discretion. What is necessary is
that the effect of any exercise is constantly monitored with a measure to ensure that the
desired effect on the related impairment is being achieved.

Exercise adherence
It does not matter how research informed and effective an exercise program is, it will not
be successful unless the patient complies with and adheres to the recommended program.
There is a growing body of research examining adherence because it is relevant for
successful management across a whole spectrum of health interventions.
Communication with a patient-centred style is valuable and can provide a motivational
basis to help the patient engage in appropriate self-management behaviours.28,29 The
clinician and patient need to work together to identify motivators or enablers as well as
barriers to exercise.30,31 A prime motivator for exercise is a decrease in neck pain. Every
opportunity should be undertaken during examination and treatment to link a proposed
exercise with pain relief, for example, how a change in spinal or scapular posture can
change neck pain and range of motion, or how facilitation of scapular or neck flexor
muscles can decrease palpable joint pain (see Chapters 9 and 14). Patients are growing
more cognizant of the need for evidence-based treatments. Thus it is relevant to both
demonstrate and discuss with them the evidence for the nature of neuromuscular
impairments that can be associated with neck pain, the fact that these impaired functions
do not automatically and consistently improve when the pain resolves and the need for
good muscle function towards preventing any recurring episodes of neck pain.
Other enablers can be as simple as adopting an established routine for exercise,
identifying and supplying equipment and intensive monitoring.31 A first criterion is that a
program is straight forward and manageable in current “time-limited” contemporary
lifestyles. Initially during the low-load movement control phase of training, we advocate a
routine of formal training for no longer than 5 to 10 minutes, twice per day (before starting
the day and after work or before retiring for the night). The formal exercises are
supplemented by functional exercises (e.g., correcting posture), which can be conducted
repeatedly during the day, without interrupting the patient’s daily activities, to gain the
necessary dosage of muscle activation or movement skill to achieve the desired change.
Small equipment such as sports tape to facilitate cervical segmental exercise (see Chapter
14), a laser and targets for position and movement sense training (see Chapter 16) and the
pressure biofeedback device for assessing and progressing deep cervical flexor training are
all very simple pieces of equipment which enable exercise and most importantly, provide
feedback on performance. It is vital to monitor progress, provide feedback on performance
and advance the exercise program to maintain a patient’s interest and adherence.
Any potential barriers to exercise need to be identified. Studies have recognized
barriers, such as pain with exercise and lack of motivation.30,31 It is counterproductive for
exercises to cause pain, especially in the motor-relearning phase. It has been shown
experimentally that nociceptive input modulates cortical neuroplasticity associated with
novel motor training and may impair the ability to learn a motor task.32 Motivation to
exercise can be promoted with links to the pain relieving effects of exercise. In addition,
motivation is enhanced with intensive monitoring of both the exercise and the gains made
by the patient.31 Measures of muscle impairment and changes in performance can be
constantly monitored both to motivate adherence and to progress the exercise program.
Effective long-term adherence is essential for good self-management.

The home program

A home program of exercises is a key element of rehabilitation and self-management
programs. The patient must actively contribute to its development to facilitate adherence.
Box 15.1 lists some pointers to consider when developing the home exercise program.
Adherence to the home exercise program is necessary for successful training and it should
be given due time for reassessment and development in each treatment session.

Box 15.1

Pointers for home exercise program development

 The program must be patient specific and tailored to the patient’s needs and not a
generic handout of exercises.
Establish patients’ preferences for recording the home program. For example, some
may prefer to receive written descriptions and illustrations of the exercises. Other
patients may prefer the clinician to video them performing the exercises on their
phones or tablets for home reference. Others may prefer a combination of
methods. Establish and act on patients’ preferences.
Assist the patient to identify suitable times for exercise that fit their lifestyle and
work—times for formal exercise and intermittent exercise during the day.
Ensure exercises are relevant and contained to a minimum. Balance the program,
too many exercises may be too time consuming, which might deter adherence,
too few exercises may be insufficient to be effective.
Ensure there is variety in exercises to capture and maintain interest.
Provide clear instruction on exercise dosage.
Establish progressive goals for training muscle groups and related outcome
measures on which to regularly monitor improvement.
Demonstrate the importance of the home exercise program by prioritizing its
review, rather than leaving it to the end of the treatment session. The latter can
give the patient the impression that it is of low priority in management.
Do not presume that the exercises are being performed correctly. Review exercises
in each treatment session to ensure that performance is correct. Correction is
required more often than not.
Ensure that as exercises are added in the progressive program, exercises that have
been superseded are removed.
When the program has progressed to strength training, it may be appropriate to
train strength on 3 days per week, refresh activation and patterning exercises on
the alternate 3 days, and have 1 day a week without formal exercises.

Neuromuscular training
Neuromuscular training consists of a program of exercise that usually commences with a
low-load exercise and posture training program and progressively adds movement
complexity and load to train:

▪ the activation and endurance capacity of the deep cervical postural

muscles (flexors and extensors) and axioscapular muscles.
▪ coordination between the deep and superficial layers of the neck muscles
and axioscapular muscles in movement and postural tasks of increasing
difficulty.
▪ muscle control within functional and work activities.
▪ muscle endurance at different contraction intensities.
▪ muscle strength tailored to the functional demands of the patient.
 Principles of motor relearning (segmentation, simplification, augmented feedback) are
followed especially in the early to intermediate phases of the program.33 Precision in
exercise is emphasized, and exercises are performed in a pain free manner and in the
initial phases, short of fatigue. Attention is given to use of correct movement patterns and
to the need for multiple repetitions in skill learning.
From the outset, it is important to ensure that improvements in muscle control from
specific training are translated to the patient’s specific functional or work activity to
address any provocative activity. It is ideal to observe the patient in their own work
environment, but when this is not possible, it is advantageous to mock-up or replicate their
pain provoking work, sporting or daily activity. Training control and muscle coordination
directly in the functional task is often necessary because it cannot be assumed that there
will always be an automatic translation from formal training to the function.34 It is also
important to review any gym or fitness program in which the patient is participating. The
patient must be given all encouragement to continue these programs, but exercises should
be reviewed to ensure that they are “neck safe” and “neck friendly”.
The precise training program for an individual patient is guided by and responsive to
the nature and extent of neuromuscular dysfunction documented in the physical
examination (see Chapter 9). In this chapter, a full training program is presented but all
exercises may not be necessary for all patients, and patients will progress through the
program at different rates. Precise exercise selection and progression, as indicated, is
based on the findings of the initial examination, continual monitoring of the patient’s
progress as well as knowledge concerning the patient’s functional demands and lifestyle.
Exercises for posture and the neck flexor, extensor and axioscapular muscles are
integrated from the first treatment as needed and continued as the patient achieves
progressive goals. Posture training is described first because it is an integral functional
exercise for training all muscle groups.

Posture training
Poor working postures or drifting into poor working postures has been implicated in neck
pain disorders of several occupations.24,35,36 Specific training of posture is indicated when
the patient interview and physical examination reveal that poor postural behaviours
contribute to the individual’s neck disorder. Correcting to the upright neutral posture
reduces passive, often end-range load on cervical structures, which can be pain relieving
in itself. “Postural correction” as an exercise is nevertheless prescribed for most patients
because it is a key functional exercise to repeatedly activate spinal postural muscles and
axioscapular muscles during the day as is required in the motor learning process.37
Assuming an upright posture will activate the deep cervical flexors,37 and further
activation can be achieved by adding a “neck lengthening” strategy to the postural
correction strategy.38 Repeated practice of the postural correction alone will improve
performance on the craniocervical flexion test,39 confirming it as an important exercise
strategy.
Postural training commences in the first treatment. As mentioned, it is an important
component of cervical and axioscapular muscle training because it provides the
opportunity for the multiple repetitions required in the motor learning process. It is a
functional exercise that can be included in a patient’s working day. Postural correction is
also beneficial as a preventative or pain-relieving strategy during the working day. These
aspects are discussed with the patient so that they understand the importance of the
exercise in their rehabilitation.

Spinal posture
Postural training is specific to the activity identified as problematic, and this is commonly
the sitting posture. The spinal regions are interdependent, and all regions are given
attention. Patients may sit in a good neutral lumbopelvic posture but often they sit in an
unacceptable extended or most commonly, a flexed lumbar posture. In this latter
circumstance, correction to a neutral lumbar lordosis is initiated from the lumbopelvic
region that facilitates lumbar multifidus activity.37,40 The thorax should move upwards and
forwards to position the shoulders over the hips. Thoracolumbar extension is undesirable
because it emphasizes activity in the thoracolumbar extensors rather than the lumbar
extensors.41 There are many ways to facilitate postural correction. One simple way, which
patients quickly learn, is to roll the pelvis to an upright position to form a normal lumbar
lordosis with faciliatory pressure on the L5 spinous process (Fig. 15.1). The patient is
taught self-facilitation by placing their own thumb on the L5 spinous process. They can
use this strategy until they gain an awareness of the position. The thoracic and cervical
postures often correct automatically with correction of the lumbopelvic position. If not,
the patient is encouraged to subtlety lift or depress the sternum to correct any residual
thoracic kyphosis or thoracic extension, respectively. On occasions, patients have
difficulty dissociating lumbopelvic movement from thoracolumbar extension. In these
cases, lumbopelvic movement may be more easily performed when the patient sits on the
edge of a raised treatment bed. Visual feedback from a photo on the patient’s mobile
phone or a set of mirrors may be helpful for patients who feel that the position is quite
foreign.
 FIG. 15.1 Facilitation of a neutral posture with a pressure stimulus on spinous
process of L5.

If the patient sits with an extended spinal posture, they first learn to relax into flexion.
The extended posture frequently includes extension from the lumbar to the thoracolumbar,
low thoracic regions. It is often necessary to first train proprioceptive awareness of
lumbopelvic movement, dissociated from thoracolumbar extension. For patients with a
very fixed pattern of extension, it may be necessary to practice lumbopelvic movement
with the thoracolumbar region set in a preflexed position in either a high-seated position
(Fig. 15.2) or in side lying. Once awareness is gained, the patient trains posture with an
unrestrained thoracolumbar region.
 FIG. 15.2 The patient preflexes the thoracolumbar region by placing the thumb on the
sternum and the little finger in the naval and drawing them together. Lumbopelvic
motion is practised in this position and once the patient learns the movement, it is
practised without the thoracolumbar restraint.

Scapular posture
Scapular posture is trained as indicated and directed by the response to scapular correction
in the physical examination. Active correction of scapular posture facilitates appropriate
muscle activity.42,43 Training usually commences in the first treatment session once the
patient has mastered correction of spinal posture with little effort and concentration. When
patients find correction of spinal posture takes much concentration, adding a second task
of scapular correction may be too challenging. In concentrating on the scapulae, they lose
the spinal position. In these cases, teaching scapular correction is undertaken in the second
session or subsequent sessions. When scapular posture is protective of neural tissue (an
elevated shoulder posture), treatment of neural tissue takes priority in management
because correction may be provocative.
As with spinal posture, instructions/methods for correcting an aberrant scapular posture
are many and the clinician should use the one that the patient finds easiest to implement.
The clinician may try to repeatedly manually position the patient’s scapula into a neutral
position to give the patient the sense of the corrected position so that they can develop
cognitive strategies to self-correct scapular posture. When patients find it difficult to
determine their own strategies, the clinician may provide them with one. One we find very
patient friendly is for them to visualize the correction from cues on the front of their chest.
The manual correction of scapular posture undertaken in the physical examination (see
Fig. 9.2C) informs the clinician on the movements required to correct scapular posture.
Patients are asked to imagine strips of elastic attached to the front of their chests. If the
scapula is in downward rotation and protraction, the elastic strip runs at 45 degrees from
mid sternum to the tip of the shoulder. The instruction to the patient is to lift up the tips of
the shoulders and spread the tips of the shoulders out to stretch the elastic. If the scapulae
are protracted, the elastic band runs across the chest horizontal to the floor. If the scapulae
are in anterior tilt, then the elastic bands run vertically (like a set of braces). Scapular
positions often contain elements of one or two directions. The clinician modifies the
angles of the imaginary elastic bands to suit the individual patient and observes, from
behind, how well the instructions correct scapular position. Some further modification of
the angles of the band/instructions may be required, but if the patient can achieve a
reasonable position, that is acceptable. Further refinement can be made in subsequent
sessions if required, but it is easy to frustrate the patient with too detailed a correction,
which can deter compliance. On occasions, taping may be used to facilitate the correct
posture.

Head and neck posture

The third element of posture correction is instructing the patient to gently lengthen the
back of their neck. This will automatically correct neck and head posture and no other
instruction is required. No mention is made of chin position. This is an important
component of the correction as it enhances activity of the deep cervical flexors and is an
important functional exercise for these muscles.38
Dosage for posture training: The patient is encouraged to gently hold the corrected
posture for 10 seconds and to practice the exercise, ideally, 3 to 4 times an hour. The
exercise is incorporated into activities in sitting, standing or walking. Appropriate muscle
activity can be augmented, (e.g., pressing the hands on the thighs or the elbows on the
arms of an office chair enhances the contraction of serratus anterior and the lower
trapezius).44 The postural correction exercise is a vital part of self-management. Although
we advocate that the exercise is performed 3 to 4 times per hour, patients in our study on
posture correction complied twice per hour for, on average, 8 hours per day. With this
dosage, they achieved a positive muscle training effect in the deep cervical flexors in 2
weeks.39 The patient needs to consider how to remember to undertake regular postural
correction. Some elect to have a sound reminder on their mobile phones or a pop up on
their computer at work. The clinician can send a strong message to the patient of the
importance of posture correction to neck health at the second treatment session, by
prioritizing enquiry of the reminders the patient has adopted for the posture exercise
before asking any other questions about their neck condition. Posture correction is a key
exercise in both management and maintenance programs.

Training the activation and endurance of the deep

cervical and axioscapular muscles
Cervical flexor training
Initial training is directed towards the deep cervical flexors, the longus capitis and longus
colli to improve the muscles’ activation and endurance capacity. Impairment in the deep
cervical flexors performance is characteristic of neck pain disorders (see Chapter 5) and
training commences in the first treatment session. There is one contraindication to the
training regime, i.e., when the upper cervical flexion neural provocation test is positive
(provokes neck pain or headache) (see Chapter 9). In these cases, training begins with
self-resisted isometric contractions against the fist positioned under the chin with a 10%
effort. Other circumstances such as high levels of pain or suspected cervical instability are
not contraindications. In relation to pain, deep cervical flexor training is a low-load
exercise performed in supine crook lying and is rarely pain provocative. When
ligamentous instability is suspected, training muscle control is indicated as a key
component of management.
The outcome measure to assess the effects of training is the craniocervical flexion test
(CCFT). The aim is for the patients to be able to perform 10, 10-second isometric holds on
the pressure level of 30 mmHg.

Training the craniocervical movement pattern

Findings in the physical examination will inform the initial approach to deep cervical
flexor training. If the patient was unable to perform appropriate craniocervical flexion and
used a retraction action or other substitution strategy (see Chapter 9), then training begins
by facilitating the correct pattern of motion. Attention is given to endurance, only when
the correct movement/muscle action is mastered. The movement of craniocervical flexion
is taught in supine crook lying with the craniocervical region positioned in a neutral
position (folded towels may be placed under the head if necessary, to achieve the neutral
position as done in the formal test). The simple instruction of “feel the back of your head
slide up the bed to nod your chin” facilitates the correct sagittal rotation action and the
patient receives feedback from the surface of the bed. A focus on the sliding sensation
negates a tendency to retract the chin. Movement is performed slowly, with control. As
large a range as possible from craniocervical extension to craniocervical flexion is used
because this makes it easier for the patient to feel and understand the correct movement.
Training the movement is augmented with eye movement to facilitate the craniocervical
flexors (eyes looking down) and craniocervical extensors (eyes up and back). The patient
can palpate the sternocleidomastoid and they practice through a full excursion of motion
without feeling sternocleidomastoid activity (Fig. 15.3). Practicing the movement, 10
repetitions, 2 to 3 times per day for a few days in a home program is usually sufficient to
learn the pattern and be able to progress to training deep cervical flexor endurance.
 FIG. 15.3 The patient trains the craniocervical flexion movement pattern through the
full excursion of the flexion, extension movement. They facilitate the flexors with eyes
looking down and monitor that the sternocleidomastoid and scalene muscles remain
relaxed.

Training the endurance of the deep cervical flexors

Training the low-level endurance of the longus capitis and colli commences when the
patient can perform the craniocervical flexion movement correctly. The pressure
biofeedback unit (Stabilizer, Chattanooga, USA) is used to teach the exercise and to
provide feedback on performance. It is very difficult without this feedback for the
clinician or patient to know if the deep cervical flexor contraction is being maintained.
Training is commenced at the pressure level, determined in the physical examination that
the patient was able to achieve with a good movement pattern and hold steady without
dominant use of the superficial flexor muscles. This is often at test levels 22 or 24 mmHg.
Again, the movement is facilitated by the feel of the back of the head sliding up the bed,
and the patient slowly nods to the target pressure level. They then hold the position using
the feedback from the dial to confirm performance. Failure is signalled when the needle on
the dial drops below the target pressure, or the patient has to constantly reposition to the
target pressure. The clinician monitors the head movement to ensure a correct movement
pattern.
The feedback assists the patient to learn the low-load, endurance exercise but they
typically train at home without the feedback. The reason is that many patients while
focussing on the dial, do not concentrate on performing the correct action and the pressure
is kept steady with an incorrect strategy. To prepare to train at home without feedback, the
patient practices first with the feedback and concentrates on the feeling to maintain the
position. They repeat the exercise with the feedback and then turn the dial away and
attempt to hold the position without feedback. Here, it is vital for the patient to be actively
looking down which is a facilitatory strategy for the deep cervical flexors (Fig. 15.4A and
B). The dial is turned back, and the patient checks their success or not. Once they can hold
the position, the patient then trains to locate the target without feedback, checking
accuracy with the feedback. The aim of the practice is that the patient can target the
training pressure and hold it steady without feedback for 10 seconds. Most patients will
learn the exercise with 5 to 10 minutes of unsupervised practice. However, this can be
challenging for a patient with poor neck proprioception and in that case, careful training
with the feedback may be necessary in the first instance. In home training, they aim to
replicate the feel of the contraction. It is helpful to include descriptors of what the patient
felt to achieve the task in the instructions for home exercise.

FIG. 15.4 Towards effective craniocervical flexor muscle endurance training at home,
(A) the patient practices first with the feedback, then (B) practices without feedback by
turning the dial away and then turns the dial back to check their performance with the
feedback.

Dosage: Home practice is encouraged at least twice daily, with a pattern of practice
being, for example, before arising in the morning and when retiring at night. The aim is
for patients to practice 10 repetitions of 10-second holds of the craniocervical flexion
exercise. On some occasions, training is commenced with a lesser dosage when the patient
fatigues or cannot retain a good pattern of craniocervical flexion for the 10 repetitions. On
return for follow-up treatment, the patient’s performance in the CCFT is retested. If
improvement is present, they then train with the assistance of the feedback to target the
next pressure level. This process continues until the patient can achieve 10 × 10-second
holds at the 30 mmHg level without effort. Most patients are capable of achieving this
goal.19 Of interest, a biproduct of this training is improvement in joint position sense,45
which probably results from the relocation practice inherent in the training protocol. The
time taken to reach the 30 mmHg target is variable but is usually achieved in 4 to 6
weeks.19 It depends on many variables including levels of pain and degree of presenting
impairment.46,47 Patients with very poor baseline movement and muscle activation often
require longer whereas others without complexities achieve the goal in a shorter time.
During this formal training period, other exercises are added to train the deep cervical
flexors (see later sections) at levels commensurate with their capacity.
Formal testing of the deep cervical flexors as well as monitoring and progressing
training with the pressure biofeedback unit promotes accuracy in performance and
prescription. Equally as important, the objective feedback is a powerful motivator for the
patient and assists in adherence to the exercise program.

Cervical extensor training

The initial training protocol for the suboccipital and neck extensor muscles replicates the
movements and tests used in the physical examination. The exercises can be performed in
the four-point kneeling position, a prone on elbows position or a forward reclined sitting
position as suitable for the individual patient. Care is taken with patient positioning in
relation to spinal and scapular postures. Ensure that the hips are positioned above the
knees and the lumbar lordosis, thoracic kyphosis and cervical lordosis are in neutral.
Muscles, such as serratus anterior and lower trapezius, may need to be facilitated so that
the patient holds a neutral position of the scapulae. All cervical extensor muscles work to
hold the weight of the head against gravity, but each exercise is designed to target muscle
groups.

Craniocervical extensors
The exercise targets rectus capitis major and minor in a craniocervical extension and
flexion (head nodding) exercise while maintaining the cervical spine in its neutral
position. This action is usually instantly learnt by the patient as the familiar action of
saying yes. These muscles have key proprioceptive functions as well as controlling
movement of the upper cervical joints.

Craniocervical rotators
The exercise targets the obliquus capitis superior and inferior muscles while the cervical
spine is maintained in the neutral position. Best instructions are to gently shake the head
as if saying no. The range should be less than 40 degrees to each side to focus on C1–2
rotation. Manual facilitation is provided for those patients identified in the physical
examination to have difficulty in localizing C1–2 rotation (Fig. 15.5). A facilitatory
strategy for home use is to have the patient fix their gaze on a spot between their hands
and rotate their head as if saying ‘no’ while maintaining their fixed gaze. This technique is
not suitable for patients who have impaired gaze stability (see Chapter 16). An alternate
cue is for the patient to imagine drawing a straight line between the hands with their nose.
 FIG. 15.5 C1–2 rotation can be facilitated by stabilizing C2 and guiding the “spin” of
the head to target activity of the obliquus capitis superior and inferior.

