Prof. H.Gusbakti, MSC, PKK, Aifm

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Prof. H.

Gusbakti, MSc,PKK,AIFM

Definitions of pain

Pain is a complex unpleasant phenomenon compos


sensory experiences that include time, space, inten
emotion, cognition, and motivation
Pain is an unpleasant or emotional experience
originating in real or potential damaged tissue

Pain is an unpleasant phenomenon that is uniquely


experienced by each individual; it cannot be adequate
adequat
defined, identified, or measured by an observer

event stimulates pain receptors


stimulus is transferred via specialized
nerves to the spinal cord
from there up to the brain- processed in
the brain,
Brain sends an impulse down the spinal
cord, via descending nerves
command the body to react eg withdraw
the hand from a very hot object.

bright,
sharp,
stabbing types of pain
dull,
throbbing,
aching types.

The experience of pain


Three systems interact usually to produce pain:
1. sensory - discriminative
2. motivational - affective
3. cognitive - evaluative

1. Sensory - discriminative system processes information abo


the strength, intensity, quality and temporal and spatial
aspects of pain
2. Motivational - affective system determines the individuals
approach-avoidance behaviours

3. Cognitive - evaluative system overlies the individuals learne

behaviour concerning the experience of pain. It may block,


modulate, or enhance the perception of pain

Pain categories

1. Somatogenic pain is pain with cause (usually kno


localised in the body tissue
a/ nociceptive pain
b/ neuropatic pain

2. Psychogenic pain is pain for which there is no kno


kn
physical cause but processing of sensitive inform
in CNS is dysturbed
Acute and chronic pain
Acute pain is a protective mechanism that alerts the
individual to a condition or experience that is immediately
harmful to the body
Onset - usually sudden

Relief - after the chemical mediators that stimulate the


nociceptors, are removed

This type of pain mobilises the individual to prompt action


to relief it

Stimulation of autonomic nervous system can be observed


during this type of pain (mydriasis, tachycardia, tachypnoe,
sweating, vasoconstriction)
Responses to acute pain
- increased heart rate

- diaphoresis

- increased respiratory rate


- elevated blood pressure
secretion

- blood sugar
- gastric acid

- pallor or flushing,
dilated pupils
viscera,

gastric motility
blood flow to the

kidney and skin

Psychological and behavioural response to acute


pain
- fear
- general sense of unpleasantness or unease
- anxiety
Chronic pain is persistent or intermittent usually defined
as lasting at least 6 months
The cause is often unknown, often develops insidiously,
very often is associated with a sense of hopelessness
and
helplessness. Depression often results

Psychological response to chronic pain


Intermittent pain produces a physiologic response
similar to acute pain.
Persistent pain allows for adaptation (functions of the
body are normal but the pain is not reliefed)
Chronic pain produces significant behavioural and
psychological changes
The main changes are:
- depression
- an attempt to keep pain - related behaviour to a
minimum
- sleeping disorders
- preoccupation with the pain
- tendency to deny pain

Pain threshold and pain tolerance

The pain threshold is the point at which a stimulus is perceiv


as pain
It does not vary significantly among healthy people or in the
person over time

Perceptual dominance- intense pain at one location may caus


an increase in the pain threshold in another location
The pain tolerance is expressed as duration of time or
the
intensity of pain that an individual will endure before
initiation
overt pain responses.
It is influenced by - persons cultural prescriptions
- expectations

Pain tolerance is generally decreased:


- with repeated exposure to pain,
- by fatigue, anger, boredom, apprehension,
- sleep deprivation
Tolerance to pain may be increased:
- by alcohol consumption,
- medication, hypnosis,
- warmth, distracting activities,
- strong beliefs or faith
Pain tolerance varies greatly among people and in
the same person over time
A decrease in pain tolerance is also evident in the
elderly,
and women appear to be more tolerant to pain than

Age and perception of pain


Children and the elderly may experience or express pain
differently than adults
Infants in the first 1 to 2 days of life are less sensitive to
pain
(or they simply lack the ability to verbalise the pain
experience).
A full behavioural response to pain is apparent at 3 to 12
month of life
Older children, between the ages of 15 and 18 years,
tend to have a lower pain threshold than do adults
Pain threshold tends to increase with ageing
This change is probably caused by peripheral neuropathies