Deep cervical extensors

The exercise targets the deep cervical extensors, the semispinalis cervicis and multifidus
by mechanically disadvantaging the more powerful torque producing extensors of the head
and neck (e.g., splenius and semispinalis capitis) by keeping the craniocervical region in a
neutral position during the extension movement.48 Even at this early stage of the exercise,
the deeper extensor muscles work in coactivation with the deep cervical flexor muscles
that control the craniocervical neutral position. The exercise is performed as per the test. A
pen is placed between the wrists (four-point kneeling) or between the elbows (prone on
elbows or inclined sitting) and the patient curls their neck down to look at their
knees/chest and then curls their neck back as far as possible but keeping their gaze fixed
on the pen. If patients are having difficulty performing the correct movement, the clinician
can guide the movement in the learning process by facilitating the movement through C2
and encouraging a craniocervical neutral position with a hand on the head (Fig. 15.6). In
addition, a more segment-specific contraction of the deep extensors, relative to the
splenius capitis is gained with localized resistance over the vertebral arch (Fig. 15.7).49,50
 FIG. 15.6 Facilitation of cervical extension. The clinician grips C2 and controls a
craniocervical neutral position with the hand on the head. The clinician can pattern the
movement with the patient in an assisted active movement.

FIG. 15.7 Manual resistance applied over the lamina of the cephalad vertebra (e.g.,
C4) can enhance the activation of the deep neck extensors (semispinalis cervicis)
relative to the superficial extensors (splenius capitis) at the caudal level (i.e., C5).

Dosage: Exercises to train all three muscle groups are performed to the patient’s
capability because correct movement and muscle use are key considerations. For example,
if the patient can only perform cervical extension from the flexed position back to the
neutral position, this range is practiced initially. With training, the range will improve, and
the patient concentrates on the quality of the movement until they can achieve the normal
excursion of approximately 20 to 30 degrees while maintaining the craniocervical region
in neutral. Training of C1–2 rotation may begin with excursions of 10 degrees to each
side. The aim is for local movement of C1–2 and facilitation of the obliquus capitis
superior and inferior. Range will increase with practice as patients gain more
proprioceptive awareness of the movement.
Craniocervical and cervical extensor muscle training is added to the home exercise
program. Initial dosage for training may be three sets of five repetitions of each of
craniocervical extension, rotation and cervical extension, with a rest between each set.
This can be progressed by improving range of movement within the exercises and adding
repetitions until the patient can comfortably perform three sets of 10 repetitions through
full excursions of movement.

Scapular muscle training

The capacity of the axioscapular muscles (particularly the three parts of trapezius and
serratus anterior) is trained to sustain correct postural alignment. Specific scapular
postural correction strategies, as well as exercise to improve scapular motion control in
specific directions, are trained progressively as required by the individual patient. Many
different exercises can be used,51 and some examples are provided.
When weakness and fatigability of the upper trapezius52 has been found in the physical
examination, often in association with a downwardly rotated scapular posture, initial
emphasis is placed on the specific action of upper trapezius. The patient is taught to
upwardly rotate their scapula by visualizing the upward movement of the distal end of the
clavicle, i.e., a controlled shrugging (Fig. 15.8). This action also relaxes the levator
scapulae which downwardly rotates the scapula. The exercise is performed in sitting or
standing and the clinician may manually facilitate the upward rotation initially. The
exercise is initially performed without load and then progressed as able, against resistance
with hand weights. In some patients, better activation of the upper trapezius may be
achieved by performing the shrug exercise with the arms abducted to at least 30 degrees
(Fig. 15.9).53
 FIG. 15.8 Facilitation of upper trapezius. The patient upwardly rotates their scapula
by visualizing the upward movement of the distal end of the clavicle to ensure a correct
action.

FIG. 15.9 The upward rotation shrug exercise for upper trapezius. The arms are
abducted to approximately 30 degrees to pre-position the scapula in upward rotation
before commencing the exercise against load.

Dosage: Upper trapezius is trained, as an example, by performing three sets of 10

repetitions of scapular upward rotation with the emphasis placed on scapular control. The
exercise is progressed with increasing arm load. Again, the dosage and progressions will
depend on the patient’s ability to perform the exercise with precision.
For a particular focus on lower trapezius, training may be commenced in side lying with
the arm elevated to approximately 140 degrees. This position deters use of latissimus dorsi
and pre-sets the scapula in some upward rotation. The exercise is easy to perform at home
using pillows to support arm weight. The cues for the patient are to lengthen their arm by
drawing the scapula upward and forward in line with their arm and actively hold and
concentrate on the forward action (upper trapezius and serratus anterior). The patient then
shortens their arm by drawing the scapula across and down their chest wall and again
holds the position (lower trapezius) (Fig. 15.10). The clinician can manually facilitate the
scapular movement to enhance learning. The angle of the arm can be varied to better target
the middle portion of the trapezius when required.

FIG. 15.10 The patient trains the endurance of the scapular muscles in side lying.
The arm is positioned in approximately 140 degrees and supported on pillows.
Serratus anterior is facilitated by an arm lengthening manoeuvre to draw the scapula
forwards and upwards. Lower trapezius is facilitated by shortening the arm by drawing
the scapula across and downwards on the chest wall.

Dosage: In the home program, the patient practices, for example, 10 × 10-second holds
in this formal exercise. This muscle training is reinforced with frequent activation of the
scapular supporting muscles in the posture training exercise which is undertaken
frequently during the day.

Training muscle control and coordination in

movement and postural tasks
The training program is progressed as the targets for training the activation and endurance
capacity of the deep cervical flexors, extensor and axioscapular muscles are met.

Training the cervical flexor and extensor muscles

Training coactivation
The deep cervical flexor and extensor muscles are described as a deep muscle sleeve
which supports the cervical segments.54 Functionally, these muscles coactivate during neck
movements.55 Once the activation of the deep flexor and extensor muscles has been
trained, this functional coactivation is trained with self-resisted alternating isometric
exercises. The exercise is performed sitting, with the posture corrected and the back of the
neck ‘lengthened’ to prefacilitate the deep cervical flexors. Gentle resistance is applied by
the palm of the patient’s hands in an axial rotation direction, alternately to the left and
right. The muscles are facilitated by the patient looking toward their hand before
resistance being applied. Resistance should match about a 10% effort so that the focus
remains on the deeper muscles. Holds for a few seconds can be performed, and this is a
portable exercise that the patient can practice at convenient times during the day.

Training control and coordination between deep and superficial

neck flexors
Cervical extension in the upright position is a common functional movement requiring
both eccentric and concentric control and coordination between deep and superficial neck
flexors. It is a movement commonly reported functionally as provocative of symptoms.
Coordinated control and sufficient strength and endurance of the deep and superficial
flexors are required to sustain the extension position in various functional tasks.
Control of the movement into extension is trained in the first instance within the
capacity of particularly, the deep cervical flexors. The movement is initiated by
craniocervical extension with the patient looking to the ceiling behind the head. The return
to neutral is initiated by craniocervical flexion. The patient only extends to a range that is
pain free and that they can control. The key feature of the exercise is the eccentric and
concentric work of the deep cervical flexors in coordination with the sternocleidomastoid
and anterior scalene muscles. Both clinician and patient should monitor the smooth
movement into extension and the ability to return to neutral initiating with craniocervical
flexion. A deficit in either component indicates that the deep cervical flexors are loaded
beyond their capacity. Extension is practised in a range that the deep cervical flexors can
control. The range to which the head is moved into extension is gradually increased as
control is improved and any pain permits.
The second stage of the exercise adds isometric holds in positions through range, which
begins the strength and endurance training of the cervical flexor synergy. The patient
extends the head and neck to a predetermined position in range that is able to be controlled
and is pain free. The clinician supports the head in this position and the patient relaxes.
The holding contraction is initiated by looking down together with a slight craniocervical
flexion action. Controlling this position, the patient then initiates a head lift, just taking the
weight of the head off the clinician’s hand (Fig. 15.11). For home practice, the support of
the clinician’s hand is replaced by that of the patient.
 FIG. 15.11 Training the endurance of the craniocervical and cervical flexors against
the load of gravity and head weight is interposed with training control in the movement
pattern of extension. Control of chin position is monitored. If the chin extends, it signals
that the load has exceeded the capacity of the deep cervical flexors.

Dosage: In the second stage of training, the aim is to hold the position for up to 5
seconds before curling the neck back up to the neutral upright position. In practice,
building up to five repetitions of 5 second holds is often a sufficient dose for most
patients, although others may require higher dosages depending on functional
requirements. The exercise is progressed by progressively increasing the range of
extension in which the exercise is performed.

Training scapular control with arm movement and

light load
As soon as the patient masters correction of scapular posture, training is progressed to
challenge this control with arm movement and then load. Such exercises are very relevant
for patients reporting aggravating activities such as keyboard or mouse use, bench top
light processing work, similar household activities or lifting and carrying. Arm activities
require a stable base of support. Emphasis is placed on maintaining a correct scapular
position while performing either open or closed chain upper limb exercises at a load that
the patient can control. Training may commence with free arm movements (e.g., shoulder
flexion, abduction [to approximately 40–60 degrees] and internal/external rotation) and
then against resistive straps such as Theraband (Pro-Med Products Inc) or light-hand
weights in line with the patient’s functional needs. Once this is achieved, the axioscapular
muscles’ control can be challenged with the addition of more rapid arm movement. In
addition, closed chain exercises can be performed in sitting with a corrected scapular
position using hand resistance against the thigh or the edge of the desk to particularly
facilitate serratus anterior in patients with scapular winging.
Scapular control often needs to be trained through full arm elevation with the focus on
the timing and quality of scapular movement.51 Patients with both idiopathic neck pain and
whiplash-associated disorders may have delayed onset of serratus anterior during arm
elevation and reduced duration of serratus muscle activity in arm elevation and lowering.56
Correcting spinal posture first has been shown to enhance the effect on serratus anterior
activity compared with exercising with a forward head posture.57
Training often needs to be progressed for serratus anterior and the tripartite trapezius
muscle for patients where winging of the scapula is an issue. The push up and push up
plus exercises are efficient exercises for this purpose.44,58 Training can be commenced by
performing the push up against the wall, and once there is good control under these lighter
load conditions, the starting position can be progressed to a four-point kneeling position.
The patient concentrates on pushing through the arms to raise the chest rather than use the
common substitution strategy of thoracic flexion. Training can be made efficient, by
combining this exercise with training for the neck extensor muscles.

Training muscle endurance and strength

As patients gain muscle control and coordination, the deficits in neck flexor and extensor
strength and endurance are addressed by progressive resistance training. Progression to
higher-load exercise is important to address the cervical muscle atrophy that may present
in patients with idiopathic neck pain or whiplash59 to promote hypertrophy.60 Muscle
endurance is trained at low-contraction, moderate-contraction and higher-contraction
intensities61 and deficits in strength are trained to meet the patient’s functional demands.

Neck flexors
Progression to higher load strength and endurance training incorporates the action of both
the deep and superficial flexors. The focus remains on performing controlled movement.
In all exercises, craniocervical flexion is monitored to ensure that the load is within the
capacity of the deep cervical flexors. A drift of the chin into extension indicates their
capacity has been exceeded and load should be reduced.
The neck flexors can be progressively challenged with antigravity head lifts by
gradually increasing the effect of gravity. Exercises can begin as head lifts off the wall
from a sitting position with the back supported at an angle such that the patient can
perform the exercise painlessly (Fig. 15.12). The exercise is initiated by looking down,
followed by craniocervical flexion and the chin position is controlled throughout the
exercise. Exercise dosage initially is usually 5-second holds × 5 repetitions, increasing to
10 repetitions or greater. The exercise is progressed by increasing the effect of gravity by
progressively moving the chair away from the wall to the extent of approximately 25 cm
from the wall. After this point, the exercise progresses to head lifts in supine from two to
three pillows using the same technique as followed in the wall exercises and building up to
10 repetitions of 5-second holds. For many patients, progression to head lifts from one
pillow is sufficient. These exercises are readily translated to a home program. Some
patients will require further training to meet the strength demands of their sport or
occupation, and in these circumstances, resistance can be increased with the use of pulleys
and weights. Alternately, a variety of equipment can be used to assist strength training
including pulleys, weights and dynamometers.62–64

FIG. 15.12 Cervical flexor endurance and strength training begins with head lifts from
the wall. The patient performs the familiar action of sliding the back of the head up the
wall to preflex the craniocervical spine, and holding that position, just takes the weight
of the head off the wall. Concentration is on keeping the chin flexed position.

Neck extensors
Exercise for the cervical extensors is progressed to isotonic strength training. Training is
conducted with the two patterns of extension, (1) with the craniocervical region in neutral
to emphasize the deeper cervical extensors and (2) allowing the movement to proceed with
craniocervical extension, which will permit a full contribution from the superficial
extensors.
Exercises can be performed in prone lying,65 four-point kneeling, sitting or standing
using weights, Theratube or a pulley system to provide resistance (Fig. 15.13).62,64
Exercises are tailored to the patient’s functional demands. For example, if the patient’s
neck pain is related to poor extensor endurance in flexion, the exercises can be undertaken
in the functional ranges of concern as well as the upright posture. The emphasis is on
endurance, and dosage is advanced proportionally more by time rather than load.
Nevertheless, for most patients, exercise should also incorporate strength parameters
(higher load and less repetitions) to address known strength deficits and muscle atrophy.59
Maintaining a neutral craniocervical position when performing any extension exercise in
prone will continue to bias the deep cervical extensors.48 Likewise, it has been shown that
when resisting an isometric flexion force in sitting with the head in a neutral posture, a
vertical resistance or a pulley angle declined 15 degrees from the horizontal, results in
higher activity in the deep extensors relative to the superficial flexors.64 As with the neck
flexors, extensor training must be designed to meet the strength demands of the patient’s
sport or occupation.

FIG. 15.13 Neck extensor strength training. Many forms of resistance can be used
including weights, Theratube or a pulley system attached to a head harness.

Dosage: Progressive resistance exercise for the neck follows guidelines for facilitating
changes in muscle endurance, strength and hypertrophy.66,67 When progressing flexor and
extensor strength and endurance training, attention is given to the relative exercise load of
these muscle groups. In healthy individuals, the cervical extensors are approximately 1.75
times stronger than the cervical flexors.68 The extensors have at least twice the capacity for
endurance compared with the flexor muscles under the same relative load (sustained
contractions at 50% of maximal strength).69 These factors should be considered in exercise
prescription. As an example, endurance exercises for the extensors may need to be
sustained for longer or more repetitions performed compared with endurance training for
the flexors, particularly in the later stages of the exercise program.

Training scapular muscle endurance and strength

Training scapular muscle strength, endurance and patterns of movement are indicated
when the examination reveals that poor scapular posture and muscle control are
contributing to the neck pain disorder. This often occurs when patients report activities
with their arms as ones provoking their neck pain (e.g., lifting, carrying).70–72 The
axioscapular muscles can be challenged with progressive resistance from pulleys,
Theraband62 or hand weights or by progressing exercises such as the push up plus on
unstable surfaces.73

Dosage and intervention timelines

There are several issues which influence the design and duration of an exercise program
making it difficult to answer the frequent question: “How long must I do the exercises
for?” For instance, there is wide variation in deep cervical flexor activation capacity
between patients.46,47 It is most probable that patients with very poor activation will require
a longer time for rehabilitation of deep cervical flexor function than those presenting with
fair activation. Furthermore, a certain dose of exercise may address one impairment but
not another. Our study of patients with mechanical neck pain revealed that after training
the deep cervical flexors for a designated 6 weeks, performance in the CCFT improved to
reflect a normal pattern of behaviour between the deep and superficial flexors.26 However
this training dosage failed to fully resolve the delay in onset of the deep cervical flexors in
response to a rapid arm movement. Unpublished pilot data suggests that it might be
possible to resolve the delay, but it could take up to 12 to 16 weeks of training. Time for
strength training is variable, and time for change can range from 6 up to 20 weeks
depending on the age of the patient, the intensity of training and goals. Thus giving
definitive training time periods for individual patients is difficult, although approximate
periods could be estimated.
Throughout the intervention period, the patient and clinician work towards effective
self-management. There are often economic pressures to curb the number of sessions with
the clinician and therefore costs of treatment. As indicated, time is needed to complete the
exercise program and patients will undertake many of the exercises within a self-
management exercise program, especially once symptoms have eased. Nevertheless,
patients should be checked (e.g., once per month) to progress exercise and to maintain
motivation, which is enhanced when the program is monitored.31 Evidence from a meta-
analysis investigating exercise adherence supports this practice with evidence that booster
sessions with a physiotherapist assisted people, albeit with hip/knee osteoarthritis, to better
adhere to exercise.74 Follow-up does not always have to be in person. The advent of
telepractice provides an alternate, convenient and inexpensive way to support
adherence.75,76 Many people have access to devices and programs that permit free video
calls. Effectiveness of self-management is enhanced when patients have access to, and
regular, support.

Maintenance program
Neck pain is a recurrent disorder17 and recovery from an acute episode is frequently
incomplete.15,16 It is pertinent to think about the potential effect of subclinical pathology
and the effect of arthrogenous muscle inhibition on muscle function following the
rehabilitation period.20,77–79 Our study of the effects of different training modes on various
measures of craniocervical flexor performance illustrate the reason for concern.63 The 10-
week follow-up of a motor relearning program showed “normalized” performance in the
CCFT. Yet by the 6 month follow-up, the performance had deteriorated, i.e.,
sternocleidomastoid activity was increasing again in the CCFT indicating a decline in
function of the deep cervical flexors80 (Fig. 15.14). An interesting observation was that the
gains in craniocervical flexor strength and endurance with an endurance training program
(training at 20% and 50% of maximum voluntary capacity) were maintained at the 6-
month follow-up.63 This is one study, but it does illustrate the vulnerability of the
neuromuscular system in neck pain disorders and, particularly, the postural supporting
muscles.

FIG. 15.14 Sternocleidomastoid (SCM) activity at each stage of the craniocervical

flexion test (A) Following a 10-week motor learning program, SCM activity decreased
significantly in all stages of the test indicating improved performance in the deep
cervical flexors after training.80 (B) Follow-up at 6 months (dotted line) indicated a
regression in muscle performance as in evidence with the increased SCM activity
across the craniocervical flexion test stages. (Modified from O’Leary S, Jull G, Kim M, et al.
Training mode-dependent changes in motor performance in neck pain. Arch Phys Med Rehabil
2012;93:1225–1233.)

The need for a maintenance program is clearly supported by factors as the recurrent
nature of neck pain, the presence of subclinical pathology, the effect of arthrogenous
muscle inhibition and the quite rapid deterioration of muscle performance following
cessation of training. The maintenance program is a long-term commitment. Only a very
small percentage of people are likely to commit in the long term, to a 30-minute program
of neck exercises 3 or 4 times a week. Thus a maintenance program must be realistic and
contain exercises with a high possibility of adherence. They should be easy to do,
convenient and not disruptive to work or lifestyle. The aim is for the patient to develop
“preventative habits” for their neck akin to other personal hygiene habits, the best example
being the lifetime preventative habit of cleaning the teeth.
At present, there is no research informed maintenance program for the neck, and if
patients search the internet for exercises, they commonly encounter advice for range of
movement exercises. However, these exercises alone do little to improve muscle
function.63 The following suggestion for developing a long-term preventative habit to
maintain muscle function has no evidence base although it does have a research-informed
rationale. The key exercises are the postural correction exercise and a mobilising exercise.
The evidence to support the suggestion of a postural correction exercise is as follows.

▪ Assuming an upright neutral lumbopelvic position facilitates lumbar

multifidus and the deep cervical flexors (longus capitis and colli).24
▪ Elongating the back of the neck facilitates longus colli,38 and there is
evidence that correction of spinal and neck posture will effectively
exercise the deep cervical flexors.39
▪ Correcting scapular posture facilitates the scapular supporting
muscles.42,43 The active correction can decrease any neck tenderness via
reciprocal relaxation of muscles as levator scapulae and the neck
extensors.9
▪ When the exercise is performed sitting in an office chair with arms,
further facilitation of serratus anterior and lower trapezius is gained by
gently pushing down on the arms of the chair through the forearms.44

Thus the postural correction exercise can help maintain the activation and low-load
endurance capacity of the deep neck and scapular postural supporting muscles. It brings
the spine into a neutral position, which will take end-range loading strains off the joints.
Based on our trial, sufficient exercise dosage could be holding posture correction for 10
seconds twice per hour for at least 8 hours of a day.39
The mobilizing exercise for the maintenance regime is the archery exercise (see Fig.
14.4C). This exercise promotes a rotation mobilization thoughout the functional cervical
spine C0–1 to upper/mid thoracic region. It is an easy and portable exercise that can be
performed at any convenient time of the day.
Future research is needed to judge whether the combination of regular performance of
the postural correction and the rotation mobility exercise are an effective maintenance
program and can lessen the frequency, intensity and duration of episodes of neck pain.
However, there is some confidence in the rationale for this simple “neck-health” program.

Relapse prevention
The chance that patients will have another episode of neck pain is relatively high based on
current evidence. Thus good advice to the patient is to self-check their ability to perform
key exercises. This could be a monthly routine, and if loss of performance is found, the
patient should have exercises to recommence to help prevent another episode of pain.
Another key part of the development of the self-management program is a discussion with
the patient on what measures they can take if their neck becomes painful or they feel that
another episode of neck pain is pending. The relapse prevention program should be based
on the key features of the individual’s neck pain and how they have responded to various
interventions. For example, advice may be to recommence a self-sustained natural
apophysial glide (SNAG) or mobilization with movement for the painful joint.81 Home
applied heat or ice or, if necessary, simple analgesics may also be useful to help settle
pain, rather than the patient resorting to NSAIDs with their inherent side effects. The
muscles will react to the pain and a list of the appropriate exercise strategies to ensure
adequate muscle control are an important component of a relapse prevention program.
Patients may need to return to low-load exercises if in pain and then progress to their
former exercise status. The strategy developed should be patient specific with the patient
feeling confident in their ability to implement the self-management program. They can be
advised to contact their health care practitioner if they are unable to successfully self-
manage.