Neuroanatomy of pain
The portions of the nervous system responsible for the
sensation and perception of pain may be divided into three
areas:
1. afferent pathways
2. CNS
3. efferent pathways
The afferent portion is composed of:
a) nociceptors (pain receptors)
b) afferent nerv fibres
c) spinal cord network

Afferent pathways terminate in the dorsal horn


of the
spinal cord (1st afferent neuron)
2nd afferent neuron creates spinal part of
afferent
system
The portion of CNS involved in the
interpretation of
the pain signals are the limbic system,
reticular
formation, thalamus, hypothalamus and cortex
The efferent pathways, composed of the fibers

From the pain receptors, the pain


stimulus is transmitted through
peripheral nerves to the spinal cord and
from there to the brain. This happens
through two different types of nerves
fibers:
A-delta "fast pain and
C-fibers slow pain nerve fibers.

A pain stimulus, e.g. if you cut yourself,


consists of two sensations.
first fast pain sensation-is experienced
as sharp.
slow pain, more a dull and burning.
Occurs after a short time
lasts a few days or weeks,
Chronic pain-if inappropriately processed
by the body, it can last several months

nerves are called A-delta fibers.


relatively thick size nerve fibers allow the
pain stimulus to be transferred very fast
(at a speed of five to 30 meter/second),
hence the name
This is all to make the body withdraw
immediately from the painful and harmful
stimulus, in order to avoid further
damage.

starts immediately after the fast pain


is transmitted by very thin nerve fibers,
called C-nerve fibers (their diameter is
between 0.2 to 1 thousandth of a
millimeter).
pain impulse can only be transmitted
slowly to the brain, at a speed of less
than 2 meters per second.
Body response -immobilization (guarding,
spasm or rigidity), so that healing can
take place.

released from their storage areas in the


brain when a pain impulse reaches the
brain,

bind to receptors in the pain pathway to


block transmission and perception of
pain.

Physiological and psychological


interactions
Suggested spinal gates in the dorsal horn
at each segment of the spinal cord
Competition at each gate for heat, touch
or pain to be transmitted at each point

Variation in pain perception between


individuals
Why do these different perceptions of
pain exist
How do midwives respond to different
expression of pain

C-fibres
Uterine smooth muscle

A-delta
traction and pressure on the peritoneum,
uterine ligaments, urethra, bladder,
rectum, lumbosacral plexus, fascia and
muscles of the pelvic floor

The brain first perceives the sensation of pa


The thalamus, sensitive cortex :
perceiving
describing
localising

of pain

Parts of thalamus, brainstem and reticular formation:


- identify dull longer-lasting, and diffuse pain

The reticular formation and limbic system:


- control the emotional and affective response to
pain
Because the cortex, thalamus and brainstem ar e
interconnected with the hypothalamus and autonomic
nervous system, the perception of pain is associated

The role of the afferent and efferent


pathways in
processing of pain information
Nociceptive pain
Nociceptors: Endings of small unmyelinated and lightly
myelinated afferent neurons
Stimulators: Chemical, mechanical and thermal noxae
Mild stimulation positive, pleasurable
sensation
(e.g. tickling)
Strong stimulation pain
These differences are a result of the frequency
and amplitude of the afferent signal
transmitted
from the nerve endings to the CNS
Location:

In muscles, tendons, epidermis, subcutanous

Nociceptive pain:

- mechanisms involved
in development

Afferent pathways:

From nociceptors transmitted by small A-delta fibers an

C- fibers to the spinal cord form synapses with neurons


in the dorsal horn(DH)
From DH transmitted to higher parts of the spinal cord
and to the rest of the CNS by spinothalamic tracts

*The small unmyelinated C- neurons are responsible for the


transmission of diffuse burning or aching sensations

*Transmission through the larger, myelinated A- delta fiber


occurs much more quickly. A - fibers carry well-localized,
sharp pain sensations

Efferent analgesic system


Its role: - inhibition of afferent pain signals
Mechanisms:
- pain afferents stimulates the neurons in
periaqueductal
gray (PAG) - gray matter surrounding the cerebral
aqueduct in the midbrain results in activation of
efferent
(descendent) anti-nociceptive pathways
- from there the impulses are transmitted through
the spinal cord to the dorsal horn
- there thay inhibit or block transmission of