Conclusion
Research has provided evidence that neuromuscular adaptations are a common and
expected reaction to neck pain and injury. Changes occur in motor output, muscle
behaviour and muscle properties. The evidence also points to the need for assessment-
driven targeted exercises for people with neck pain if neuromuscular function is to be
improved. Relief of pain does not guarantee that the many aspects of neuromuscular
function will return to their preinjury status. Neck pain is frequently characterized by
recurrent episodes over many years. Training the neuromuscular system is vital to not only
restore muscle function in respect of the current episode of pain but as a protection against
future episodes of pain. In this respect, maintenance programs are an important element of
self-management.

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16

Management of Sensorimotor Control

Disturbances
Management of disturbances in proprioception, eye movement control, coordination and
postural stability have not been studied as extensively as the management of other cervical
musculoskeletal impairments. However, evidence is growing for the efficacy of specific
rehabilitation strategies to positively influence altered sensorimotor control and
cervicogenic dizziness. Strategies include treatments directed locally to the neck muscles
and joints as well as exercises to integrate the visual, vestibular and cervical sensorimotor
control systems. The close connections between these systems and the adaptations that
occur in the sensorimotor control system warrants problem orientated, tailored,
multimodal management that addresses both the primary cervical musculoskeletal causes
as well as any secondary adaptive sensorimotor control changes.

Approaches to management
Addressing the cervical musculoskeletal pain and
dysfunction
Several different treatments for neck pain and cervical musculoskeletal dysfunction have
improved dizziness and sensorimotor control. More specifically, dizziness has improved
with the use of manual therapy for cervical joint dysfunction,1–4 specific neck muscle
training,5 acupuncture,1 and multimodal treatment (manual therapy, electrotherapy and
muscle relaxation exercises).6 Cervical joint position sense (JPS) has improved following
manual therapy,1–4 craniocervical flexion training,7 and acupuncture.1 Likewise balance
has shown some improvement following cervical extensor muscle endurance training8 and
acupuncture.9
Studies are beginning to provide evidence of long-term benefits for patients with
chronic cervicogenic dizziness from treatments of cervical musculoskeletal dysfunction.
(10,11)
Malmstrom et al.11 showed that multimodal cervical musculoskeletal treatment
reduced neck pain and dizziness in the long term. Reid et al.10–12 demonstrated the
effectiveness of short periods of manipulative therapy to reduce dizziness (both sustained
natural apophysial glides [Fig. 16.1] and posteroanterior glides) over four to six
treatments. Both methods of manual therapy had immediate and sustained (up to 2 years)
effects and reduced the intensity and frequency of chronic cervicogenic dizziness.
 FIG. 16.1 Sustained natural apophysial glides used in the management of
cervicogenic dizziness when the patient reports dizziness on cervical extension.

Treating cervical musculoskeletal pain and dysfunction will improve the symptoms of
cervicogenic dizziness, but treatments must also be directed towards the sensorimotor
impairments to enhance treatment outcomes. Reid et al.3,10 found that although manual
therapy improved dizziness, objective changes in sensorimotor control (joint position error
and balance) in these patients were minimal. Similarly, specific neck muscle exercises
improved dizziness in some patients with whiplash-associated disorders (WAD), but many
others continued to report dizziness and still had signs of impaired sensorimotor function
after the intervention.5 Thus the aims of specific training are to improve not only the
symptoms but also the sensorimotor impairments, to normalize the system with the aim of
preventing recurrence and optimizing function.

Addressing the adaptive changes in the sensorimotor

control system
Specific training to improve disturbances in sensorimotor control should address the
adaptive changes in the sensorimotor control system that occur with altered cervical
afferent input. Specific training of sensorimotor impairments has been investigated and
there is evidence of wider effects of training. For instance, training gaze stability, eye-head
coordination and head on trunk relocation can improve both sensorimotor impairments
and patients’ neck pain and disability without any treatment of local cervical
musculoskeletal dysfunction.13–16 Revel and colleagues,13 with an 8-week training program
consisting of gaze stability exercises, eye head coordination and head on trunk relocation
practice, improved neck pain and disability as well as cervical joint position error (JPE).
Similar outcomes were described by Jull et al.7 and Humphreys et al.14 for multimodal
sensorimotor programmes. Balance has improved with a program of oculomotor
rehabilitation.16 In turn, balance training has improved JPE17 and JPE training has
improved cervical flexor neuromuscular control.18,19 Cervical movement sense/accuracy
has been improved with cervical kinematic training using either a virtual reality
environment or a laser on a target20,21. In other examples, Heikkila and Astrom22 tested a
multimodal approach (body awareness training, a behaviour therapy–based exercise
approach and multiprofessional advice and education) and demonstrated improvements in
JPE. Moreover, Hansson and colleagues23 used a vestibular rehabilitation program for
patients with chronic WAD and demonstrated improved balance and reduced dizziness.
Vestibular rehabilitation programmes may also be useful for persons with concussion.24,25
Of note, although vestibular training improved dizziness and balance, it did not improve
neck pain or movement in a cohort of patients with chronic WAD.26
Despite these examples of cross-over effects of training, there is little direct correlation
between the various sensorimotor measures, i.e., proprioception, eye movement control
and balance.27,28 This suggests that exercises used to treat eye movement control for
instance, may not be the most effective for balance or JPS deficits. Thus even though there
might be some cross over in training effects, the preferred approach is to prescribe
exercises for each deficit found in the evaluation of cervical joint position and movement
sense, oculomotor function, co-ordination and static and dynamic balance. The exercise
program is individualized and responds to each specific deficit identified in the physical
examination. We regard this as the best clinical approach.29–31 A clinical trial is currently
underway to confirm whether this specificity is always justified in sensorimotor
programs.32

Combining cervical musculoskeletal and

sensorimotor approaches
Patients with neck pain and symptoms of dizziness have impaired musculoskeletal and
sensorimotor function. Not surprisingly, several studies have combined management of
the cervical musculoskeletal and sensorimotor systems.1,33,34 The success of combining
cervical musculoskeletal and vestibular interventions was apparent in the management of
young adults with persistent neck pain, dizziness and headaches following concussion.
The combined treatment approach resulted in improved times to return to sport35 and
stimulated recommendations for its adoption for patients with neck trauma and
concussion.36–38
A combined approach is supported for the management of patients with cervicogenic
dizziness and visual disturbances. It is logical that attention is paid directly to any
impaired proprioception, eye movement control, coordination or postural stability as well
as to the source of the altered cervical somatosensory input (e.g., impaired muscle
function, painful restricted joint motion). A multimodal program might include education,
assurance to assist any anxiety, manipulative therapy and active exercise, specific muscle
rehabilitation as well as a tailored program to train as indicated, cervical joint position and
movement sense, oculomotor control, coordination and balance. The program recognizes
the associations between the cervical somatosensory, vestibular and ocular systems and
addresses all potential causes of altered cervical somatosensory input.

Principles for tailored sensorimotor control exercises

Sensorimotor changes occur early after the onset of neck pain39–41 and thus exercises
should be commenced as soon as possible. A progressive program is devised based on
specific impairments identified in the examination. The level of difficulty of initial
exercises will depend on the presenting symptoms, their degree of severity as well as the
level of impairment. The program is progressed to the functional requirements of the
patient.
The home program is vital as repetition is required to achieve improvements. Exercises
for each impairment should be performed in short sessions (e.g., 30 seconds or 5–10
repetitions as fits the exercise), 2 to 5 times per day depending on severity and irritability
of the patient’s symptoms. Temporary reproduction of mild to moderate dizziness or visual
disturbances is acceptable however exacerbation of nausea, neck pain or headache is not.
If the latter occurs, the exercises can be modified by decreasing the number of repetitions,
range of motion or altering the patient’s position to a more supported one such as supine
lying.
Starting levels for the exercises are adjusted to suit the individual patient, their
presenting symptoms and the degree of impairment demonstrated in the physical
examination. Subsequent progression of each exercise set is directed by constant
reassessment of performance. Exercises are progressed by altering the duration,
repetitions, frequency and the degree of difficulty of the task. Degrees of difficulty can be
increased by altering the speed and range of head movement, the amount of visual
feedback (eyes open, restricted peripheral vision or eyes closed) and the visual focus point
(single point compared with a word or group of words), background (plain, striped or
checkered), position of the patient (supine, sitting, standing) and condition. Exercises can
also be progressed by combining activities. For example, oculomotor tasks, cervical
movement or position sense practice can be undertaken with a balance task, for example,
while sitting on an unstable surface such as a therapy ball or standing with an unstable
base of support (e.g., tandem or single leg stance).
All exercises should be performed at a speed, movement range and starting position that
allows the patient to perform the task with precision and without exacerbating pain or
headache. Larger ranges of motion at slower speeds will bias the cervical afferents and
should be conducted first. Faster smaller ranges will challenge the vestibular system and
can be used as a progression when indicated.

Exercises to train sensorimotor control

A variety of exercise strategies are used to train the various aspects of sensorimotor
control assessed to be impaired in the particular patient. Patients must be carefully
instructed in the exercises. As indicated, short sessions of training are used, and the patient
must be provided with a clear self-management program to be performed at home.
Regular review is important to progress the exercise program. How quickly a patient
progresses and how quickly symptoms resolve is a very individual characteristic.

Training cervical joint position sense

The test of relocation to the natural head posture used in assessment of cervical JPS
converts to a training method. A target is printed on A4 size paper to the dimensions
calculated by Roren et al.42 and provides feedback to the patient on performance—the
inner three circles reflect a good performance (0–3 degrees of error) the next circle a fair
performance (3–4.5 degrees of error) and the outer circle and beyond an abnormal
performance greater than 4.5 degrees of error is used (see Fig. 9.19). The patient sits
90 cm from the wall wearing a laser mounted on a headband. The target is placed on a
wall so that the laser projects into the centre of the target. The patient practices the
relocation task in directions assessed to be abnormal (> 4.5° relocation error). This may be
any or all of flexion, extension, right and left rotation directions depending on the
assessment findings. The patient concentrates on the starting position, closes their eyes
and moves in the direction to be trained. They return to the neutral position as accurately
as possible, then open their eyes to check their performance, using the feedback from the
laser beam on the target. The patient readjusts their head back to the neutral position as
required before practising the task again. Some patients find this task very difficult and, in
those cases, patients can perform the movement initially with the eyes open to gain
constant feedback from the laser. When ready, they again attempt the task with the eyes
closed. The position sense task can be progressed by the patient attempting to find
different points in range, for example, at 20° intervals throughout the available range of
movement with their closed eyes, again checking and correcting performance with eyes
open at each interval. Further progressions can include performing the tasks in standing
and then with decreasing bases of support.
For most effective training of JPS, the patient is provided with a laser and a printed
target for home use. Commercial head mounted lasers or simple inexpensive homemade
head mounted lasers (plastic head band, key chain laser and self-adhesive cord clip to
maintain the “on” button of the laser) and targets are given or loaned to the patient. The
accurate feedback not only helps to enhance performance, but it provides the patient with
a powerful incentive to perform the exercise and improve adherence.

Retraining cervical movement sense

Movement sense is trained using the head mounted laser to project on to targets consisting
of patterns of various difficulty. Patients again sit 90 cm from the wall. They perform fine
head movements to trace lines and patterns with the laser as accurately as possible
concentrating on accuracy rather than speed. Again, the level chosen to start training will
depend on the findings in the assessment of cervical movement sense. The easiest level of
training is tracing simple, short straight lines, progressing to larger ranges of movement
and patterns. The task is further increased in difficulty with the patient tracing more
complex patterns such as curves, zigzags and the alphabet presented on A4 size paper
(Fig. 16.2). Again, for best practice, a laser and target are given to the patient to practise
movement sense exercises at home.

FIG. 16.2 Movement sense training. The patient practises to accurately trace a pattern with the laser
mounted on the headband (see also Fig. 9.21). As the patient improves, the task can be progressed
by having them trace more complex patterns. Tracing the alphabet as shown is a challenging task.
The laser guides and provides feedback on performance.

Recently Sarig-Bahat et al.20 assessed the use of a neck virtual reality system to train
cervical movement sense/accuracy. In the virtual environment, the patient had to
accurately follow a target moving at 10° per second in single movement planes. It was
tested against a system to train cervical movement accuracy similar to that described
earlier where the patient had to trace stationary lines in different movement directions
(initially flexion, extension, rotation left and right) and then progressing to more complex
patterned movements) on a larger target (70 cm × 70 cm) using a laser attached to a
headband for feedback. Improvements were evident in both the short and intermediate
terms with both the virtual reality system and the target and laser tasks.20,21 Thus the
choice of which application to use could be the availability of a device or the patient’s
preferred method of training—an important feature to encourage adherence.

Smooth-pursuit eye-movement exercises

Training eye-movement control initially uses the same task as the smooth-pursuit neck
torsion test. The starting position chosen is dependent on the assessment findings. The
patient can commence the exercise with the head in the neutral position if this is impaired.
However, the exercise can be commenced with the trunk prerotated, if assessment has
shown poorer eye follow performance in the torsioned (compared with neutral) position of
the neck. The patient follows a slow (20° per second) moving target with their eyes
through visual angles of about 40° without moving their head. Different movement
directions can be practised but horizontal movements are most often required. The moving
target can be provided by the patient themselves which aids home practice. They hold the
laser and project it onto a wall and move it in backward and forward, up and down
directions as required (Fig. 16.3). Alternatively, the patient can throw a ball from one hand
to the other while following the trajectory of the ball with the eyes. The instruction is to
follow the moving object as accurately as possible with the eyes, while keeping the head
still. Again, it is advantageous for accuracy and compliance with practice, to provide the
patient with a laser for home practice.

FIG. 16.3 Training smooth pursuit eye follow in neck torsion. The patient holds the laser and slowly
moves their hand projecting the laser back and forwards on a wall to provide the visual feedback.
The patient follows the laser with their eyes without moving their head. Training can be conducted
with the neck in the neutral or in the more challenging torsioned position.

Gaze stability exercises

Exercises to train gaze stability are usually commenced in sitting but can be performed in
supine lying if pain is exacerbated in the sitting position. In these circumstances, the
clinician performs passive or assisted active head movements. The patient is to maintain
focus on an object directly in the midline as the head is moved.
Most patients commence training in sitting. The patient keeps their eyes fixed on a point
while performing slow controlled head and neck movements. Movement may be into
rotation and/or flexion-extension as directed by assessment findings. The patient aims to
perform “pure plane” movements. If the patient performs awkward or combined plane
motions, the gaze stability exercise is practised in front of a mirror. A focus point is
marked on the mirror and the reflections provide feedback to the patient on the quality of
the head movement. The patient practises the task with slow movements initially,
concentrating on accuracy and quality of head movement.
Exercise difficulty can be advanced by progressively increasing the range of movement
to approximately 45° or by providing increased visual conflict, by changing the fixation
point from a dot, to several words, to a busy background (stripes or a checkerboard pattern
under the dot or group of words) (Fig. 16.4). These exercises are similar to gaze stability
exercises in vestibular rehabilitation protocols.43 The differences are that movements are
performed slowly and through larger ranges of head motion to bias the cervical afferents.
Exercises are usually practiced in smaller doses and thus are more easily tolerated by the
patient. It is important that clear instruction is provided to the patient for home practice at
every stage of progression.
 FIG. 16.4 Gaze stability. The patient trains gaze stability by keeping their eyes fixed on a point while
performing slow controlled head and neck movements. An example of more advanced gaze stability
training is depicted where a single focus point is placed on a busy background.

Eye-head coordination exercises

The movement directions (vertical; horizontal) practised in the eye-head coordination
exercises are guided by examination findings. The aim of the exercises is for the patient to
perform dissociated head and eye movements. Training is undertaken in sitting and the
patient is asked to look between two points. The two points can be created by the patient
holding their fingers approximately 30° apart from the midline or two dots can be placed
on a wall 30° apart. The patient focuses on the point in the midline, then moves the eyes
first, without moving the head, to the point at 30°. Once there, eyes remain focused on the
point while the patient brings the head in line with this target. They then return their eyes
back to the midline without moving the head and next bring the head back to that point
while maintaining their focus.
The exercise can be progressed in several ways. The patient can practise moving the
head to one direction, while their eyes maintain focus on a target, which is moving to the
opposite direction. The patient can perform progressively larger ranges of arm, head and
trunk movement to challenge the control of eye movements. The focus point and
background can be altered as was done for the gaze stability exercises. Finally, peripheral
vision can be restricted by blackening out some swimming goggles to increase the
difficulty level of this task. Of importance, the patient’s performance must be continually
evaluated and the program progressed accordingly. The home program must also be
continually adjusted.

Trunk head coordination exercises

For training trunk head coordination, movement of the body is best performed by rotating
from the hips and torso on stable feet, rather than using thoracic rotation. The patient is
asked to keep the head still while rotating the trunk, pelvis and hips to the left and/or right
as directed by assessment findings. Initially, patients often require feedback on
performance and this can be gained by looking into a mirror to ensure that the head is kept
still while they move the trunk. The clinician can assist by keeping the head still while the
patient moves the trunk, or alternatively, the patient maintains head stability while the
clinician passively rotates the trunk.
Training trunk head coordination is progressed by increasing the range and speed of
trunk motion. The exercise increases in difficulty by using the head-mounted laser beam
projected onto a target (as per joint position and movement sense training). The patient
must hold the laser point still, which more precisely keeps the head still while moving the
trunk (Fig. 16.5). Use of the mirror and then the laser is easily incorporated in the home
program.

FIG. 16.5 Trunk head coordination. The patient tries to hold their head still while rotating their trunk
to the left and right. The precision of the exercise is enhanced by the patient aiming to hold the laser
light on a target. Alternatively, a mirror can be used to make this task easier.

Static balance training

Balance training and progressions follow relatively standard procedures. Starting positions
and progressions are based on the assessed deficits and the patient’s functional
requirements respectively. Static balance is trained with eyes open and then closed, on a
firm then soft surface (such as a piece of foam or a soft mat). Stance positions are
progressed in difficulty starting in comfortable stance and advancing to narrow, tandem
and single leg stance. The patient trains to maintain each increasingly difficult position for
up to 30 seconds at a time without excessive movement or rigidity.
Balance training can be further challenged by adding head movement, oculomotor tasks
and or coordination exercises to the balance task. Patients with neck pain disorders often
need to be challenged by these higher-level exercises. It is important when developing the
home program with the patient that they are conscious of performing the balance exercises
in a safe environment, for example, in a corner with the safety of two walls or near a fixed
bench or table.
Functional, dynamic balance training
Dynamic balance training is a functional progression. It is particularly indicated in patients
who report functional difficulties such as feeling light headed or unsteady when walking
or moving quickly and in whom this task is found to be impaired on examination. Training
focuses on the skill of walking with head movement. It commences with the patient
walking with a shoulder width base, slowly turning the head as far as possible to one side
and then the other. Walking is also practised moving the head up and down through full
range of head motion. The patient should not try to focus on a specific point. Rather the
head and eyes should move together in the same direction. If the task is too difficult or
provokes symptoms, the gaze can be stabilized to the midline initially. Training can be
progressed to faster neck movements and also to tandem walking while performing neck
movements (Fig. 16.6). Again, when developing the home program, an emphasis must be
placed on safety. Performing these exercises in a hallway is safe practice.

FIG. 16.6 Walking with head turns. The patient is asked to walk in tandem walk, slowly moving the
head through full range of flexion and extension.

Vestibular rehabilitation and vision therapy

Some patients may have concomitant vestibular and visual deficits. For example, when a
person sustains trauma to the neck they also suffer a concussion or, vice versa, trauma to
the head may involve the neck. In these cases, specific oculomotor and balance exercises
are directed more specifically towards the vestibular and oculomotor systems. Treatment
for Benign paroxysmal positional vertigo (BPPV) might also be provided when indicated.
Vestibular rehabilitation aims to assist the individual to habituate, compensate or adapt to
any explicit deficits or imbalance in the vestibular system. In general, when the patient has
both neck pain and vestibular disorders, cervical sensorimotor and musculoskeletal
deficits are best managed in the first instance to facilitate performance of exercises for the
vestibular system that might involve fast head motion.43 There is some overlap in the
exercises used for cervical sensorimotor rehabilitation with those used for vestibular
rehabilitation, especially exercises for balance and oculomotor control. These can be
useful as a starting point in patients with concomitant sensorimotor and vestibular deficits.
Visual disturbances can exacerbate cervical symptoms. When the visual system is of
particular concern, it is often the first focus of management. Treatment includes
oculomotor exercises. Some patients may require multidisciplinary management with
treatment also from a behavioural or neuro-optometrist or vision therapist who may
prescribe prism glasses, lenses, filters or other devices to encourage specific eye
movements to facilitate and maximize the effects of training.44,45

Psychological considerations
Just as pain and general distress can be related, so can symptoms of dizziness interact with
psychological distress. In some individuals, dizziness may contribute to psychological
distress, whereas in others, psychological distress can manifest as vertigo or dizziness.
Anatomic and neurophysiological overlap between the vestibular system and the pathways
implicated in emotional states might explain these close links.46 Thus, the clinician should
be aware that psychological factors may affect clinical presentations and therapeutic
outcomes in some47 but not others.48 Likewise addressing the symptoms and signs of
sensorimotor disturbances may help to decrease psychological distress.49

Self-management
Best management tailors treatment to address the impairments identified in the physical
examination of the individual patient. As emphasized throughout this chapter, a home
program of training must be developed with the patient, and it must be constantly
modified as the patient progresses through their individualized rehabilitation program. Part
of the development of the self-management program is a discussion with the patient on
measures they can take if they feel that symptoms of light headedness or unsteadiness, for
example, are returning so that any relapse is prevented or minimized.
Individual patients have different presentations and comorbidities with respect to their
musculoskeletal and sensorimotor deficits of cervical, visual and/or vestibular origin. The
nature and amount of rehabilitation that the patient requires to improve sensorimotor
control may depend on the nature and magnitude of concomitant disturbances in the
vestibular and/or visual systems and the extent to which cervical function may need to be
optimized to compensate for any permanent changes in the visual or vestibular systems.
This is particularly important in older patients who have age-related changes to vision and
the vestibular system and in persons with permanent vestibular impairment associated
with vestibular pathology or trauma. In these circumstances, more extensive rehabilitation
is often required. Patients with any permanent changes in the visual or vestibular systems
should routinely be provided with strategies and remedial exercises for relapse
management and prevention because they will require the cervical spine to be functioning
at an optimal level to compensate for such deficits. This usually includes exercises to
maintain and optimize both cervical musculoskeletal and sensorimotor function.