Enk enkefalinergic
PAG paraaqueductal gray
EAA excitatory amino acids
RVM rostral ventro-medial medulla

Descendent antinociceptive systm

The role of the spinal cord in pain processin

Most afferent pain fibers terminate in the dorsal horn of th


spinal segment that they enter. Some, however , extend
toward the head or the foot for several segments before
terminating

The A- fibers, some large A-delta fibers and small C- fiber

terminate in the laminae of dorsal horn and in the substan


gelatinosa
The laminae than transmit specific information (about
burned or crushed skin, about gentle pressure) to 2nd
afferent neuron

2nd afferent neurons transmit the impulse from the


substantia
gelatinosa (SG) and laminae through the ventral and
lateral horn,
crossing in the same or adjacent spinal segment, to the
other side
of the cord. From there the impulse is carried through the
spinothalamic tract to the brain. The two divisions of
1. the neospinothalamic tract - it carries information to the
spinothalamic tract are known:
mid brain, thalamus and post central gyrus (where pain
is perceived)
2. the paleospinothalamic tract - it carries information to
the
reticular formation, pons, limbic system, and mid brain
(more synapses to different structures of brain)

PAG periaqueductal gray


PB parabrachial nucleus in pons
VMpo ventromedial part of the posterior
nuclear complex
MDvc ventrocaudal part of the medial dorsal nucleus
VPL ventroposterior lateral nucleus
ACC anterior cingulate cortex
PCC posterior cingulate cortex
HT hypothalamus
S1, S2 first and second somatosensory cortical areas
PPC posterior parietal complex
SMA supplementary cortical areas
AMYG amygdala
PF prefrontal cortex

Theory of pain production and modulation

Most rational explanation of painproduction and modulatio

is based on gate control theory (created by Melzack and Wall)


According to this theory, nociceptive impulses are
transmitted to the spinal cord through large A- delta and
small C- fibers
These fibers create synapses in the SG
The cells in this structure function as a gate, regulating
transmission of impulses to CNS
Stimulation of larger nerve fibers (A-alfa, A-beta)
causes
the cells in SG to "close the gate".
A closed gate decreases stimulation of T-cells (the 2nd

Stimulation of small fiber input inhibits cells in SG and


"open the gate".
An open gate increases the stimulation of T-cells
transmission of impulses enhances pain perception
In addition to gate control through large and small fibers
stimulation, the central nervous system, through efferent
pathways, may close, partially close, or open gate.
Cognitive functioning may thus modulate pain perception

Action of endorphins(ED)
All ED act by attaching to opiate receptors on the plasma
membrane of the afferent neuron. The result than is
inhibition of releasing of the neurotransmitter, thus
blocking the transmission of the painful stimulus

Neuropathic pain
It occurs as a result of injury to or dysfunction of the
nervous system itself, peripheral or central
Deaferentation pain - form of neuropathic pain: a term
implying that sensory deficit in the painful area is
a prominent feature (anesthesia dolorosa)

Phantom pain- pain localizei into non-existing organ (tissu


Long-lasting pain after short-lasting pain stimulus

What causes neuropathic pain?


Neuropathic pain often seems to have no obvious cause;
but, some common causes of neuropathic pain include:
Alkoholism, Amputation, Back, Leg, and Hip problems,
Chemotherapy,
Diabetes mellitus, Facial nerve problems, HIV infection or AIDS
Multiple sclerosis, Shingles (Herpes yoster), Spine surgery

What are the symptoms of neuropathic pain?


Symptoms may include:
Shooting and burning pain,
Tingling and numbness

Hypersensitivity increased sensitivity of the system


involved in the pain processing

Hyperalgesia increased the pain sensitivity to noxious


stimuli

Allodynia - phenomenon characterised by painful

sensations provoked by non-noxious stimuli,


(e.g. touch), transmitted by fast- conducting
nerve fibres

Mechanism: changes of the response characteristics of


second - order spinal neurons so that normally
inactive or weak synaptic contact mediating
non-noxius stimuli acquire the capability to
activate a neuron that normally responds only
to impulses signaling pain

Peripheral neuralgias after trauma or surg


Common forms of neuropathic pain

lumbosacral and cervical rhizotomy,


peripheral neuralgia

Most peripheral neuralgias are the result of trauma or


surgery. Such a conditions does not necessary occur as
a result of damageing a major nerve trunk but may be

caused by an incision involving only small nerve branche


(incisional pain)
Mechanism: the pain is due to neuroma formation in the
scar tissue (?)

Deaferentation pain following spinal cord in

Incidence of severe pain due to spinal cord and cauda equin


lesions ranges from 35 to 92 % of patients
This pain is ascribed to 3 causes:
1. mechanically induced pain (fracture bones,
myofascial pain)
2. radicular pain (compression of nerve root)
3. central pain (deaferentation mechanism)

Clinical Manifestation of Pain


Acute Pain
We can distinguish two types of acute pain:
1. Somatic
2. Visceral
referred
Somatic pain is superficial coming from the skin or close to
the surface of the body.

Visceral pain refers to pain in internal organs, the abdomen,


or chest.
Referred pain is pain that is present in an area removed or
distant from its point of origin. The area of referred pain
is supplied by the nerves from the same spinal segment
as the actual site of pain.

Different types of chronic somatic pain


I. Nervous system intact
1. nociceptive pain
2. nociceptive - neurogenic pain
(nerve trunk pain)
II. Permanent functional and/or morphological
abnormalities of the nervous system
(preganglionic, spinal - supraspinal)
1. neurogenic pain
2. neuropathic pain
3. deafferentation pain

The most common chronic pain


1. Persistent low back pain
result of poor muscle tone,inactivity,
muscle strain, sudden vigorous exercise

2. Chronic pain associated with cancer

3. Neuralgias - results from damages of peripheral nerves

a) Causalgia - severe burning pain appearing 1 to 2 weeks a


the nerve injury associated with discoloratio

changes in the texture of the skin in the affe


area.
b) Reflex sympathetic dystrophies - occur after peripheral

nerve injury and is characterised by continuo

severe burning pain. Vasomotor changes are

present (vasodilatation vasoconstriction

4. Myofascial

cyanotic and edematous extremities).


pain syndromes - second most common cau
of chronic pain.

These conditions include: myositis, fibrositis, myal


muscle strain, injury to the muscle and fascia
The pain is a result of muscle spasm, tenderness
and stiffness

5. Hemiagnosia
is a loss of ability to identify the sorce of pain on one
side
(the affected side) of the body. Application of painful
stimuli
to the affected side thus produces anxiety, moaning,
agitation
and distress but no attempt to withdrawal from or
push aside
the offending stimulus. Emotional and autonomic
responses

6. Phantom
limb
- is pain that an individual feels in
to the pain
mypain
be intensified.
amputated limb
Hemiagnosia is associated with stroke that produces

paralysis and hypersensitivity to painful stimuli in the

Pathophysiology of muscle pain


Muscle pain - a part of somatic deep pain,
(MP)

- it is common in rheumathology and sports


medicine
- is rather diffuse and difficult to locate

MP is not a prominent feature of the serious progressive dise

affecting muscle, e.g. the muscular dystrophies, denervation

or metabolic myopathies, but it is a feature of rhabdomyolys

Muscles are relatively insensitive to pain when elicited by ne


prick or knife cut, but overlying fascia is very sensitive to pa
Events, processes which may lead to muscular pain are:
metabolic events:
metabolic depletion ( ATP muscular
contracture)
accumulation of unwanted metabolities (K+,

Pathophysiology of visceral pain


Visceral pain:
Types - angina pectoris, myocardial infarction, acute
pancreatitis, cephalic pain, prostatic pain,
nephrlolytiatic pain
Receptors: unmyelinated C - fibres
For human pathophysiology the kinds of stimuli apt to
induce pain in the viscera are important.

It is well-known that the stimuli likely to induce cutaneous


cutaneou
pain are not algogenic in the viscera. This explains why in
the past the viscera were considered to be insensitive
to pain

Adequate stimuli of inducing visceral pain:


1. abnormal distention and contraction of the hollow
viscera muscle walls
2. rapid stretching of the capsule of such solid visceral
organs as are the liver, spleen, pancreas...
3. abrupt anoxemia of visceral muscles
4. formation and accumulation of pain - producing
substances
5. direct action of chemical stimuli (oesophagus, stomach )
6. traction or compression of ligaments and vessels
7. inflammatory processes
8. necrosis of some structures (myocardium, pancreas)