Conclusion
Evidence is growing for the need to target sensorimotor control disturbances in persons
with neck pain disorders. Problem orientated, tailored, multimodal management that
addresses both the primary cervical musculoskeletal causes as well as any secondary
adaptive sensorimotor control changes is currently recommended. Tailored sensorimotor
control exercises could include exercises aimed at addressing impairments in
proprioception, head and eye movement control, coordination and postural stability. In
some patients, additional management directed towards the vestibular and/or visual
systems may be required and consideration of any psychological components when
present, should be part of the approach.

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17

Management of Nerve Tissue

Some neck pain disorders involve sensitized or compromised nerve tissue that require
specific management approaches targeting nerve tissue. Correctly identifying involvement
of nerve tissue is essential (see Chapters 4 and 9) because it may indicate the need for a
change in management strategy. Significantly compromised nerve function in the presence
of a severe cervical myelopathy or radiculopathy, signals a safety concern for the patient
and may require immediate specialist medical consultation. For the most part, neck pain
disorders involving nerve tissue do not involve immediate safety concerns for the patient
and are effectively treated conservatively. Nerve related cervical conditions do, however,
require a gentle approach because they may easily be aggravated by overzealous physical
treatments. The status of nerve function may occasionally deteriorate and requires diligent
monitoring over the duration of management. There is the potential for conditions
presenting initially as only a sensitized nerve state, to progress to a state of compromised
function (i.e., worsening nerve conduction) with potentially irreversible longer-term
consequences for the patient if not identified early. Effective management of nerve-related
neck pain disorders requires an understanding of the potential mechanisms underlying the
condition (see Chapter 4), so that management approaches can be applied appropriately,
and symptoms and signs signalling worsening of the condition can be identified and
interpreted accurately. This chapter discusses the management strategies for nerve-related
neck pain disorders, including neurophysiological mechanisms proposed to underlie
successful management approaches.

Neurophysiological mechanisms underpinning nerve

tissue management
Mechanisms of effect underlying nerve tissue management approaches are underpinned by
neurophysiological processes to restore homeostasis in and around the affected nerve.1

Restoring homeostasis around the nerve

In the first instance, the neuropathy may be addressed by treating the musculoskeletal
tissues determined in the examination to be directly causing the nerve irritation and/or
compression. Treatments aim to resolve perineural inflammation resulting from injury or
pathology of interfacing musculoskeletal structures (e.g., disc lesions).2–4 Acute or chronic
perineural inflammation along a nerve trunk is known to induce nerve pain, potentially
nerve damage5–11 as well as nerve mechanosensitivity.12–15 Furthermore, degenerative or
injured spinal or peripheral musculoskeletal interfaces may entrap or compress the nerve,
potentially affecting nerve conduction and mechanosensitivity.16–19 Restoring the normal
status of these musculoskeletal tissues by resolving inflammation, as well as restoring
normal movement (joint mobility) and physical support (neuromuscular function) will
directly reduce nerve interface factors contributing to a neuropathy. In one experimental
animal study20 where inflammatory mediators were placed around the dorsal root ganglion
of a rat, spinal mobilization resulted in faster resolution of dorsal root ganglion
hyperexcitability and resultant hyperalgesia compared with no intervention. The authors
hypothesized that potential mechanisms of effect of the spinal mobilization may have
included improved blood supply and nutrition to the affected dorsal root ganglion with a
faster resolution of inflammation and excitability.

Restoring homeostasis within the nerve

An aim of management is to return homeostasis within injured nerve tissue that may have
been disturbed by injury and associated perineural oedema or nerve
entrapment/compression. Disturbances in intraneural homeostasis may include reduced
circulation to the nerve, intraneural ischaemia, neuroinflammation and intraneural
oedema21–25 that can result in nerve conduction loss and mechanosensitivity.16–19
Neurodynamic treatment methods, usually in the form of manual therapy or exercise
directed at the nerve tissue or nerve-musculoskeletal interfaces, aim to have positive
mechanical and neurophysiological effects. Movement/mobilization of the nerve and its
connective tissues results in intraneural pressure changes that are proposed to decrease
excitability of dorsal horn cells by altering axoplasmic flow, improving intraneural
circulation, and reducing intraneural oedema.1,26 Mechanistic studies have supported the
effect of neural mobilization modalities on dispersion and reduction of intraneural
oedema.27–29 Neurodynamic mobilization in animal studies has also shown that such
mobilization may impact neuro-inflammatory responses (decreasing nerve growth factor
concentration and glial cell activation) in the dorsal root ganglia and spinal cord that
potentially influence mechanisms associated with the occurrence of more widespread pain
in neuropathic pain states.30,31

Restoring tolerance to motion and resolving

mechanosensitivity
Treatment may be directed towards restoring the capacity of nerves to tolerate motion,
compression and stretch forces relative to their musculoskeletal interfacing structures
during movement.32–35 Studies have shown that affected nerves may have a reduced
capacity for motion or mechanosensitivity to motion and/or compression.13,14 This is
detected in the examination as a positive response to neurodynamic tests and palpation
(see Chapter 9).33,36–39 Manual therapy techniques, such as the lateral glide mobilization,
can improve the tolerance of nerve tissues to motion, and have been shown to reduce
protective muscle responses during neurodynamic tests in mechanosensitive individuals.40
Furthermore, neurodynamic techniques both in humans41 and animals42 have shown
mechanisms (e.g., reduced temporal summation) suggestive of the activation of
descending inhibitory systems. Although there is evidence that treatment may improve
nerve tolerance to motion, there is little evidence currently that treatment can increase the
excursion of nerve motion1 known to be reduced in some compressive neuropathies such
as carpal tunnel syndrome.43–46

Matching management to the nature of the nerve-

related condition
Management approaches to nerve-related neck pain disorders vary depending on the
patient’s presentation and examination findings. In some presentations, involvement of
nerve tissue may be a minor secondary component of the condition (i.e., mild
mechanosensitivity) that resolves spontaneously as other more substantial musculoskeletal
impairments are addressed. In other conditions, the nerve component may be more
significant with more marked signs of nerve mechanosensitivity or changes in nerve
conduction. Techniques aimed specifically at resolving these nerve tissue–related
impairments are a priority. Where there is marked nerve mechanosensitivity, other
examination findings (e.g., elevated scapular postures, marked active or passive
movement restrictions) may be protective responses to mechanosensitive nerves. Attempts
to improve scapular posture or perform exercise may aggravate the condition. Instead,
attention is given immediately to resolving the underlying nerve mechanosenstivity. In
summary, interpreting the level of nerve involvement and priority for specifically
addressing nerve tissue within a management approach will depend on the findings from
the patient examination, and may change over the duration of a management period as the
patient’s condition progresses.
When specific attention to nerve tissue is a priority, techniques chosen will depend on
the stage of the condition and the nature of the nerve involvement. For example, in the
acute stages of a condition, there may be an emphasis on reducing perineural and/or
intraneural inflammation. In subacute and chronic conditions, the focus may be more on
restoring pain free mobility, the function of nerve tissue and the musculoskeletal
interfaces. If it is suspected that a nerve is compressed or entrapped, treatment is focused
on reducing compression to the nerve. Irrespective of approach, the potentially irritable
nature of mechanosensitive nerve tissue warrants that physical treatments be undertaken
with care so as not to further provoke the patient’s symptoms.47,48
A multimodal mechanistic approach to management of cervical nerve-related conditions
is taken because mechanisms underlying conditions, such as cervical radiculopathy, may
vary from individual to individual. Nerve tissue exposed to perineural inflammation
and/or compression secondary to injury of a musculoskeletal structure, may present as a
loss of nerve conduction,49 as a mechanosensitive nerve painful to movement or
pressure13,14 or as a variable mix of both. Therefore there is no one set approach to
managing conditions such as radiculopathy. The presentation of this disorder may vary
significantly between patients, thus requiring a patient-centred management approach.
Determining an appropriate course of management requires judicious initial examination
and continual reassessment of treatment response.
Patient education and advice
Management is underpinned by comprehensive patient education and advice regarding the
clinical presentation with collaborative discussion concerning management strategies.
Informing patients of the involvement of nerve tissue within their disorder is important for
safety reasons for certain nerve-related cervical conditions. Firstly, patients with
compromised nerve conduction, such as cervical radiculopathy or myelopathy, should be
informed of signs of deteriorating nerve function and the need to seek advice if
deterioration is suspected. Secondly, nerve tissue has a propensity to be irritable. Patients
who have been given exercises to address nerve mechanosensitivity need to be cautioned
to commence and progress slowly and be analytical regarding their symptomatic response
to a new exercise intervention. The concept of performing exercise for nerve
mechanosensitivity is usually foreign to patients and careful explanation as to the rationale
for their inclusion is necessary for optimal compliance.

Addressing contributing factors

There may be significant patient (e.g., postural) and environmental (e.g., ergonomic)
factors that underlie nerve irritation in neck pain disorders.

Postural/movement–based strain to nerve

When considering nerve tissue mechanosensitivity, clinicians need to be cautious in
addressing aberrant postures if they appear to be protective of nerve tissue. However, it is
also possible for postures to be contributing to the nerve mechanosensitive state. Poor
cervical and shoulder girdle muscle control can underlie persisting nerve-related disorders.
Some cases of persistent cervicobrachial mechanosensitivity appear to be related to
aberrant shoulder girdle function. In particular, a downwardly rotated and/or depressed
scapula (a sensitizing component of neurodynamic tests of the brachial plexus) may
induce continuous excessive strain to the brachial plexus. Patients with symptoms (pain
and/or paraesthesia) in relaxed upright standing may experience immediate reduction in
these symptoms when the clinician manually corrects this aberrant scapular posture. A link
between scapular posture and nerve symptoms may be confirmed by taping the corrected
scapular posture over a longer time period. Although these patients demonstrate positive
signs of nerve mechanosensitivity, mobilizing techniques to address mechanosensitivity
may have limited effect if the underlying postural and movement–based impairments of
the scapula are not addressed first (see Chapter 15).
Adequate neuromuscular function of the cervicothoracic region and shoulder girdle is
essential in the long-term management and prevention of recurrence of nerve-related
conditions including cervical radiculopathy and cervical myelopathy. If pain is severe in
the early stages of management, gentle isometric exercises are commenced initially.
Exercise to improve neuromuscular function can be progressed (see Chapter 15), as long
as an exercise does not compromise integrity of the neural structures and nerve function.
Ergonomic factors and nerve strain
Consistent with the management approach to other cervical conditions, ergonomic and
work-related modifications may need to be considered in cervical nerve-related
conditions. This is particularly relevant for ergonomic factors affecting the upper limb
such as overreaching associated with poor work station design. Nerve entrapments of the
upper limb such as carpal tunnel syndrome, which may be associated with concurrent
cervical disorders (i.e., double crush), often have ergonomic or work-related contributing
factors that need to be addressed. For example, the prevalence of carpal tunnel syndrome
is approximately 3.8% in the general population50 and 21% in occupations involving
repetitive hand tasks.51 Similarly the ulnar nerve may become entrapped as it passes
through the cubital tunnel of the elbow particularly in individuals in occupations that
involve repetitive tasks such as manipulating tools.52 Addressing these work-related
contributing factors may include the modification of work equipment or work practices
(e.g., technique modification, incorporation of work breaks).

Manual therapy
This section considers the application of manual therapy techniques for both nerve
mechanosensitivity and nerve conduction deficits. For many patients, these features
coexist in a variable mix. The choice of technique and progression will depend on the
priority features of the condition, and the continued evaluation of the response to
treatment.

Manual techniques directed at nerve mechanosensitivity

Manual therapy techniques targeting the nervous system are well described for managing
neck pain disorders exhibiting positive signs of neuromechanosensitivity.53,54 Techniques
may either directly mobilize the relevant musculoskeletal interface (e.g., joint
mobilization), or specifically mobilize nerve tissue. Techniques such as a cervical lateral
glide mobilization (Fig. 17.1) target the restoration of pain-free relative motion of the
cervical nerve-musculoskeletal interface.53,54
 FIG. 17.1 Cervical lateral glide. This technique is applied with the clinician’s index
finger gently wrapped around the posterolateral aspect of the uppermost vertebrae
(i.e., C5 for a C5–6 technique) on the symptomatic side such that a lateral glide can be
applied to C5 relative to C6. In this example, the clinician’s force application produces
a left lateral glide for a right sided neural mechanosensitivity issue. The clinician’s right
hand stabilizes the patient’s right shoulder girdle. The patient’s right arm can be
positioned in neutral or in a progressively more advanced upper limb neurodynamic
test position.

Signs of cervical nerve mechanosensitivity may resolve with manual therapy techniques
targeted at improving painful or restricted cervical segmental motion without the need for
specific nerve-based techniques. However, in many cases, a better effect is gained from
manual therapy techniques directed to the nerve interface. The cervical lateral glide
mobilization technique has been shown to immediately reduce protective muscle
responses associated with neurodynamic tests40 with positive effects on mobility and
pain55 in those who are mechanosensitive. In a clinical trial, Nee et al.56 showed that
management including education, manual therapy (lateral glide technique) and nerve
mobilizing exercises provided immediate clinically relevant benefits beyond advice to
remain active. Evidence from a systematic review and meta-analysis supports the use of
cervical lateral glide techniques in people with nerve-related neck and arm pain. The
technique had a positive effect on pain, with clinically meaningful effect sizes.57 The
lateral glide technique is often progressed by prepositioning the arm from the neutral
position to a progressively more advanced upper limb neurodynamic test position, as well
as incorporating active mobilization of the upper limb.
Dosage: Manual therapy techniques directly addressing nerve tissue mechanosensitivity
are initially conservative (e.g., 1–2 sets of 30 second durations of mobilizations, at a grade
short of symptom reproduction). They can be progressed with regard to increased sets,
repetitions, and grade of mobilization. Once the risk of an adverse response to treatment
has been negated, techniques may be progressed to symptom reproduction within the
individual’s tolerance. As indicated, the cervical lateral glide mobilization may be
progressed by progressively increasing positions of the relevant positive upper limb
neurodynamic test (e.g., median nerve biased test) or reported provoking functional upper
limb position (e.g., arm overhead). Progression is guided by symptom response and
symptom irritability.

Manual techniques for altered nerve conduction

For conditions such as cervical radiculopathy with changes in nerve conduction, traction
may assist in alleviating symptoms associated with this nerve compression.58 Traction
generally has not shown efficacy in the management of non-specific neck pain
disorders,59–61 but in cervical radiculopathy, mechanical traction may provide additional
clinical benefit to other therapeutic modalities such as exercise.58 Nevertheless, evidence
of the benefits of traction have been mixed.62–64 If traction is to be trialled in a patient with
cervical radiculopathy, the preference is to first apply manual traction (e.g., traction to
C5/6 in the presence of C6 radiculopathy) to permit the appropriate adjustment of
technique in response to patient comfort for these potentially irritable nerve conditions.
Cervical radiculopathies may also respond well to manual techniques targeting
restricted or painful cervical segmental motion, including cervical lateral glide techniques
as described for neural mechanosensitivity. In the early stages of management, techniques
that potentially compromise an already compressed or inflamed nerve (e.g., C5/6 right
lateral flexion mobilization in the presence of right C6 nerve conduction deficits) may
need to be avoided. Irrespective of the technique applied, there needs to be diligent
monitoring of nerve conduction status to ensure techniques are having a positive impact,
and importantly, not an adverse impact.
Dosage: Techniques addressing cervical radiculopathies should initially be
conservative. Traction and other mobilization techniques should not reproduce symptoms
and initially be applied in a trialled manner to assess the effect on symptoms. Traction can
be progressed in duration and force and mobilization techniques by increased
sets/repetitions, once the risk of an adverse response to treatment has been negated.

Self-mobilization with home exercise

Exercises to self-mobilize neural tissue for the management of nerve mechanosensitivity
have long been advocated. Techniques broadly include those commonly referred to as
sliders that combine movements which simultaneously shorten and lengthen the nerve bed
at adjacent joints (Fig. 17.2A–C), respectively. The other techniques are referred to as
tensioners that aim to mobilize a nerve by elongation of the nerve bed (Fig. 17.3A and
B).54,65,66 Mechanistic studies in the upper limb have shown that nerve sliding techniques
may result in greater nerve excursion compared with tensioning techniques67 particularly
between the two moving joints.68 As such, sliding techniques for managing neural
mechanosensitivity are generally recommended because they expose the nervous system
to more mobilization and less strain.35,68 However, the choice and progression of neural
mobilizing exercises may differ depending on the initial presentation and stage of
individual’s recovery. For example, tensioning techniques may be appropriate in non-
irritable presentations if sliding techniques are not proving effective, particularly if they
best expose the nerve and musculoskeletal interface to the mechanical forces that they will
need to tolerate for optimal return to function (e.g., fully outstretched positions such as
reaching, tennis serve). The initial choice of exercise and exercise progressions are based
on clinical reasoning processes.69

FIG. 17.2 Nerve “slider” self-mobilization technique (median nerve bias). The neural
tissue mobilization techniques combine movements which simultaneously shorten and
lengthen the nerve bed at adjacent joints to create gentle excursion of nerve tissue
relative to their interfaces. (A) The nerve bed is lengthened in the cervical spine and
shortened at the wrist and elbow. (B) The nerve bed is lengthened at the wrist and
elbow and shortened in the cervical spine. (C) the nerve bed can be moved in the
cervical region by shortening and lengthening the nerve bed alternately in each upper
limb.

FIG. 17.3 Nerve “tensioner” self-mobilization technique (median nerve bias). These
neural tissue mobilisation techniques combine movements which move and then
elongate the nerve bed from (A) the starting position to (B) end position of the exercise

Exercise to address nerve mechanosensitivity may also involve exercises directed

towards sensitive dura. Some presentations of headache and neck pain appear to be related
to movement sensitivity of the dura as evident by pain with cervical (or craniocervical)
flexion (see Chapter 9). Exercises may target dural tissue initially with slider type
exercises using pain-free ranges of concurrent craniocervical flexion/ankle plantarflexion,
alternated with concurrent craniocervical extension/ankle dorsiflexion. Exercises are
progressed as able to a sitting position incorporating cervical flexion/knee flexion
alternated with cervical extension/knee extension. When symptoms are severe or irritable,
nerve mechanosensitivity may need to be addressed with manual therapy initially because
these direct neural mobilizing exercises may be potentially aggravating.
Dosage: Exercises to mobilize nerve tissue should be commenced at a low dosage (e.g.,
1 set of 10 or less repetitions per session, twice per day) and short of symptom
reproduction. Exercises can be progressed with increased sets and repetitions once the
absence of an adverse response has been ascertained.
Referral to medical physicians
Although most neuropathies can be managed conservatively, some may require medical
attention or a multidisciplinary approach. In particular, neurological signs of absent or
significantly altered reflexes or muscle strength may indicate severe compressive
neuropathy (or myelopathy). Further investigation, such as magnetic resonance imaging,
may be indicated to determine the presence of nerve or spinal cord compromise, with
potential treatment options that may include surgery. Patients with severe or recalcitrant
neuropathic pain usually require good pharmaceutical pain management by a medical
practitioner. Such medications currently include tricyclic antidepressants, pregabalin,
gabapentin and lidocaine patches.70 However, even in these more severe cases where
medication is required, there is a still a role for physiotherapy within a multidisciplinary
approach. Physiotherapy is particularly important with regard to education on activity
modification and the restoration of pain-free postural and movement function with the use
of manual therapy techniques and progressive exercise as is appropriate to the patient’s
condition.

Conclusion
When neck pain disorders involve sensitized or compromised nerves, management
approaches may need to specifically target nerve tissue. Correctly identifying the nature of
nerve involvement will guide management. Some presentations involving significantly
compromised nerve function may signal safety concerns for the patient requiring medical
consultation, however most neck pain disorders involving nerve tissue can be effectively
treated conservatively. Effective management requires an understanding of the potential
mechanisms underlying the condition so that interventions can be applied appropriately
and the status of neural function can be judiciously monitored.

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18

Case Presentations

Clinical Reasoning and Clinical Decision Making

Conservative physical therapies are the primary interventions for the management of neck
pain disorders. However, neck pain presentations vary between patients as does the
clinical reasoning processes underpinning management decisions. The text to this point
has discussed clinical reasoning and considered the use of several interventions in relative
isolation. In this chapter, we present patient cases to practically demonstrate the clinical
reasoning processes underlying differential diagnosis and/or selection of integrated
management approaches. Cases are used to illustrate how various therapies may be
selected and integrated, based on the outcomes of clinical reasoning of findings of the
patient interview, the physical examination and progressive assessments. The cases have
different emphases to illustrate different components of examination and management and
associated reasoning. The reader is referred to relevant chapters to refresh details of
particular treatment techniques/regimes.

Case 1: Directionally biased persistent neck pain (Fig.

18.1)
For many patients, an informative relationship can be established between their movement
behaviours and symptoms. The following case is a prime example of this relationship. The
case highlights the need for a thorough patient interview, particularly with regard to the
behaviour of symptoms and identification of aggravating factors to neck pain that share a
common provocative movement component. This case also highlights the powerful impact
that patient education, advice and compliance has on recovery.
 FIG. 18.1 Case 1: Body chart. GH general health; MEDS medications, INVEST
investigations, P & N pins and needles.

Patient presentation and key examination findings

PS, a 28-year-old primary school teacher, presents with a 5-year history of daily left-sided
neck and upper thorax pain that occasionally spreads into the left upper arm. This
condition started when she returned to university to commence studies in education in her
mid-twenties. PS reported that in the initial 2 to 3 years, her condition was episodic and
seemingly related only to her study. However, symptoms persisted and progressively
worsened well beyond the completion of her degree. They were now affecting multiple
aspects of her life. Over the past 3 years she had sought treatment for her neck condition
from many health professionals. Management strategies included manual therapy, exercise
(predominantly stretches), acupuncture and dry needling, chronic pain education and pain
management. To date, none of these interventions had been effective for any length of
time, with no sustainable positive change in symptoms over time.

Reported aggravating factors and functional examination

The salient factor in this case was that PS reported key aggravating factors that had a
common mechanical element relevant to her persisting symptoms, i.e., flexion of the
lower cervical spine. These specific activities were computer work on a laptop, working
with young children at schools on low desks, and driving her car with the head rest
pushing her head forward. When asked to replicate these activities in the clinic as best as
possible, it was evident that all activities positioned her in mid-range to end-range lower
cervical flexion, a position that PS was required to function in for a large proportion of her
days. Replication of these activities in the clinic resulted in a familiar feeling of strain to
her neck that resolved when the neck was returned to a more neutral position.

Other examination findings

Examination of active movements revealed that, although mildly uncomfortable, there
were no limitations to PS’s cervical flexion range of motion, or any other motion
direction. Manual segmental examination revealed marked pain provocation on palpation
of the (L) C5–6 motion segment in the absence of any apparent intersegmental mobility
loss. The most notable finding during formal examination of the cervical motor system
was a marked reduction in cervical extensor muscle endurance, with self-reported fatigue
after less than five repetitions of lower cervical extension. There were no apparent
impairments in thoracic mobility or the neural system (nerve conduction or
neurodynamics). Although the patient expressed frustration with the persistence of her
disorder and the lack of improvement with previous treatment, these emotional responses
were understandable based on the longevity of the condition and were not considered as
potential barriers to recovery. Furthermore, the patient appeared very positive about
recovery once the link between her aggravating activities, physical findings and
persistence of pain was established, providing her a sense of empowerment.

Diagnosis and clinical reasoning

The diagnosis considered the condition from both a movement-related and structure-
related perspective. A diagnosis was made of a chronic flexion related C5–6 motion
segment strain. The movement disorder aspect of the condition was driven by identifying
the common element to all reported aggravating activities. Specific and comprehensive
questioning that transferred to activity replication during the physical examination
demonstrated that a flexed position of the lower region of the neck was related to the
provocation of symptoms. Although it was uncertain as to what specific structure of the
lower neck region was responsible for the persistence of symptoms, findings from the
manual examination suggested the C5–6 segment may be implicated. Importantly, the
examination findings indicated that this lower-neck condition was of a postural overuse
strain nature, perpetuated by habitual loading to the neck in flexion and a deconditioned
muscular system. The success of management would therefore require PS’s full
participation to change the habitual loading pattern and condition the muscular system.

Management approach
Advice and education
A key aspect of management was to adequately inform PS that her neck condition was not
caused by a lack of neck flexibility, but rather habitual patterns of movement and muscle
deconditioning. This was important because she had been told in the past that stretches
would help her neck condition, which they did not. Instead it was reinforced that resolving
the habitual movement pattern of her neck was the most relevant factor that would be
complimented by conditioning exercises of her neck muscles. This included strategies to
reduce the time and excursion of cervical flexion in which PS functioned by changing the
work environment when able, as well as her work practices and behaviours. Strategies
included use of a laptop holder and external keyboard, and an inclined reading board, to
remove the need for excessive cervical flexion when working on the laptop computer, or
reading documents, respectively. Although PS could not avoid sitting at lower desks while
supervising school students, the need for more regular breaks during this work with
children was emphasized and undertaken. PS also modified her car seat position so that
her head felt comfortable and not in a flexed position.

Exercise therapy
Exercise included both postural correction training as well as specific conditioning of the
cervical muscles. Postural correction training incorporated the practice and familiarity of
attaining a neutral upright posture. PS incorporated this into work postures with use of
memory joggers. A neutral posture was also facilitated with the use of the laptop holder
and inclined reading board. Training also included progressive lower cervical extensor
training. Training initially incorporated through-range coordination and low-load
endurance training in the prone on elbows position. The exercise was subsequently
progressed to resistance exercise directed towards higher load and sustained contractions
to attain gains in muscular strength and endurance. Although PS was only seen over a 6-
week period as her symptoms had markedly improved, she was encouraged to continue
progression of her exercises for several months. This was justified to her based on the
longevity of her condition and the expected time frame required to achieve sustainable
changes in muscle conditioning, as well as the prevention of recurrence.

Reflection and clinical message

PS responded well to this intervention with substantial alleviation of pain and increased
comfort during the relevant activities. The key element to the success of this intervention
was identifying the association between the aggravating factors, the patient’s habitual
movement behaviour, and the neuromuscular impairments, that were collaboratively
identified by the patient and the clinician. This was very motivating and empowering for
PS because she could immediately implement the strategies (changes in movement
behaviour, work practices and ergonomics, muscular training) that clearly complimented
each other. It should be noted that such strong and consistent directionally based clinical
presentations do not always exist. Many mechanical neck pain presentations are more
clouded, with multiple aggravating directions of motion and more widespread motor
impairments. However, even within these more clouded presentations there may be a
certain pattern of movement disorder that is dominant and can be prioritized in
management.

Case 2: Headache—differentiating the role of the neck

(Fig. 18.2)
Neck pain is a common feature of frequent intermittent headache types such as migraine,
tension-type headache, cervicogenic headache, and headaches associated with
craniomandibular dysfunction. The neck pain can arise from cervical musculoskeletal
dysfunction or it may be part of the headache symptom complex. Thus cervical
musculoskeletal dysfunction can be the primary cause of headache (cervicogenic
headache), a contributor or comorbid feature of the headache symptomology, or have no
role in the headache syndrome. The use of local treatments to the neck (e.g., manipulative
therapy, therapeutic exercise) in headache management is relevant only when a link is
established between the neck pain, relevant cervical musculoskeletal dysfunction and the
headache.

FIG. 18.2 Case 2: Body chart. VAS visual analogue scale; GH general health; MEDS
medications, INVEST investigations, P & N pins and needles.

This case presents a patient whose primary reason for seeking a physiotherapy
consultation was to know if her headaches had a neck cause/component and, if so, what to
do about it. The reasoning will be narrated through the examination to expose the
clinician’s thinking in determining the presence or not and possible role of cervical
musculoskeletal dysfunction in this person’s headache.

Patient presentation
JD is a 62-year-old office manager. She reports a history of menstrual migraine since the
age of 16 years. In the last 10 years or more, she reports feeling more neck pain with her
headaches and is also getting headaches more frequently. They still feel like her usual
migraines although the intensity has lessened, and she no longer experiences auras. JD has
always found that if she pushes at the base of her skull, she can change the headache.

Reasoning.
First thoughts are that JD has experienced an improvement in her menstrual migraines
likely coinciding with the end of menopause and she may be describing a transition to
either a frequent common migraine, tension-type or cervicogenic headache or is
developing a mixed headache. Changing the headache by pushing on the base of the skull
is not helpful in differential diagnosis. It is a non-specific sign because it is possible to do
this with migraine, tension-type or cervicogenic headache.
JD reports a headache frequency of at least two headache days per week, their intensity
at worst is a 6/10, and duration is several hours. She now takes Nurofen (an over the
counter nonsteroidal antiinflammatory drug) to control the headache (up to 6 per day on
headache days). The time of onset of headache is variable and does not appear to be
related to any particular activity or posture. She can wake with a headache, or the
headache comes on in the afternoon, either at work or at home, often on a Saturday.

Reasoning.
Waking with a headache could be as a result of sleeping position of the neck, but it is also
a common feature of migraine. Headaches on a Saturday could be suggestive of a stress-
release migraine or tension-type headache. JD is not relating headache onset to any
particular neck-related activity at this time, which is lessening thoughts about cervicogenic
headache. She is managing headaches with Nurofen, which can assist some persons with
any of migraine, tension-type or cervicogenic headache types.
JD describes her headaches as an intense ache, felt in the frontal region. They are
usually worse on the left side but can involve the whole head and neck. Headaches usually
start in her forehead and JD reports that the top part of her neck begins to ache when she
has a headache. She really thinks that her neck is triggering her headaches. Her neck is
usually more bothersome when she has the headache than when she is headache free.
When she has a headache, JD reports she is sensitive to light and computer work can be
aggravating.

Reasoning.
Headaches are unilateral and seem to be relatively side consistent, which is consistent with
cervicogenic headache but does not dismiss migraine. Cervicogenic headaches usually
start in the neck and then spread to the head, but JD reports a pain onset in the head, which
is more commonly a characteristic of migraine. Sensitivity to light and computer work
while a headache is present are often generic complaints of headache sufferers. Of interest,
JD’s neck pain seems to be very closely related to the headache (i.e., it is not so
bothersome on non-headache days), yet her view is that it appears that the neck is
triggering the migraine. Although it is important to acknowledge her beliefs, the
inconsistent presence of neck pain in the absence of headache further lessens thoughts
about cervicogenic headache.
JD has a family history of migraine (mother). Apart from the headaches, JD reports no
other health issues, has had no surgeries and takes no medication (with the exception of
Nurofen). She is working full time, and manages on headache days with Nurofen, but
would prefer not to rely on medication. Outside work, she is involved in several
community organizations, and is rather busy. All children have left home, and she and her
husband enjoy four grandchildren.

Hypotheses from the patient interview

There is well recognized symptomatic overlap between headache types and, as often
occurs, JD is not presenting with classical features of one headache type. Based on
information from the patient interview, it is reasoned that JD’s headache is, in descending
order of possibility, chronic migraine (the neck pain is part of the pain of migraine), a
mixed headache or a cervicogenic headache. Tension-type headache was ruled out at this
stage for lack of defining characteristics. This rather mixed symptomatic picture realizes
the importance of the physical examination to determine whether or not the neck pain is
associated with a pattern of musculoskeletal dysfunction to confirm or rule out a cervical
cause or contributor to JD’s headaches.

Physical examination: key findings

▪ Posture: JD demonstrated a generally mildly flexed spinal posture, with
flexion of the cervicothoracic region and an associated slight forward head
posture. Her scapulae were slightly downwardly rotated bilaterally.
Correction of both spinal and scapular postures made no immediate
difference to the test movement of (L) neck rotation (range or perceived
stiffness).
▪ Articular system: Examination of cervical mobility revealed that cervical
rotation was symmetrically restricted bilaterally (60 degrees) with no
reproduction of symptoms. Cervical extension was limited to
approximately 20 degrees but was also asymptomatic. The cervical
flexion rotation test (C1/2 rotation) was unremarkable. The
cervicothoracic region was generally hypomobile. Manual examination
revealed (L) C2/3 moderate hypomobility and slight pain provocation.
There was general hypomobility in the lower cervical and upper thoracic
regions.
▪ Neuromuscular system: Examination of the muscle system revealed that
JD could achieve 24 mmHg in the craniocervical flexion test (CCFT) with
good movement patterning and sustain a holding contraction at this level
without difficulty. There was premature fatigue (5 repetitions) in the
scapular holding test and no immediate change in palpation findings
(reassess: passive accessory intervertebral movements (PAIVMs) C2–3—
no major change) immediately afterwards. Testing of the cervical extensor
muscles demonstrated a good pattern of motion in the craniocervical and
cervical muscle tests but some premature fatigue in performing 10
repetitions of cervical extension.
▪ Examination of sensorimotor function and the neural system were
unremarkable.

Clinical reasoning and reflections

The physical examination did reveal a pattern of musculoskeletal dysfunction consistent
with a neck pain disorder. The examination revealed a slightly reduced (for age) range of
active cervical movements, there were joint signs of moderate hypomobility but little pain
at the (L) C2–3, and muscle function (e.g., CCFT achieved the 24 mmHg stage) was fair
but not optimal. Given the frequency and severity of JD’s headache, it was reasoned that
the cervical musculoskeletal dysfunction was not comparable in severity to the headache
complaint. This, in conjunction with the information from the patient’s history, led to the
conclusion that JD did not have a cervicogenic headache. Rather it was hypothesized that
she continued to suffer from chronic migraines and as well, had a mild comorbid neck
disorder. However, it was possible that the cervical musculoskeletal dysfunction was a
contributor or augmenting the migraine. A trial of treatment might confirm or refute this
hypothesis.
The findings and the reasoning behind the diagnosis and neck pain hypothesis was
discussed with JD as was the various relationships between headaches and neck pain. She
was keen to try a trial of treatment and to learn appropriate exercises for her neck. She
attended for treatment on four occasions over a 4-week period. Management included
manual therapy for the hypomobile C2–3 segment and cervicothoracic region and a
comprehensive self-management program of neuromuscular training and mobility
exercises was developed. Further discussions took place about different headache types
and the role of the neck as JD was interested to know more. JD was followed-up by
telephone 1 month after discharge, at which time she reported that the exercises had
definitely helped her neck and it felt a lot freer. Headaches were at best, possibly a little
less severe, but there had been no substantive change in their pattern.
The definite change in neck symptoms together with the lack of change in the headache
pattern, confirmed retrospectively, the hypothesized diagnosis of chronic migraines and a
comorbid mild neck disorder.

CASE 3: (1) Learning from past treatment response;

(2) Importance of differential diagnosis to guide
management of complex patients after a whiplash
injury (Fig. 18.3)
Patient presentation and key examination findings
JR is a 35-year-old female who was involved in a motor vehicle crash on her way to work
4 months ago. She briefly lost consciousness and has little memory of the crash. Head and
neck scans revealed no significant findings. All symptoms were severe in the first few
weeks after the accident. They gradually improved, but in the last month, there had been
no change. JR had 6 weeks off work and then commenced a graduated return to work. JR
is a medical registrar at a large city hospital and she currently works 30 hours per week.
She manages work by changing positions regularly but is now not doing any physical or
specific exercise because she has found that this exacerbates her symptoms. She has no
history of neck pain or trauma, has a history of intermittent mild migraine (2 per year) and
her general health is good. Before the crash, JR worked full time and enjoyed regular
ballet and jogging for fitness.
 FIG. 18.3 Case 3: Body Chart. P pain; GH general health; MEDS medications,
INVEST investigations, P & N pins and needles.

JR presented with bilateral neck and thoracic pain, daily moderate left occipital
headache, once monthly left orbital migraines, regular sleep disturbance, intermittent
unsteadiness, visual disturbances and general fatigue. Her neck, thoracic and headache
symptoms were exacerbated by driving, sustained sitting, computer work, lifting and
carrying and physical activity. Unsteadiness and visual disturbances were exacerbated
when neck pain and headache increase. Symptoms eased temporarily when exacerbating
activities were avoided and with heat, simple analgesics and rest. JR is anxious while
driving and avoids driving if possible. She works on bi-monthly rotations in wards
throughout the hospital and her work environment and tasks can differ between rotations.
JR has attended physiotherapy. The focus was on strengthening and physical activity
exercises which exacerbated symptoms. Subsequently, she stopped doing all types of
exercise and is not sure of where to go from here. She consults her GP regularly and sees a
psychologist to manage her posttraumatic stress symptoms. JR has also consulted a
neurologist who prescribed medication for the migraines. JR takes simple analgesics and
antiinflammatories as required.
Current levels of pain and disability were scored as followed:

Neck disability index (NDI): 30%

Pain visual analogue scale (VAS): 4/10
Patient specific functional scale (PSFS/10)
Sleeping: 7
Sustained sitting (40 minutes): 5
Lifting/carrying: 7
Dizziness handicap inventory (DHIsf) score: 5/13.

Clinical reasoning
Important points to highlight in this case are that the previous treatment of strengthening
and physical activity aggravated JR’s symptoms, she is not getting better, and she has
stopped doing any exercise at all as a result, which is a poor and undesirable outcome. It is
important to determine the reasons for this outcome. JR’s NDI and pain score (VAS)
indicate moderate neck pain and disability. It is possible there is an element of sensory
hypersensitivity that might explain this adverse reaction to strengthening exercises and it
should be explored in the physical examination. JR has several symptoms other than pain,
and a single focus modality, i.e., strengthening exercises, is unlikely to address all
symptoms. The physical examination needs to include a full movement, neuromuscular
and sensorimotor assessment, directed by her complaints to differentially diagnose
symptoms particularly headache, dizziness and visual complaints, as a basis for
developing a best practice management program.
Given JR’s description of symptoms and relationship to activity, it could be
hypothesized that her neck and thoracic pain and occipital headache arise from cervical
musculoskeletal dysfunction. The trauma may have exacerbated JR’s preexisting orbital
migraine or now, may be an additional trigger. JR’s description and behaviour of her
unsteadiness, visual disturbances and fatigue suggest they are related to cervical
sensorimotor dysfunction. A vestibular pathology is unlikely, but the examination should
screen for vestibular and oculomotor dysfunction, in light of the concussion that JR
sustained at the time of the crash. JR has some symptoms of posttraumatic stress, which
may impact on physical symptoms, but she is managing these with the help of a
psychologist. The nature of JR’s work and the potential long hours requires monitoring.
Besides posttraumatic stress symptoms, JR has few yellow flag indicators and seems to
have good self-efficacy and coping strategies.

Key physical examination findings

▪ Sensory testing: Tests of pressure pain thresholds revealed widespread
mechanical hyperalgesia. There was no evidence of thermal hyperalgesia.
▪ Neural examination: Neurodynamic testing of the upper limbs (median
biased) revealed marked bilateral elbow extension and pain provocation
(unfamiliar arm pain) with no relevant symptom modification with the
addition of sensitizing manoeuvres.
▪ Movement examination: There was a slight restriction overall in cervical
range of motion and a positive (L) C1–2 flexion rotation test. The manual
segmental examination determined joint dysfunction (palpable muscle
spasm and pain provocation) in the (L) C0–1, C1–2 and (R) C5–6
segments, as well as general thoracic hypomobility.
▪ Neuromuscular examination: JR performed poorly in the CCFT as well
as in the tests for the craniocervical and cervical extensors and right
middle and lower trapezius. JR demonstrated poor movement patterns
altered muscle activation and premature fatigue.
▪ Sensorimotor examination: Impaired performance was evident in tests of
joint position sense, trunk-head and eye-head coordination, balance, and
 gaze stability. The visual oculomotor screen identified an abnormal near
point of convergence (NPC) distance.

Diagnosis and clinical reasoning

JR’s responses to sensory and neurodynamic testing suggested the presence of sensory
hypersensitivity, which may be why previous high-load and general exercise approaches
exacerbated her symptoms and were counter-productive. This highlights the importance of
considering the potential for pain provocation when implementing and progressing
exercise programs and implementing a program of graduated return to physical activity
and work.
Differential tests supported the hypothesis of a cervicogenic basis of the daily headache
dizziness, and visual symptoms. The diagnosis of cervicogenic headache is supported by
the presence of a pattern of painful cervical (and thoracic) segmental joint dysfunction
(C1–2), decreased range of cervical motion and altered neuromuscular function. Poor
neuromuscular function appears to be relevant to the persistence of the disorder and
requires management. JR’s migraine exacerbation may have been triggered by the neck
injury; its response to management strategies for the neck will need to be monitored. A
neck trigger would be confirmed if migraines decrease as neck pain and dysfunction
improve.
Signs of altered cervical sensorimotor control were consistent with symptoms of
dizziness and visual disturbances. Treating sensorimotor deficits including NPC should
address any central vestibular oculomotor contributions to symptoms as management
methods for peripheral and central disturbances overlap. Prior treatment did not address
these specific sensorimotor impairments, which might contribute to her lack of recovery.

Overall management approach

JR required multimodal management as directed by the impairments found in the physical
examination in the articular, neuromuscular and sensorimotor systems. Advice and
education for graduated return to physical activity and full-time work were important
components of management. In addition, the psychologist’s contribution to JR’s stress
management and modulation was a vital part of management.
Specific physiotherapy management included manual therapy (without pain
provocation) to address pain and improve segmental motion. This was complimented with
active segmental exercises for C1/2 and the cervicothoracic region to capitalize on the
effect of manual therapy. These exercises were also included as part of the home program.
Extensive rehabilitation was undertaken to train neuromuscular control because the
physical examination revealed impaired function of flexors, extensors and right
axioscapular muscles. A comprehensive progressive training regime was undertaken (refer
to Chapter 15), which progressed from training appropriate patterns of muscle use to
challenging the muscle system with load. Training was undertaken over several weeks and
was monitored carefully to avoid pain exacerbation. It was altered at times to cope with
occasional relapses.
The impaired sensorimotor control found in the physical examination was addressed
with exercises to challenge (L) eye-head coordination and gaze stability, trunk head
coordination and tandem stance with eyes closed. As JR coped with these exercises, Joint
position error (JPE) training in (L) rotation, walking with head rotations and
flexion/extension as well as near-point convergence practice were added to the program
and progressed accordingly (refer to Chapter 16).
Graded physical activity was commenced early in the program with specific instructions
for the amount of activity. Over a 6-month period, JR progressed from walking, to water
running, to walk/run progressing to running and eventually returned to ballet. As JR’s
work requirements changed when she went to a new hospital ward, attention was given to
recognizing any foreseeable problems. Collaborating with JR on how to solve any issues
was important. Advice and education regarding stress management and mindfulness were
also provided as well as strategies for rescue management if pain exacerbation occurred.