Characteristic feature of true visceral


pain
a) it is dull, deep, not well defined, and differently
described by the patients
b) sometimes it is difficult to locate this type of pain
because it tends to irradiate
c) it is often accompanied by a sense of malaise

d) it induces strong autonomic reflex phenomena


(much more pronounced than in pain of somatic
origin)
- diffuse sweating, vasomotor responses, changes
of
There
are many
visceraland
sensation
that are
unpleasant
but below
belo
arterial
pressure
heart rate,
and
an intense
the level of pain, e.g. feeling of disagreeable fullness or acidity o
psychic
stomach or undefined and unpleasant thoracic or abdominal
alarm reaction -"angor animi" - in angina
sensation. These visceral sensation may precede the onset of vi
v
pectoris)
pain

Refered visceral pain (transferred pain)


Refered pain = when an algogenic process affecting a
viscus recurs
frequently or becomes more intense and prolonged, the location
becomes more exact and the painfull sensation is progressively
felt in
more superficial struftures

Mechanisms
involved
in refered pain
creation:
Refered pain
may be accompanied
by allodynia
and

a) convergence of impulses from viscera and from the skin


cutaneous
in the CNS:
and muscular hyperalgesia
Sensory impulses from the viscera create an irritable focus in the
segment at which they enter the spinal cord. Afferent impulses fro
skin entering the same segment are thereby facilitated, giving rise
cutaneous pain.
b) senzitization of neurons in dorsal horn

Painful visceral afferent impulses activate anterior


horn
motor cells to produce rigidity of the muscle
(visceromotor
reflexes)

A similar activation of anterolateral autonomic cells


induces
pyloerection, vasoconstriction, and other
sympathetic
phenomena
These mechanisms, which in modern terms can be defined
as positive sympathetic and motor feedback loops, are
fundamental in reffered pain

It is clear that painful stimulation of visceral

It has been observed that the local anesthetic block of the

sympathetic ganglia led to the disappearance, or at least to


t

marked decrease, of reffered pain, allodynia, hyperalgesia

In some conditions, reffered somatic pain is long-lasting,


increases progressively, and is accompanied by
dystrophy
of somatic structures.
Possible mechanisms:
- onset of self-maintaining vicious circle impulses:
peripheral tissue afferent fibers

central nervous system

peripheral tissue somatic and sympathetic efferent

Intricate conditions - in some types of pain, e.g. chest pain, is


difficult
to distinguish the true cause of pain because such kind of pain
may be
related to cervical osteoarthrosis, esophageal hernia, or
cholecystitis. It is
diffcult to ascertain whether these intricate conditions are due to

a simple
It has been demonstrated that the mnemonic process is facilitated if
i
the experience
to be from
retained
is repeated
is accompa
addition
of impulses
different
sourcesmany
in thetimes
CNS or to
pleasant or unpleasant emotions.
somatovisceral

and viscerosomatic reflex mechanisms.


Pain is, at least in part, a learned experience - e.g. during the first re
colic, true parietal pain followed visceral pain after a variable interva
In subsequent episodes of renal colic pain, parietal pain developed p
and was not preceded by true visceral pain.
This is probably due to the activation of mnemonic traces .

Silent myocardial ischemia (SMI)


Chest pain is only a late and inconstant marker of episodes

of
transient MI in vasospastic angina (30 %), in stable angina
Mechanisms of SMI
(50 %)
a) Lack of the pain is, in part, related to the duration and sev

of MI. Episodes shorter than 3 min, and those accompanied

a modest impairment of left ventricle ( in end-diastolic p


inferior to 6 mm Hg) are always painless.

Longer and more severe episodes are acccompanied by che


pain in some instances but not in others.
b) Pacients with predominantly SMI appear to have a
generalized
defective perception of pain ( threshold and
tolerance).

Disturbances in pain perception and nocicep


Most of the disturbances are congenital

a) Congenital analgesia - nociceptive stimuli are not process


and/or integrated at a level of bra
Patient does not feel a pain

b) Congenital sensoric neuropathy - nociceptive stimuli are no


transmitted by peripher
nerves or by spinal affe
tracts.
Acquired disturbances in pain perception and nociception

They may occur at syringomyely, disturbances of parietal lobe


brain, in patients suffering from neuropat
(e.g. chronic diabetes mellitus)

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