Reflection and clinical message

The management of whiplash-associated disorders can be challenging with some patients
not recovering well. JR did achieve a good outcome when initially she was on a projection
for a poor outcome. The modification to exercise load, the addition of specific
interventions to address sensorimotor impairments, and a sensible graduated approach to
work and physical activity, were key aspects of the change in her path of recovery.
Following a 6-month period of management (10 treatment sessions), JR had returned to
full-time work with minimal neck pain and no headaches (NDI 10%). She self-manages
her neck pain and continues regular maintenance exercise.
JR’s presentation demonstrates the importance of avoiding pain exacerbation in the
presence of sensory hypersensitivity. This applies to all aspects of management, but in
JR’s case this particularly pertained to high-load exercises and general physical activity
that exacerbated her symptoms. Exercises for training cervical neuromuscular and
sensorimotor control were vital in JR’s case. They were directly relevant to her symptoms
and reduced capacity for physical function. A particular advantage of these programs is
that training commences with low-load exercises. All exercises were tailored and
progressed within JR’s capabilities and symptom tolerance. Nevertheless, graded physical
activity was included as early as possible. It was vital that a specific collaborative plan
was established with JR to progress a return to exercise and physical activity. Several
months of an appropriately paced program was required, which is not unlike a time-frame
for rehabilitation following for example, a major knee injury.
Different patients respond differently to physical rehabilitation. JR’s response to the
initial treatment (i.e., pain exacerbation) suggested that any further exercise and the return
to physical activity had be progressed and planned carefully. In addition, JR needed to be
equipped with the awareness, knowledge and strategies, to pre-empt and effectively self-
manage any potential relapses. This case is a prime example that warns against assuming
that a patient presenting with sensory hypersensitivity will not have a favourable outcome.
Rather an unfavourable response may be a reflection of a misdirected management
approach for that individual.

Case 4: Clinical reasoning in the physical examination

guides treatment decisions (Fig. 18.4)
This case presents a patient with neck pain and headache related to office work to
illustrate the importance of clinical reasoning in the physical examination to guide optimal
treatment, rather than delivering a standard protocol of care. Even though patients may
have a similar history and symptoms, slight variations in the findings of the physical
examination can significantly modify the treatment approach as will be illustrated in this
case presentation.

FIG. 18.4 Case 4: Body chart. VAS visual analogue scale; GH general health; MEDS
medications, INVEST investigations, P & N pins and needles.

Patient presentation
SJ is aged 22 years, and he presented with a 3-month history of insidious onset neck pain.
Occipital headaches began 1 month ago. He started work as a programmer 6 months ago
after finishing his degree in information technology. He likes his job and is working within
a good team to develop innovative applications. SJ has neck pain most days and it usually
comes on around midday. The neck pain increases in the afternoon and on days when it
gets quite bad, a headache develops on the same side. Recently, neck pain is coming on
earlier in the day.
SJ sits at work, uses a three-screen set-up and mainly works on the screen directly in
front. He admits that he tends to slump in his chair and usually has coffee breaks at his
desk. Turning his head hurts his neck especially when he uses the right screen for a
prolonged period. Neck pain generally eases with activity, although SJ admits he often
uses electronic devices in the evenings as well. He used to get an odd ache in the neck
when he was at university, but this is the first time his neck pain has really bothered him
consistently. He is otherwise in good health.

Clinical reasoning from the patient interview

SJ’s clinical presentation is consistent with a diagnosis of neck pain and cervicogenic
headache. The headache fulfils the main criteria for cervicogenic headache, it is unilateral,
without side shift, associated with ipsilateral neck pain, pain begins in the neck and
headache is aggravated by neck movement or neck postures.
Work postures and work habits are likely contributors to his condition. For all case
scenarios, education and training in better work postures and practices is an essential part
of management as is a discussion on his use of electronic devices in the evenings.

Scenario 1
Physical examination—key findings

▪ Postural assessment: When replicating his working sitting posture, SJ

slump sits in lumbopelvic flexion. His (R) scapula is downwardly rotated
and anteriorly tilted. Movement to test for the effect of posture correction:
(R) rotation, restricted to 50 degrees with neck pain (3/10).

Facilitation of a corrected spinal posture increased (R) rotation to 75 degrees with a

concurrent reduction in neck pain (1/10). The addition of scapular posture correction
resulted in no further changes in range of motion (i.e., remains 75 degrees) but it
completely eliminated the pain (0/10).

▪ Articular system: Active cervical movements are painful and limited;

extension 20 degrees; (R) lateral flexion (little head tilt) 30 degrees; and
(R) rotation 50 degrees resulting in neck pain of 3/10. Upper cervical
flexion and extension are unremarkable. The flexion-rotation test revealed
normal mobility of (L) C1–2 rotation with (R) C1–2 rotation limited to 35
degrees (slightly hypomobile).

Manual examination added further confirmation, Passive accessory intervertebral

movements (PPIVMs), C1–2, moderately hypomobile and PAIVMs, C1/2 moderately
hypomobile with pain provocation (6/10). Tests of adjacent joints/regions
(temporomandibular joint (TMJ); shoulder) were unremarkable.

▪ Neural system: No abnormality detected.

▪ Tests of muscle function: A poor retraction pattern of motion was noted
during the CCFT. SJ could not extend beyond neutral during the cervical
 extension test and fatigued within 5 repetitions. Craniocervical extension
and rotation muscle tests were unremarkable. Scapular holding tests
revealed marked endurance deficits of the trapezius muscles with notable
incapacity to sustain the test position for greater than 3 repetitions of 5
second holds. Reassessment of C1–2 PAIVMs (slight hypomobility, pain
1/10) immediately following the test revealed a notable improvement,
despite a poor test performance.
▪ Sensorimotor function: No abnormality detected.

Clinical reasoning for diagnosis

The physical examination confirmed the pattern for cervicogenic headache (reduced
motion, upper cervical joint signs, reduced cervical muscle function) and substantiates the
diagnosis of cervicogenic headache.

Clinical reasoning for the initial treatment approach

The physical examination suggests that adverse strains from posture and attendant muscle
loading are major provocative factors of the neck pain because correction of spinal and
scapular posture significantly reduced neck pain and improved range of movement. In
addition, reassessment of C1–2 PAIVMs following the scapular holding test significantly
changed (but did not eliminate) joint signs and pain. The test targeting lower trapezius
encourages reciprocal relaxation of the scapular elevators, suggesting that adverse muscle
forces have a major role in aggravating the joint. Muscle tests indicated very poor
neuromuscular control.
Based on these findings, it was hypothesized that poor posture and muscle function
were the primary drivers of the condition. Thus management will have a strong focus on
facilitating and reeducating correct sitting and working postures and neuromuscular
training (cervical flexors [pattern initially], extensors and axioscapular muscles) to both
help alleviate this episode of neck pain as well as prevent it reoccurring. It could be
reasoned that the painful C1–2 joint dysfunction is a secondary consequence. Although
manipulative therapy may have a role to address any residual joint dysfunction (depending
on subsequent reassessment findings), its role is lesser than that of reeducating sitting,
working postures and neuromuscular training.

Scenario 2
Physical examination
The patient has similar findings in the physical examination but there are some key
differences from Scenario 1. The same findings are presented, and differences are
highlighted and inform a different management focus for this patient.

Physical examination
 ▪ Postural assessment: When replicating his working sitting posture, SJ
slump sits in lumbopelvic flexion. His (R) scapula is downwardly rotated
and anteriorly tilted. Movement to test for the effect of posture correction:
(R) rotation, restricted to 50 degrees with neck pain (3/10).
Neither correction of spinal posture or scapular posture resulted
in changes in (R) rotation range or pain response
▪ Articular system: Active cervical movements are painful and limited;
extension 20 degrees; (R) lateral flexion (little head tilt) 30 degrees; and
(R) rotation 50 degrees resulting in neck pain of 3/10. Upper cervical
flexion and extension are unremarkable. The flexion-rotation test revealed
normal mobility of (L) C1–2 rotation with (R) C1–2 rotation limited to 25
degrees (moderately hypomobile).
Manual examination added further confirmation, PPIVMs, C1–2,
moderately hypomobile and PAIVMs, C1/2 moderately
hypomobile with pain provocation (6/10). Tests of adjacent
joints/regions (TMJ; shoulder) were unremarkable.
▪ Neural system: No abnormality detected.
▪ Tests of muscle function: A poor retraction pattern of motion was noted
during the CCFT. SJ could not extend beyond neutral during the cervical
extension test and fatigued within 5 repetitions. Craniocervical extension
was unremarkable. Rotation muscle tests revealed a poor ability to
perform C1–2 rotation, which improved with facilitation. Scapular
holding tests revealed marked endurance deficits of the trapezius muscles
with notable incapacity to sustain the test position for greater than 3
repetitions of 5 second holds. Reassessment of C1–2 PAIVMs following
the scapula hold test revealed little change (moderate hypomobility, pain
(5/10).
▪ Sensorimotor function: No abnormality detected.

Clinical reasoning for the initial treatment approach

Although the basic findings of the examination are similar in this scenario, an important
difference was that strategies that may relieve joint and muscle loading (facilitating the
neutral posture, placing the scapula in a neutral position and the effects of the scapular
muscle test on manual examination of C1–2) had little effect on neck movement and pain.
It could therefore be reasoned that C1–2 joint dysfunction is the primary problem. The
poor ability to rotate in the craniocervical rotation test, and the improvement with
facilitation suggests an element of poor joint proprioception at the C1–2 joint which
supports the hypothesis of articular dysfunction.
Based on these findings, it was hypothesized that articular dysfunction at C1–2 was a
stronger feature than in scenario 1, and more emphasis on manipulative therapy was
needed to address this joint dysfunction. Active segmental exercises and exercises to
improve C1–2 movement sense were included to augment the effects of manipulative
therapy. The neuromuscular findings were still very relevant, but attention to them alone
may not result in as rapid recovery if not undertaken in conjunction with techniques to
address the C1–2 joint dysfunction.

Scenario 3
Physical examination
Again, the patient has similar findings in the physical examination but there are some key
differences from Scenario 2. They are highlighted and inform yet another different
management focus for this patient.

▪ Postural assessment: When replicating his working sitting posture, SJ

slump sits in lumbopelvic flexion. His (R) scapula is downwardly rotated
and anteriorly tilted. Movement to test for the effect of posture correction:
(R) rotation, restricted to 50 degrees with neck pain (3/10).
Neither correction of spinal posture or scapular posture resulted in
changes in (R) rotation range or pain response
▪ Articular system: Active cervical movements are painful and limited;
extension 20 degrees; (R) lateral flexion (little head tilt) 30 degrees; and
(R) rotation 50 degrees resulting in neck pain of 3/10. Upper cervical
flexion reproduces a pulling feeling in the neck. Upper cervical
extension is unremarkable. The flexion-rotation test revealed normal
mobility of (L) C1–2 rotation with (R) C1–2 rotation limited to 25 degrees
(moderately hypomobile).
Manual examination added further confirmation, PPIVMs, C1–2,
moderately hypomobile and PAIVMs, C1/2 moderately
hypomobile with pain provocation (6/10). Tests of adjacent
joints/regions (TMJ; shoulder) were unremarkable.
▪ Neural system: Upper cervical flexion with the addition of a straight
leg raise reproduced neck pain and headache.
▪ Tests of muscle function: The CCFT was not performed because of
these positive signs of neural mechanosensitivity specific to upper
cervical flexion. SJ could not extend beyond neutral during the cervical
extension test and fatigued within 5 repetitions. Craniocervical extension
was unremarkable. Rotation muscle tests revealed a poor ability to
perform C1–2 rotation, which improved with facilitation. Scapular
holding tests revealed marked endurance deficits of the trapezius muscles
with notable incapacity to sustain the test position for greater than 3
 repetitions of 5 second holds. Reassessment of C1–2 PAIVMs following
the scapula hold test revealed little change (moderate hypomobility, pain
(5/10).
▪ Sensorimotor function: No abnormality detected.

Clinical reasoning for the initial treatment approach

Despite similar basic findings of the examination in this scenario compared with scenario
2, the important variable is the positive response to the test of neural mechanosensitivity.
Attention to neural tissue mechanosensitivity takes priority. Despite the importance of
rehabilitating neuromuscular control, exercises for the craniocervical flexors at least must
be delayed or modified as the training movement stands to provoke the
mechanosensitivity. Thus based on the examination findings, treatment in this case will be
directed initially to resolve the neural mechanosensitivity. This may be achieved with a
combination of manual therapy to address an interface possibly contributing to the
sensitivity (i.e., the C1–2 joint arthropathy) and gentle active mobilizing exercise for the
neural structures (sliding exercises).

Case 5: Neck pain associated with neuropathy (Fig.

18.5)
Identifying the presence and nature of neuropathy in neck pain disorders relies on a
comprehensive structural differential examination that will subsequently guide
management approaches. The most appropriate and safe course of conservative care
depends on determining the relative presence of signs of nerve conduction and nerve
mechanosensitivity. The following case describes a patient with cervical radiculopathy
with dominant features of neural mechanosensitivity that directly guided a successful
management approach.

FIG. 18.5 Case 5: Body chart. GH general health; MEDS medications, INVEST
investigations, MRI magnetic resonance imaging.
Patient presentation and key examination findings
JL, a 46-year-old male, presented with discomfort on the right side of the neck and
shoulder girdle accompanied by pain and paraesthesia in the right arm extending down to
the lateral forearm and hand, particularly his fingers and thumb. These symptoms had
been present for 3 weeks. Although no single event or incident could be recalled, JL
suspected he had strained his neck while lifting heavy customer travel bags off the
conveyer belt during his work as an international airline customer service officer. He
reported that more recently, he would spend up to 5-hour shifts checking in bags, 4 to 5
days a week. JL reported that lifting heavy bags (with a tendency to use his dominant right
arm) off the conveyer belt would often result in neck tightness. However, over the past 3
weeks, this had progressed to a discomfort in his neck and progressive symptoms into the
right upper limb. His general medical practitioner had arranged a magnetic resonance
imaging that revealed moderate levels of degenerative change including lateral stenosis at
the C5–6 level on the right.

Examination findings strongly indicating neural

mechanosensitivity
JL’s main aggravating activity was elevation of the right upper limb. When replicated in
the clinic, this reproduced the upper limb symptoms and feelings of strain to the neck.
These symptoms were magnified if arm elevation was performed with the wrist and hand
in extension suggesting neural mechanosensitivity. Structural differentiation during
neurodynamic tests further implicated neural tissue mechanosensitivity. Familiar
symptoms were reproduced during the median nerve biased neurodynamic test in a
combined position of right shoulder abduction/external rotation/80-degree elbow flexion,
with symptoms able to be altered (increased/reduced) with either the addition of
sensitizing movements of the wrist (wrist extension/flexion) or cervical spine (lateral
flexion left/right), respectively. The clinical neurological examination (for nerve
conduction) revealed normal muscle strength and reflexes, and mild reduction in sensation
to light touch (7/10) in the right C6 dermatome.
The patient had also reported some discomfort with right cervical rotation. When
examined, this movement reproduced familiar discomfort locally at the neck only.
Cervical extension was also mildly restricted and when combined with right lateral flexion
reproduced neck pain and very mild arm symptoms. Manual examination revealed the
presence of protective muscle spasm and mild segmental reduction in mobility evident on
examination of (R) lateral flexion of C5–6. Cervical lateral glides directed at C5–6 were
markedly restricted to the left (protective muscle spasm) when the (R) upper limb was
prepositioned in the neural provoking position (shoulder abduction and external rotation),
compared with when lateral glides were applied to the right with the left arm in the same
posture.

Other relevant examination findings

In relaxed standing, the patient demonstrated downwardly rotated and protracted shoulder
blades bilaterally, especially on the right side. This scapular posture on the right was
magnified when arm elevation was lightly resisted. Examination of the craniocervical
flexors (CCFT 26 mmHg) revealed a fair to good performance in the test whereas the
cervical flexors and extensors revealed premature fatigue during the head lift test and
cervical extensor test, respectively. Poor patterns of movement were observed after 3 to 4
repetitions of the tests, which worsened with further repetitions. These scapular and
cervical muscle test findings were considered relevant to the pathomechanics of the
disorder, potentially indicating suboptimal physical support to the cervical spine and
brachial plexus structures at the neck when lifting. This thought process was further
supported when manual elevation of the shoulder girdle to a more neutral posture relieved
feelings of tension at the neck. A general lack of thoracic spine extension and rotation was
noted which was of potential relevance to both scapular function and mobility demands at
the lower neck. There were no apparent impairments of the glenohumeral joint or rotator
cuff muscles.

Diagnosis and clinical reasoning

A diagnosis was made of a C6 radiculopathy associated with a strain of the right C5–6
motion segment. Examination findings suggested a predominant pattern of neural
mechanosensitivity to motion (very positive neurodynamic tests including structural
differentiation). Although there was some evidence of nerve conduction deficits (sensory
changes) these were mild. The observed radiologic stenosis was probably present and
asymptomatic before the injury, therefore it was considered a relevant finding. In
particular, the presence of a degenerative stenosis may have increased the risk of
developing a neuropathy when combined with the injury induced perineural inflammation.

Management approach
Advice and education
The patient had initially expressed concern regarding his “pinched nerve”. Time was
devoted initially to reassure JL that this was a completely reversible condition that would
cease once the inflammation had resolved and pain-free motion restored. An emphasis was
therefore placed on modifying any factors that were aggravating to the condition. In
particular, this included the organization of suitable duties for a period in his workplace
that did not involve lifting heavy bags.
Although the resolution of neural inflammation was the short-term goal of management,
the patient was also advised that the long-term management would incorporate specific
training of neuromuscular function of his shoulder girdle, neck and thorax to optimize the
physical support of the neck and brachial plexus to prevent recurrence.

Manipulative therapy
Manual therapy targeted the restoration of a pain-free cervical lateral glide in progressive
pre-set positions of the neurodynamic test position. This was targeted because it was the
most substantial and relevant finding during the physical examination. Treatment was
enhanced by the performance of daily neural sliding exercises. Diligent reassessment
showed this approach to have positive effects on both the neural mechanosensitivity and
cervical movement signs.

Exercise therapy
Exercise initially focused on the correction of habitual scapular posture (corrected towards
upward rotation and retraction) incorporating the use of memory joggers and strapping
tape. To train the capacity to lift baggage at work with minimal strain to the neck, specific
daily strengthening of his scapular upward rotators using progressive resisted shrugging
exercises were also commenced immediately. In subsequent sessions, this was combined
with lifting practice specific to JL’s work duties (i.e., removing baggage from the conveyer
belt—arm in low-elevation position and controlling shoulder girdle and neck orientation
under load) with progressive increase in load as able. Progressive resistance exercises with
an emphasis on movement control for the cervical flexors and extensors were incorporated
to foster optimal physical support of his neck particularly in light of the physical demands
of his work. At discharge, the patient was encouraged to continue shoulder girdle and neck
strengthening exercises 3 times a week as a maintenance program.
Initially, the exercise program also included thoracic mobility exercises (thoracic
rotation and extension) and neural mobilization exercises (neural sliding—elbow
flexion/extension in wrist extension in progressive shoulder elevation) 3 times daily. As no
residual signs of neural mechanosensitivity were evident at discharge, neural mobilizing
exercises were ceased and JL was encouraged to continue the thoracic mobility exercises
as a work break for maintenance purposes.

Reflection and clinical message

Not all cervical pain disorders associated with neuropathy are the same and this case
featured predominant signs of nerve mechanosensitivity that guided the management
approach. If the presentation had implicated nerve conduction deficits, the management
approach would have differed. In this case, the single mild sign of nerve conduction deficit
(reduced sensation) resolved quickly with intervention. Neural mechanosensitivity
progressively resolved over an 8-week period (mostly in the first 3–4 weeks) with milder
fluctuating residual symptoms experienced over the last 4 weeks associated with the
progressive return to normal work duties including lifting bags. Collaborative reasoning
with the patient concerning the fluctuations in recovery associated with his progressive
return to lifting over this final 4 weeks was paramount. This was particularly so because it
reinforced to him the importance of the work-specific neuromuscular conditioning
element of the management approach, which permitted his return to normal work duties
while maintaining a healthy neck-nerve status.

Conclusion
Clinical practice is not an exact science and at present, research evidence although very
informative, can only guide management approaches. As such best practice relies on a
collaborative effort incorporating the perspectives of the patient, the clinical expertise of
the therapist and the scientific evidence. With conservative care, the majority of patients
with neck pain will gain some to complete relief of symptoms, gain improved function and
acquire knowledge and strategies to self-manage their necks. Such patients have been
presented in this chapter. Nevertheless, there are limitations to the benefits that
conservative therapies can achieve, particularly for those patients who have very high pain
states, severe or advanced pathology or neuropathic pain states. In these cases,
multiprofessional management is required which includes adequate pharmacotherapeutics
for pain relief, which might help facilitate rehabilitation. In some cases, interventional
management may prove to be a suitable option. However, conservative management is the
first treatment of choice.
19

Concluding Remarks

Focusing on Prevention
There would be little argument against a claim that knowledge has increased substantially
over the last decade in the basic and clinical sciences pertinent to neck pain disorders. Yet
during this same time, the burden of neck pain has increased worldwide.1 Systematic
reviews report that effect sizes of benefits for various interventions in the management of
neck pain remain relatively small whether interventions are medical, educational, physical
or psychological. The contrast between increasing knowledge yet increasing burden and
lack of major change in treatment outcomes encourages thought about directions for future
research (and its design) and health care practice.
The rate of increase in the burden of neck pain has been quite rapid. Its incidence
globally, rose by 21% between 2005 and 2015, and in terms of the metric of years lived
with a disability, neck pain ranked 4th of 301 chronic conditions in 2013, but rose to 1st of
310 chronic conditions by 2015, together with low-back pain.1,2 Several factors
undoubtedly contribute to this escalating problem. The ageing population is one factor.
Even though ageing may not cause osteoarthritis, the frequency of osteoarthritis increases
with age. The incidence of osteoarthritis increased by 33% in the last 10 years, which
might, in part, account for the increase in neck pain.1 Another factor impacting negatively
on the neck is the technology revolution, which is transforming both the world of work
and lifestyle. Workplaces have become more computerized and more sedentary across a
spectrum of occupations. Computer work has been linked with the development of neck
pain.3–6 Lifestyles are incorporating increasing use of various electronic devices and
applications for communication, education and entertainment with the net result of more
sedentary lifestyles outside work. Of most concern, is that this change in lifestyle is
beginning in early childhood. This was well illustrated by Howie et al.7 who measured the
body movements of children from 3 to 5 years of age while they played games on tablet
computers, watched television or played with toys. Compared with the other two
conditions, playing with the tablet computer was linked with more neck and thoracic
flexion, lesser postural variation, more time sitting and less physical activity—a potential
recipe for the development of neck pain and other health concerns. A focus on prevention
at primary, secondary and tertiary level is crucial.

Prevention
The adage that prevention is better than cure is certainly an aim to strive for, even though
it may be idealistic. Neck pain is unlikely to ever be eliminated as, in the first instance,
age is a non-modifiable factor and it would impossible to eliminate all trauma.
Nevertheless, many adverse lifestyle, personal and work-related behaviours that may
underlie neck pain are modifiable. The concept of prevention is not new, but systematic
reviews suggest current workplace prevention and intervention programs are not providing
the answers.8 Further creative work in primary, secondary and tertiary prevention are key
and critical to reduce the burden of neck pain.

Primary prevention
Primary prevention is an urgent area of need. New and inventive approaches are required
to influence all people across their lifespan. At the current time, there is no effective,
evidence-base primary public health prevention program for neck pain, despite the internet
being full of advice from diverse perspectives. The desired endpoint is evidence-based
primary prevention programs, but in the first instance research informed programs must be
created, developed and tested. The development of a fresh and forward-thinking primary
prevention strategy could be an initiative of a collaboration between international leaders
in neck pain representing all relevant parties from the health sector and community. Such a
strategy might consist of concerted, multiple and coordinated levels of educational and
effective practical interventions. The world’s connectivity via the internet could support a
major international public health campaign, with targeted information on healthy work and
lifestyle habits and a few simple, yet effective preventative active strategies for posture,
muscles and movement that could easily be incorporated into the daily routines of all age
groups, from children and their parents through to the aged. Any such internet campaign
would need to be supplemented with work on the ground at all levels—in schools, in
training colleges and universities9 (where students need to learn not only about the nature
of their chosen work but how to perform it safely from the perspective of their own
neck/musculoskeletal health), in workplaces, as well as applications relevant to everyday
life activities for all ages. Consistent education locally reinforces the global public health
program and caters to local cultural, personal,10 work and activity variables.

Secondary prevention
Recent decades have witnessed a focus on patient-centred care that is fully supported. This
focus is evident in randomized controlled trials (RCT) and systematic reviews where the
primary outcome is usually a patient self-rated, numerical measure of neck pain or a rating
on a questionnaire of neck pain and disability. This focus on pain seems to have lessened
the emphasis on rehabilitation to restore normal neuromuscular and sensorimotor function
to reestablish safe function after an episode of neck pain. Exercise programs are frequently
trialled in the management of neck pain, but the primary outcome of interest is pain relief,
not measures of the exercise effects on muscle or other physical functions.
Patients desire pain relief; it is frequently their primary goal. Neck pain is a recurrent
disorder. It could be argued that an equally vital patient-centred outcome is to prevent
recurrent episodes of pain. Yet the current model of care is principally concerned with
relieving the presenting episode of neck pain, not on physical and functional rehabilitation
towards lessening recurrence rates. Many personal and environmental factors are likely to
contribute to neck pain recurrence. It would be naïve to suggest that rehabilitation of good
posture, movement and neuromuscular and sensorimotor control will provide the complete
answer for prevention of recurrence. Likewise, it is naïve to continue a very narrow focus
on management of current pain only and to pay no attention to whether physical function
has been restored towards addressing the real burden, which is the recurrent episodes of
pain.
There is always pressure to contain and even lessen costs of care and provide minimal
intervention. Controlling costs is understandable—but is this false economy? The costs are
not in a single episode of neck pain, they are in the costs of repeated episodes of neck
pain, the costs of repeated demands on health care, the costs on productivity of
absenteeism and presenteeism, the costs of harm (e.g., opioid addiction, side effects of
nonsteroidal antiinflammatory drugs), as well as the personal costs in quality of life.
Reflection and reappraisal on several fronts is necessary towards providing appropriate
treatment and secondary prevention for a presenting episode of neck pain. Three points are
presented for thought and discussion.

Defining the desired outcomes of exercise prescription.

Exercise has many different modes, physiological responses and benefits. It is important to
clearly define what outcomes are being sought from the exercise intervention to direct
both clinical practice and research. Take the example of two RCTs both of which are
testing the intervention of a resistance training program. RCT 1 has the primary outcome
of decreasing neck pain whereas the primary outcome of RCT 2 is to increase muscle
strength to meet a patient’s functional demand. The outcomes in these trials are
underpinned by different neuroscience and physiological rationales and mechanisms of
effect. It could be expected that the nature and dosage of a resistance training program for
achieving a hypoalgesic effect without concern for changes in motor output would be
quite different to a program for increasing cervical muscle strength. This example casts
doubt on the wisdom of prescription of exercise without careful consideration of the
desired outcome. Furthermore, several studies have already shown that quite specific
modes of exercise are required to improve different cervical muscle behaviours and motor
outputs and address sensorimotor deficits in patients with neck pain disorders.11–15 More
work regarding the physiological effects of various exercise modes and matching exercise
with specific outcomes of interest is required to ensure we develop optimal exercise
protocols for secondary prevention programs.

Prescribing appropriate exercise dosage.

Dosages to achieve the desired outcomes of an exercise intervention have not been
researched to any great extent in relation to neck pain disorders. It could be expected that
different exercise applications and dosage would be required if the primary outcome is to
modulate pain, versus it being to reach a certain level of muscle function. Unlike
rehabilitation protocols for many extremity disorders, there is little information on dosage
requirements to successfully address altered motor and sensorimotor behaviours in neck
pain conditions. The diverse times used in RCTs to test various interventions suggest that
dosage prescription in many cases is not scientifically based but rather is an arbitrary
choice. Dosages of exercise to achieve an effect will vary between individuals but urgent
areas of research are to determine if (1) all neuromuscular and sensorimotor impairments
can be restored to a “normative” status and (2) the average exercise dosage (e.g.,
frequency, intensity, duration) to achieve a normative or satisfactory status. Once
guidelines for dosage are established, RCTs can be conducted to determine the impact of a
full rehabilitation program on recurrence rates. The evidence suggests that a progressive
multimodal exercise program is required that is tailored to the individual patient (see
Chapters 15 and 16).

Adequate treatment of the presenting episode of neck pain.

Time to manage and settle the neck pain and to fully rehabilitate an individual who has
suffered an episode of neck pain will vary greatly between different persons and different
neck pain disorders. Judging by the time allowed for rehabilitation protocols for disorders
of the extremities, rehabilitation programs may range from a few weeks to 3 or even 6
months for some individuals. Pain will usually settle well within that time. Facilitating
understanding that pain relief alone may be an inadequate outcome in the context of
prevention of recurrence will require a change in mind set of health care providers,
patients and funding bodies alike. Treatment may be over a prolonged period, but much
will be within the context of self-management. Thus the number of occasions of care and
costs of management of the episode of neck pain do not have to increase greatly. However,
essential to success is consistent interest in and support of the patient, monitoring of
adherence, evaluation of performance and progression of the program (see Chapters 15
and 16).

Tertiary prevention
A percentage of patients have persistent neck pain as a result of trauma, degenerative
conditions or of undetermined aetiology. Tertiary prevention aims to assist the person
manage the impact of their ongoing neck pain in order to maintain their function and
quality of life. Tertiary prevention is topical with the ageing population and the increase in
incidence of osteoarthritis and requires particular attention in practice and research.
Tertiary prevention will include major components of self-management. Nevertheless,
self-management does not mean “no” management from a health care provider. Provision
of personnel resources or a clinical review intermittently can have positive benefits. The
effects of booster sessions or occasional provision of treatment needs further investigation.
Because a person is older and has persistent pain does not negate good outcomes from
conservative management as was illustrated in a recent RCT evaluating the effectiveness
of manual therapy and specific exercises for seniors with chronic neck pain and
headaches.16
Tertiary management for some patients with persistent neck pain can be challenging to
all health professionals. These include the relatively small cohort of patients who have a
poor recovery following a whiplash injury (10%–15% of those seeking care).17,18 Effective
secondary and tertiary management of this group remains rather illusive. Likewise,
patients who develop neuralgias in association with spondylitic changes remain a
challenge. Patients in these categories sometimes require interventional management such
as radiofrequency neurotomies albeit pain relief when attained is usually temporary.

Conclusion
Prevention at all levels is an important aim of practice. Outcomes at all levels of
prevention have to be enhanced if the burden of neck pain is to be lessened. The
effectiveness (effect sizes) of various interventions have to be improved. This is
challenging because even though RCTs remain the gold standard, they have limitations for
translation to clinical practice. Population mean outcomes of RCTs do not reflect an
individual patient’s needs and responses. Effect sizes reflect the average response to an
intervention, and often suffer a wash out effect. Participants who actually benefit from the
intervention trialled in the RCT are usually not identified. From another perspective, many
RCTs test the effect of a single modality. This does not reflect real life practice where
multimodal management is provided on an individual basis. Thus RCTs miss the
cumulative and potentially interacting effects of a treatment program. All fault does not lie
in the RCT design. Further research is needed to improve diagnostics and interventions.
Indications for certain management methods need to be clearly defined in future
research and practice. For instance, despite the long history of use of manipulative
therapy, there is a lack of international/interdisciplinary consensus on clear indications for
its use.19 It is possible that the common indications of impaired neck movement and
associated symptomatic segmental joint dysfunction are appropriate. Clinicians may
intuitively recognize associations between treatment and effects, but there needs to be an
empirical demonstration that manipulative therapy does resolve symptomatic segmental
joint dysfunction and restores impaired neck movement and that these changes are
associated with relief of symptoms.19 Clinical examination methods are the cornerstone to
guide management of neck pain disorders. Clinical tests are proving to have diagnostic
validity in identifying segmental sources of pain.20,21 Further research into diagnostics is
required in several areas. For instance, differential diagnosis of headache, visual
disturbances, dizziness, light headedness and unsteadiness from the perspective of a
cervical musculoskeletal cause or contributor is necessary to identify patients who will
benefit from management of cervical spine
There is always room for improved application of current interventions whether in
prescribing accurate dosages or improving ways to help clinicians develop high-level
therapeutic skills to deliver the intervention. Research will lead to the development of new
interventions and these may intervene at the periphery or directly on the central nervous
system.22 Neck pain will never be successfully managed by monotherapy. To further the
understanding of mechanisms and capabilities of both current and new treatments, it is
essential to assess their effect on outcomes representing relevant components within and
across domains of the biopsychosocial model. This will improve knowledge about what an
intervention can and cannot achieve, which will contribute to the development of best
practice multimodal and multiprofessional programs.
Progressive experimentation both in the clinic as well as the laboratory will inform on
best combinations of multimodal approaches towards optimal management of persons
with neck pain disorders. There has been a rapid increase in knowledge in the last 2
decades in particular and with that foundation, the next decade promises more significant
advances.

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Index
Page numbers followed by “f” indicate figures, “t” indicate tables, and “b” indicate boxes.
A
Aδ fibres, 18
Acoustic neuroma, 152
Active exercise, 195–196
range of motion in, 195–196, 196f
for training movement velocity and accuracy, 196, 197f

Adrenomedullary hormonal system (AHS), 23

Adult cervical motion segment, 31
Advice
in directionally biased persistent neck pain, 242–243
in neck pain associated with neuropathy, 254

Ageing, neck pain and, 257

Allodynia, 18, 21–22
Anatomy, education in, 184
Ankylosing spondylitis, 126
Anterior scalene muscle, 52
Anterolateral system, 18
Anxiety, 24
as “apprehension”, 182
in neck pain disorders, 88
pain perception and, 24

Articular system
cervical musculoskeletal dysfunction and, 163–164
headache in, 245

Assessment
of cardinal planes of motion, 116–121
cervical and craniocervical motion, 117–118
in cervicothoracic region, 119
 movement diagnostic tests for, 120
movement speed and velocity profile in, 118–119
movement tests for, 119–120
for vertebral artery insufficiency, 120–121

of neuromuscular system, 128–135

cervical extensor muscle tests for, 132–134
cervical extensors for, 134–135, 134f
cervical flexor strength and endurance for, 132
craniocervical flexion test for, 130–132
scapular muscle tests for, 128–130

oculomotor, 138
eye follow, 138, 139f, 139t
eye-head coordination, 138–139, 139f
gaze stability, 138, 138f
trunk-head coordination, 138–139, 140f, Physical examination

Atlanto-axial (C1-2) articulation, 30

Atlanto-occipital (C0-1) articulation, 30
Axioscapular muscle, 32–33
activation and endurance of, 206–212
length tests, 130

B
Balance training, static, 227
Behavioural strategies, education and, 184–185
Benign paroxysmal positional vertigo (BPPV), 151–152, 155t
Biomechanics, education in, 184
Biopsychosocial model, of neck pain disorders, 4–5, 5f, 173
Booster sessions, in neck pain prevention, 259
Brachial neuropraxia, 42–43
Brain injury, minor, dizziness and, 151
C
C fibres, 18
Cardinal planes of motion, assessment of, 116–121
cervical and craniocervical, 117–118
cervicothoracic region, 119
movement diagnostic tests for, 120
movement speed and velocity profile in, 118–119
movement tests for, 119–120
for vertebral artery insufficiency, 120–121

Case presentation, 241–255

Catastrophization, in neck pain disorders, 88
Catechol O-methyltransferase (COMT) gene, 23–24
CBT, Cognitive behaviour therapy
Central connections, 71, 72f, 73b
Central neuropathic pain, 20
Central sensitization, 21–22, 23f
Central vestibular disorders, 150–152, 155t
Cervical afferent input, altered
causes of, 73–74, 74b, 74t
cervical dizziness and, 149–150

Cervical afferents, 71
Cervical artery dissection (CAD), 120–121, 150–151
Cervical cord, 45
Cervical dizziness, 149–150, 155t
Cervical dystonia, 103
Cervical extension, 117–118, 117f
Cervical extensor, 134–135, 134f
muscle tests, 132–134
strength and endurance of, 135
training, 208–210

Cervical flexion rotation test, 120

Cervical flexor
activation and endurance of, 206–208
muscle control and coordination of, 212–213, 212f
strength and endurance of, 132

Cervical force sense, disturbances in, 75

Cervical joint position sense, 75
exercise for, 223–224

Cervical lateral glide mobilization, 234, 234f

Cervical lordosis, 29
Cervical motion
analysis of, 116
assessment of, 117–118

Cervical movement sense

 assessment of, 136, 136f
exercise for, 224–225, 224f

Cervical musculoskeletal dysfunction, 161–170

articular system and, 163–164
definition of, 163–165
in headache, clinical decisions for, 165–166, 166f
in neural system, 165
in neuromuscular system, 164
posture and, 164–165
sensorimotor dysfunction and, 165

Cervical musculoskeletal examination, in sensorimotor control disturbances, 153

Cervical myelopathy, degenerative, 44–45
Cervical nerve mechanosensitivity, manual therapy for, 234–235
Cervical position sense, 135–136, 136f
Cervical posteroanterior glides, 128–129
Cervical proprioception
assessment of, 135–136
disturbances in, 75–76

Cervical radiculopathy, 45–46

manual techniques for, 235
neuropathic pain in, 20
Spurling’s test for, 120

Cervical region
movements of, 31, 31f
neck pain and, 4
relationships to adjacent regions, 32–34

Cervical segments (C2-7)

manual examination of, 120, 123–125, 124f–125f
movements in, 31

Cervical sensorimotor control, altered

signs of, 74–78, 79b
cervical proprioception as, 75–76
coordination as, 78
eye movement control as, 77–78
postural stability as, 76–77
symptoms of, 74

Cervical sensorimotor examination, in sensorimotor control disturbances, 156

Cervical somatosensory input, artificial disturbance to, 73
Cervical spine
movement of, 29–32
disturbances in neck pain disorders, 35
performance, 35–36
psychological considerations, 36
neck pain and, 4
nerve conditions related to, 44–46
posture in, 29
neck pain disorders and, 34–36

relationships to adjacent regions, 32–34, 34f

craniomandibular region and, 33–34
shoulder girdle, 32–33
thorax, 29
upper limb, 32–33, 34f

Cervical traction, 8
Cervical vascular disorders, 150–151
Cervicobrachial disorders, 45–46
Cervico-collic reflex (CCR), 72
Cervicogenic headache
diagnosis of, 164
history of, 163
neck pain and, 162–163

Cervico-ocular reflex (COR), 72

Cervicothoracic junction, 29
Cervicothoracic region
assessment of, 119
extension, 119
movements of, 31, 31f, 33f

Chronic pain, 7, 17
Chronic pain syndrome, 7
Clinical decision making, 241–255
Clinical neurological examination, 121–122
Clinical practice guidelines (CPGs), 174–175
Clinical prediction rules (CPRs), 175
defining neck pain by, 8

Clinical reasoning, 101, 241–255

in directionally biased persistent neck pain, 242
in headache, 245–246
 in neck pain associated with neuropathy, 254
from patient interview, 250
in physical examination, guiding treatment decisions, 249–252, 249f
in whiplash injury, 247

Cognitive behaviour therapy, 184–185

Cold hyperalgesia, 20
Communication, 181–187
language and, 182–183
listening and, 181–182
through touch, 182–183

Computer work, neck pain and, 257

Coordination
changes in, between muscles, 54–57, 54f, 56f–57f
disturbances in, 78

CPRs, Clinical prediction rules

Craniocervical extension, 118
Craniocervical extensor, 209
Craniocervical flexion, 32f
Craniocervical flexion test (CCFT), 130–132, 164, 206, 207f–208f
formal test procedure of, 131–132
preparation for, 130, 131f

Craniocervical motion
assessment of, 117–118
training for, 207, 207f

Craniocervical region, movements of, 30, 31f

Craniocervical rotators, 209, 209f
Craniomandibular region, cervical spine and, 33–34
C-reactive protein (CRP), 21
D
Deep cervical extensors, 209–210, 210f
Deep cervical muscles
activation and endurance of, 206–212
training for, 207–208, 208f

Degenerative cervical myelopathy, 44–45

Depression
 chronic pain and, 24
in neck pain disorders, 88

Directionally biased persistent neck pain, 241–243, 242f

advice and education in, 242–243
diagnosis and clinical reasoning in, 242
exercise therapy for, 243
management approach in, 242–243
patient presentation and key examination findings in, 241–242
reflection and clinical message for, 243
reported aggravating factors and functional examination in, 241–242

Dizziness
clinical examination of, 152–157
history and interview in, 153
physical assessment in, 153–157
symptom differentiation in, 153, 155t
differential diagnosis of, 149–152
acoustic neuroma as, 152
benign paroxysmal positional vertigo as, 151–152
central vestibular disorders as, 150–152
cervical vascular disorders as, 150–151
labyrinthitis as, 152
Ménière disease as, 152
minor brain injury as, 151
perilymph fistula as, 152
peripheral vestibular lesions as, 151
vestibular migraine as, 151
vestibular neuronitis as, 152

manipulative therapy for, 191

in neck pain disorders, 104

Double crush syndrome, 42

Down syndrome, 126
Dynamic Gait Index, 137–138
Dynamic tasks, disturbances in, 77
Dynamometry, 132
E
Education, 181–187
in anatomy, 184
behavioural strategies and, 184–185
in biomechanics, 184
in directionally biased persistent neck pain, 242–243
in neck pain associated with neuropathy, 254
in neck pain disorder, 183–184
En-bloc trunk torsion, in sensorimotor control disturbances, 156
Encoding, nociceptive pathway, 17–18
Endurance
of cervical extensor, 135
of cervical flexor, 132, 206–208
of neck extensor, 214–215, 214f
of neck flexor, 213–214, 214f
of scapular muscle, 210–212, 211f

Episodic disorder, of neck pain, 10

Exercise
active, 195–196
dosage, 259
for neck pain, 258
associated with neuropathy, 254
directionally biased persistent, 243
neuromuscular adaptations to, 64–65
for neuromuscular dysfunction, 202–203
outcomes of, 258–259
in self-management, 185
sensorimotor control
for cervical joint position sense, 223–224
for cervical movement sense, 224–225, 224f
eye-head coordination exercises in, 225–226
functional, dynamic balance training, 227, 227f
gaze stability exercises in, 225, 226f
psychological considerations in, 228
smooth-pursuit eye-movement exercises in, 225, 225f
static balance training in, 227
tailored, principles for, 223
trunk head coordination exercises in, 226, 226f
vestibular rehabilitation and vision therapy in, 227–228

variability in symptomatic response to, 63–64, 64f

Extension
cervical, 117–118, 117f
cervicothoracic region, 119
craniocervical, 118

Extension rotation test, 120

Eye follow, 138, 139f, 139t
Eye movement control, disturbances in, 77–78
Eye-head coordination exercises, 78, 138–139, 139f, 225–226
F
Fear avoidance, in neck pain disorders, 88–89
Flexion
cervical, 32f, 117
cervicothoracic region, 119
craniocervical, 32f, 118

Flexion Rotation Test, 30f

Force sense, cervical, disturbances in, 75
Forward head posture (FHP)
cervical musculoskeletal dysfunction and, 164–165
posture analysis and, 112–113

Four-point kneeling, 112t

Functional dynamic balance training, 227, 227f
Functional tasks, disturbances in, 77
“Fuzziness”, 182
G
Gaze stability, 138, 138f
exercises, 225, 226f

H
Hallpike-Dix manoeuvre, 140
Head impulse test, 140
Headache
cervical musculoskeletal dysfunction and, 161–170
clinical decisions for, 165–166, 166f
definition of, 163–165

neck pain and, 161–163, 243–246, 244f

clinical reasoning and reflections, 245–246
patient presentation, 244–245
physical examination, 245

Home program, for neuromuscular dysfunction, 203, 203b

Homeostasis, of nerve, 231–232
Hyoid muscle, 52
Hyperalgesia, 21–22
cold, 20
mechanical, 22

Hypoesthesia, 22
Hypothalamic-pituitary adrenocortical (HPA) axis, 23
I
IASP, International Association for the Study of Pain
Inflammatory pain, 21, 103–104
Integrated segmental motion, 31–32, 32f
International Association for the Study of Pain (IASP), 17, 20
International Classification of Functioning, Disability and Health (ICF), 4–5
J
Joint and movement dysfunction, management of, 189–200
active exercise as, 195–196
range of motion in, 195–196, 196f
for training movement velocity and accuracy, 196, 197f

clinical reasoning in, 189, 190f

manipulative therapy for, 189–195
approach to, 193
benefits of, 189–191
clinical reasoning in, 192
contraindications and cautions to, 192
limitation of, 191
pain in adjacent areas, 195
patients suitable for, 191–192
technique for, selection and application of, 193–195, 193f–195f
self-management as, 196–197

Joint position error (JPE), 135, 156

Joint position sense (JPS), cervical, 75
exercise for, 223–224

K
Kinematic disturbances, 75
Kyphosis, 113
L
Labyrinthitis, 152
Language, 182–183
Lateral flexion
cervical, 118
cervicothoracic region, 119, 119f
craniocervical, 118

Levator scapulae muscle, 52–53

Ligament, transverse, 30
Listening, 181–182
Longus capitis muscle, 52
Longus colli muscle, 52
Lordosis, cervical, 29
Low-back pain, nonspecific, 106
Lower socioeconomic status, 24–25
M
Magnetic resonance imaging (MRI), for neck pain, 6
Management
interventions in, selection of, 176–177
of joint and movement dysfunction, 189–200
active exercise as, 195–196
clinical reasoning in, 189, 190f
manipulative therapy for, 189–195
self-management as, 196–197

of neck pain disorders, 9–10

physiological features of, 89–90, 91b
of neuromuscular disturbances, 62–65
neuromuscular adaptations to exercise, 64–65
variability in symptomatic response to exercise, 63–64, 64f
principles of, 173–179
strategies for, selection of, 174–176
of whiplash injury, 246–249, 246f
clinical reasoning in, 247
diagnosis and clinical reasoning in, 247–248
key physical examination findings in, 247
overall management approach in, 248
patient presentation and key examination findings in, 246–247
reflection and clinical message in, 248–249, Exercise

Manipulable lesion, 191–192

Manipulative therapy
for joint and movement dysfunction, 189–195
approach to, 193
benefits of, 189–191
clinical reasoning in, 192
contraindications and cautions to, 192
limitation of, 191
pain in adjacent areas, 195
patients suitable for, 191–192
technique for, selection and application of, 193–195, 193f–195f

for neck pain associated with neuropathy, 254

for stiffness, 191
unsteadiness and, 191
Manual examination, 123–127
cervical segments, 120, 123–125, 124f–125f
instability tests for, 126–127, 127f
prone lying position, 123–125, 124f–126f

Manual therapy, for nerve mechanosensitivity, 234–235, 234f

Mechanical diagnosis and therapy (MDT), 175–176
Mechanical hyperalgesia, 22
Mechanical neck pain, 6
Mechanoreceptors, cervical, 71–73, 72b
Mechanosensitivity, nerve, 44, 234f
Memory consolidation, 23
Ménière disease, 152
Migraine, 162
chronic, 162

Minor brain injury, dizziness and, 151

Motion
adult cervical segment, 31
craniocervical, 30
integrated segmental, 31–32
range of, 35
sagittal plane, 35

Motor outputs, 258–259

in neck pain, changes in, 53–54, 54f

Movement diagnostic tests, 120

Movement examination, in whiplash injury, 247
Movement sense, cervical, disturbances in, 75
MRI, Magnetic resonance imaging
Multifidus muscle, 53
Multifocal neuropathy, 42
Muscles
axioscapular, 32–33
coordination between, changes in, 54–57, 54f, 56f–57f
hyoid, 52
levator scapulae, 52–53
longus capitis, 52
 longus colli, 52
multifidus, 53, 134
obliquus capitis
inferior, 53, 133–134
superior, 53, 133–134
rectus capitis
major, 133
minor, 133

rectus capitis anterior, 52

rectus capitis posterior
major, 53
minor, 53

rotatores, 53
scalene, anterior, 52
semispinalis capitis, 53
semispinalis cervicis, 53, 134
splenius capitis, 53
sternocleidomastoid, 52
transversospinalis, 53
trapezius, upper, 52–53

Muscle activity
delayed offset, 58–59
delayed onset, 58, 59f
distribution of, variations in, 57–58
temporal characteristics of, changes in, 58–59

Muscle spindles, 71
Muscle trigger points, cervical musculoskeletal dysfunction and, 164
Musculoskeletal disorders, recognition of, in patient interview, 102
Musculoskeletal injury, 42
Myelopathy, cervical, degenerative, 44–45
N
Neck Disability Index, 59–60
Neck extensor, endurance and strength of, 214–215, 214f
Neck flexor
control and coordination of, 212–213
endurance and strength of, 213–214, 214f

Neck muscles, peripheral properties of, changes in, 61

Neck pain
associated with neuropathy, 252–255, 253f
 advice and education for, 254
diagnosis and clinical reasoning in, 254
exercise therapy for, 254
management approach in, 254
manipulative therapy for, 254
neural mechanosensitivity, 253
patient presentation and key examination findings in, 252–254
reflection and clinical message in, 254–255

basic tenets of, 3–5

cervicogenic headache and, 162–163
classification of, 5–9
defined, 3
by clinical prediction rules, 8
by mechanism of onset, 6
by mechanisms, 7–8
by pathoanatomy, 6–7
by predictors, 8
by subgrouping, 8–9
by time, 7
effectiveness and ineffectiveness, 9
episodic or recurrent disorder, 10
headache and, 161–163
source of, 163

mechanical, 6
migraine and, 162
presenting episode of, treatment of, 259
prevention of, 257–261
primary, 258
secondary, 258–259
tertiary, 259–260

single or multimodal interventions for, 9–10

tension-type headache and, 162
traumatic onset, 6

Neck pain disorders, 3–13, 87–97

biopsychosocial model of, 4–5, 5f
cervical posture in, 34–36
cervical spine-related nerve conditions in, 44–46
contemporary issues in, 5–10
education on, 183–184
management of, 9–10
movement and posture in, 29–39
nerve injury and, 41
neural tissue in, 41–50
neuromuscular disturbances in, 51–70, 65f
anatomical considerations to, 52–53
coordination between muscles in, changes in, 54–57, 54f, 56f–57f
 development of, time course for, 61–62, 62f
management of, 62–65
motor adaptations in, 59–61, 60f
motor output in, changes in, 53–54, 54f
neck muscles in, changes in peripheral properties of, 61
temporal characteristics of neck muscle activity, changes in, 58–59

pathophysiological mechanisms of neuropathy in, 41–43

psychological features of, 87–90
anxiety in, 88
assessment and management of, 89–90, 91b
biological associates of, 92–93
catastrophization in, 88
depression in, 88
fear avoidance in, 88–89
patient expectations in, 89
self-efficacy in, 89
stress in, 88
sensorimotor control disturbances in, 71–85
social features of, 90–93
biological associates, 92–93
changing face of work in, 90–92
return to work, 93
workplace psychosocial factors, 92

Neck torsion, in sensorimotor control disturbances, 156

Nerve conduction
altered, manual techniques for, 235
integrity of, 43–44, 43b

Nerve entrapment, compression and, 42

Nerve homeostasis, 231–232
Nerve injury
neck pain disorders and, 41
pathophysiological mechanisms of, 41–44

Nerve mechanosensitivity, 44
manual techniques for, 234–235, 234f
tests of, 122–123
nerve palpation as, 123
neurodynamic tests as, 122–123, 123f–124f

Nerve palpation, 123

Nerve strain, ergonomic factors and, 234
Nerve tissue, management of, 231–239
nerve-related condition and, 232–236
addressing contributing factors for, 233–234
manual therapy for, 234–235, 234f
patient education and advice for, 233
 referral to medical physicians in, 236
self-mobilization with home exercise in, 235–236, 235f–236f

neurophysiological mechanisms underpinning, 231–232

Nervous system, examination of, 121–123

clinical neurological examination, 121–122
nerve mechanosensitivity, tests of, 122–123

Neural examination, in whiplash injury, 247

Neural system, cervical musculoskeletal dysfunction, 165
Neuromuscular disturbances, in neck pain disorders, 51–70, 65f
anatomical considerations to, 52–53
coordination between muscles in, changes in, 54–57, 54f, 56f–57f
development of, time course for, 61–62, 62f
individual variability in motor adaptations to pain, 59–61, 60f
management of, 62–65
neuromuscular adaptations to exercise, 64–65
variability in symptomatic response to exercise, 63–64, 64f

motor output in, changes in, 53–54, 54f

neck muscles in, changes in peripheral properties of, 61

Neuromuscular dysfunction, 201–220

dosage and intervention timelines for, 215–216
exercise adherence and, 202–203
home program for, 203, 203b
maintenance program for, 216–217
neuromuscular training for, 203–204
posture training for, 204–206
for head and neck posture, 206
for scapular posture, 205–206
spinal, 204–205, 205f
for spinal posture, 204–205, 205f

Neuromuscular examination, in whiplash injury, 247

Neuromuscular system
assessment of, 128–135
cervical extensor muscle tests for, 132–134
cervical extensors for, 134–135, 134f
cervical flexor strength and endurance for, 132
craniocervical flexion test for, 130–132
scapular muscle tests for, 128–130

cervical musculoskeletal dysfunction and, 164

headache in, 245

Neuromuscular training, 203–204

Neuropathic pain, 20–21
Neuropathy, 41
clinical manifestations of, 43–44, 43b
nerve conduction integrity, 43–44, 43b
nerve mechanosensitivity, 44
patient reported symptoms, 43
multifocal, 42
neck pain associated with
advice and education for, 254
diagnosis and clinical reasoning in, 254
exercise therapy for, 254
management approach in, 254
manipulative therapy for, 254
neural mechanosensitivity, 253
patient presentation and key examination findings in, 252–254
reflection and clinical message in, 254–255
pathophysiological mechanisms of, 41–43
stretch-induced, 43

Neuropathy, neck pain associated with, 252–255, 253f

Neuropraxia, brachial, 42–43
Nociception, 17–28
Nociceptive pain, 19–20, 19f, 103–104
Nociceptive pathway, 17–19
Nonspecific low-back pain, 106
Non-specific neck pain, 6, 106
O
Obliquus capitis inferior muscle, 53
Obliquus capitis superior muscle, 53
Occipital neuralgia, 46
Occupations, in neck pain disorders, 91
Oculomotor assessment, 138
eye follow, 138, 139f, 139t
eye-head coordination, 138–139, 139f
gaze stability, 138, 138f
trunk-head coordination, 138–139, 140f

Optokinetic reflex (OKR), 72

P
Pain
chronic, 7, 17
defined, 17
 inflammatory, 21
mechanisms of
provisional decision of, 103–104
sensory testing and, 121

neck, Neck pain

neuropathic, 20–21
nociceptive, 19–20, 19f
perception, 17–28
noxious stimuli to, 17–19
psychosocial influences on, 24–25

psychological factors of, 22–25

relief of, 10
threshold, 22, 190

Pain education, 183

Pain matrix, 18
Pain relief, 258
Pain self-efficacy, 89
painDETECT questionnaire, 20–21
Palpation
nerve, 123
of segmental tenderness, 120

Pathoanatomic lesions, 19
Patient compliance, self-management and, 185
Patient expectations, 89
Patient interview, 101–110
elements of, 101
outcomes of, 101–107, 102b
functional limitations in, 104–105
musculoskeletal disorder recognition, 102
pain mechanism, provisional decision on, 103–104
patient-clinician rapport and collaborative relationship, 102
physical provocative factors in, 104–105, 105b
prognostic features in, 107
provisional diagnosis, 106–107
psychological or social moderators in, 105–106
red flag recognition, 102–103
sensorimotor disturbances, provisional decision on, 104
sleep, provisional decision on, 104

treatment goals and outcome measures of, 107–108

Patient reported symptoms, 43

Patient Specific Functional Scale (PSFS), 107
Patient-centred care, 101
Patient-clinician rapport, and collaborative relationship, in patient interview, 102
Perception, pain, 17–28
noxious stimuli to, 17–19
psychosocial influences on, 24–25

Perilymph fistula, 152, 155t

Perineural inflammation, 42
Peripheral neuropathic pain, 104
Peripheral sensitization, 18, 21–22, 23f
Peripheral vestibular lesions, 151, 155t
Persistent neck pain, directionally biased, 241–243, 242f
advice and education in, 242–243
diagnosis and clinical reasoning in, 242
exercise therapy for, 243
management approach in, 242–243
patient presentation and key examination findings in, 241–242
reflection and clinical message for, 243
reported aggravating factors and functional examination in, 241–242

Physical examination, 111–147, 112t, 113f–114f

cervical motion analysis, 116
four-point kneeling, 112t
manual examination, 123–127
cervical segments, 123–125, 124f–125f
instability tests for, 126–127, 127f
prone lying position, 123–125, 124f–126f

of nervous system, 121–123

clinical neurological examination, 121–122
nerve mechanosensitivity, tests of, 122–123

of neuromuscular system, 128–135

cervical extensor muscle tests, 132–134
cervical extensors, 134–135, 134f
cervical flexor strength and endurance, 132
craniocervical flexion test, 130–132
scapular muscle tests, 128–130

of posture, 112–116, 114f

adjacent regions of, 116
scapular, 115–116, 115f

of prone lying position, 112t

manual examination of, 123–125, 124f–126f
scapular holding test in, 128, 128f

of provocative movement or posture, 112, 113f

of sensorimotor control disturbances, 135–141
 cervical proprioception, 135–136
oculomotor assessment, 138
other causes of, 140–141, 140f–141f
standing balance, 137–138, 137f

sensorimotor tests, 112t

sensory testing and pain mechanisms, 121
of sitting position, 112t
of standing position, 112t
of supine lying position, 112t

Physical provocative factors, knowledge of, 104–105, 105b

Posttrauma vision syndrome, 152
Posttraumatic stress disorder, 23
Postural stability, disturbances in, 76–77
Posture
analysis of, 112–116
adjacent regions of, 116
scapular, 115–116, 115f
spinal, 113, 114f

cervical musculoskeletal dysfunction and, 164–165

headache and, 245
neck pain disorders and, 29–39
training, 204–206
for head and neck posture, 206
for scapular posture, 205–206
for spinal posture, 204–205, 205f

Prescription, exercise, 258–259

Primary neurotransmitter, of nociceptors, 18
Primary prevention, 258
Prognosis, in patient interview, 107
Prone lying position, 112t
manual examination of, 123–125, 124f–126f
scapular holding test in, 128, 128f

Proprioception, cervical, disturbances in, 75–76

Provisional diagnosis, in patient interview, 106–107
Provocative factors, physical, knowledge of, 104–105, 105b
Psychological features, of neck pain disorder, 87–90
anxiety in, 88
assessment and management of, 89–90, 91b
biological associates of, 92–93
 catastrophization in, 88
depression in, 88
fear avoidance in, 88–89
patient expectations in, 89
self-efficacy in, 89
stress in, 88

Psychological moderators, knowledge of, 105–106

Q
Quantitative sensory testing (QST), 121
R
Radiculopathy, cervical, 45–46
manual techniques for, 235

Randomized controlled trials (RCTs), 9, 258

Range of motion, 195–196, 196f
RCTs, Randomized controlled trials
Rectus capitis anterior muscle, 52
Rectus capitis posterior major muscle, 53
Rectus capitis posterior minor muscle, 53
Recurrent disorder, of neck pain, 10
Red flags, recognition of, in patient interview, 102–103
Reduced smoothness of movement, 36
Reflex
cervico-collic, 72
cervico-ocular, 72
optokinetic, 72
tonic neck, 73
vestibulo-collic, 72
vestibulo-ocular, 72–73

Reflex-mediated activity, 72–73, 72f, 73b

Rehabilitation, Exercise
Rheumatoid arthritis, 126
Rotation
cervical, 118
cervicothoracic region, 119, 119f
craniocervical, 118
Rotatores muscle, 53
S
Scapular holding test (lower trapezius), 128, 128f
Scapular muscle
activation and endurance of, 210–212, 211f
control, 213
endurance and strength, 215

Scapular posture, 113–114, 114f

control of, 115–116, 115f

Secondary prevention, 258–259

Segmental tenderness, palpation of, 120
Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS),
20–21
Self-efficacy, in neck pain disorders, 89
Self-management, 181–187, 196–197, 259
Self-mobilization, for management of nerve tissue, 235–236, 235f–236f
Semispinalis capitis muscle, 53
Semispinalis cervicis muscle, 53
Sensitization, defined, 21
Sensorimotor control disturbances, 135–141
causes of, 140–141, 140f–141f
cervical musculoskeletal and sensorimotor approaches for, 222–223
cervical musculoskeletal pain and dysfunction, 221, 222f
cervical proprioception, 135–136
differential diagnosis of, 149–160
clinical examination in, 152–157
dizziness and, 149–152
history and interview in, 153
physical assessment in, 153–157
symptom differentiation in, 153, 155t
tinnitus and, 152
visual system disturbances and, 152

exercise for
for cervical joint position sense, 223–224
for cervical movement sense, 224–225, 224f
eye-head coordination exercises in, 225–226
functional, dynamic balance training in, 227, 227f
gaze stability exercises in, 225, 226f
psychological considerations to, 228
smooth-pursuit eye-movement exercises in, 225, 225f
 static balance training in, 227
tailored, principles of, 223
trunk head coordination exercises in, 226, 226f
vestibular rehabilitation and vision therapy in, 227–228

management of, 221–230

mechanisms underlying, 73–74
in neck pain disorders, 71–85
oculomotor assessment, 138
onset of, 78–79
provisional decision on, 104
relationships between sensorimotor measures, 79, 79f
self-management of, 228
sensorimotor control system, adaptive changes in, 222
standing balance, 137–138, 137f

Sensorimotor deficits, exercise for, 258–259

Sensorimotor dysfunction, cervical musculoskeletal dysfunction and, 165
Sensorimotor examination, in whiplash injury, 247
Sensorimotor incongruence, 75–76
Sensorimotor tests, 112t
Sensory testing, 121
in whiplash injury, 247

Serratus anterior test, 129–130

Shoulder girdle, relationship with cervical spine, 32–33
Sitting position, examination in, 112t
Sleep, provisional decision in, 104
Sliders, nerve, 235–236, 235f
Smooth pursuit neck torsion test (SPNT), 78, 138, 139f, 139t
Smooth-pursuit eye-movement exercises, 225, 225f
Social moderators, knowledge of, 105–106
Spinal posture, 113, 114f
training for, 204–205, 205f

Spine-related nerve conditions, cervical, 44–46

cervical radiculopathy, 45–46
cervicobrachial disorders, 45–46
degenerative cervical myelopathy, 44–45
occipital neuralgia, 46
thoracic outlet syndrome, 46
Splenius capitis muscle, 53
Spurling’s test, 120
Standing balance, 137–138, 137f
Standing position, examination in, 112t
Static balance training, 227
Sternocleidomastoid muscle, 52
Stiffness, manipulative therapy for, 191
Stress, in neck pain disorders, 88
Stretch-induced neuropathies, 43
Subgrouping, 175–176
Suboccipital muscle, test for, 133–134, 133f
Supine lying position, examination in, 112t
Sway, 76
Sympathetic nervous system (SNS), 23
Systematic reviews, 258
T
Technology revolution, neck pain and, 257
Tensioners, nerve, 235–236, 236f
Tension-type headache, 161
neck pain in, 162

Tertiary prevention, 259–260

Thoracic outlet syndrome, 46
Thorax, relationship with cervical spine, 29
Time, neck pain prevention and, 259
Tinnitus, 152
Tonic neck reflex (TNR), 73
Touch, communication through, 182–183
Transduction, nociceptive pathway, 17–18
Transmission, nociceptive pathway, 17–18
Transversospinalis muscle, 53
Trapezius muscle tests, 129
Traumatic nerve injury, 42–43
Traumatic onset neck pain, 6
Trunk-head coordination, 78, 138–139, 140f
exercises, 226, 226f

U
Unsteadiness, manipulative therapy and, 191
Upper cervical extension, 118
Upper cervical flexion, 118
Upper limb, cervical spine and, 32–33, 34f
Upper trapezius muscle, 52–53
V
Vertebral artery, 155t
Vertebral artery insufficiency, positional tests for, 120–121
Vertebrobasilar insufficiency (VBI), 120–121, 150
Vertical perception, disturbances in, 75
Vestibular migraine, 151, 155t
Vestibular neuronitis, 152
Vestibular oculomotor screening test (VOMS), 157
Vestibular rehabilitation, 227–228
Vestibular tests, in sensorimotor control disturbances, 156–157
Vestibulo-collic reflex (VCR), 72
Vestibulo-ocular reflex (VOR), 72–73, 140
Vision therapy, 227–228
Visual system disturbances, 152
Visual tests, in sensorimotor control disturbances, 156–157
W
WAD, Whiplash-associated disorders
Whiplash injury, 8
management of, 246–249, 246f
clinical reasoning in, 247
diagnosis and clinical reasoning in, 247–248
key physical examination findings in, 247
overall management approach in, 248
patient presentation and key examination findings in, 246–247
reflection and clinical message in, 248–249
Whiplash-associated disorders (WAD), 6, 20, 88, 174
categories of, 174

Work environment, in neck pain disorders, 90–93

X
X-rays, for neck pain, 6
Z
Zygapophysial joint capsules, 19