Neurology Examination On Unconscious Patient

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Astra Dea Simanungkalit

CONSCIOUSNESS is a state of awareness


of self and the environment.

This state id determinded by two separated


function:
 Arousal ( level of consciousness)
 Awareness (content of consciousness)
Consciousness depends on two component
:

 an intact ascending reticular activating


substance (ARAS) in the brainstem as
the alerting or awakening element of
consciousness → level of
consciousness or arousal

 a functioning cerebral cortex of both


hemisphere which determines the
content of that consciousness or
awareness

Content depends on arousal


but normal arousal does not guarantee normal
content
 THE ARAS
extending from the medulla through the pons to the midbrain
which is continous caudally with the reticular intermediate
grey lamina of the spinal cord and rostrally with the
subthalamus, the hypothalamus and the thalamus
 Receives input from numerous somatic afferents
 Projects to midline thalamic nuclei (which are in a circuit with
cortical structures) and the limbic system
Function of ARAS-Thalamic-Cortical system
depends on:
 Anatomic integrity of structures
 Metabolic integrity (circulatory integrity)
 Communicative integrity (neurotransmitter
function)
 cholineric system
 monoaminergic system
 GABA (-aminobutyric acid) system
COMA is…

A state in which the patient makes no


purposeful response to the environment
and from which subject cannot be
aroused
COMA implies dysfunction of :
 ARAS or
 Both hemi-cortices

Anatomically, this means


 Central brainstem structures (bilaterally)
from caudal medulla to rostral midbrain
 Both hemisphere
Causes of Coma:
 Intracranial origin
 Head injuries
 Cerebrovascular accident
 CNS infection
 Tumours
 Increased ICP

 Extracranial origin
 Vascular disorders (shock, hypotension caused by severe
hemorrhage)
 Metabolic disorders (hypoglicemia, uremia, hepatic coma, electrolite
imbalance)
 Intoxication (alcohol, barbiturates, narcotics, Carbonminoxide)
 Miscellaneous (hyperthermia, severe systemic infection)
NEUROLOGICAL ASSESMENT OF
COMA
Level of cosciousness: GCS  Eye opening
 Motor Respon
 Verbal Response

Brainstem function
Cranial nerve examination •Pupillary reactions
•Corneal responses
•Spontaneous eye movement
Respiratory pattern •Oculocephalic response
•Oculovestibular respon
•Gag Reflex
Motor function Motor response
Muscle tone
Tendon reflexes
Seizures
Level of consciousness
 The Glasgow Coma Scale is the most useful
assessment of the level of consciousness
 The response to command, calling the
patient’s name, and painful stimuli are
observed for eye opening, limb movement and
voice.
 Painful stimuli: supraorbital pressure, sternum
pressure, nail bed pressure
 Asymmetry between the responses may be
importance  may evidence for a focal lesion
BRAINSTEM FUNCTION

 The brainstem reflexes are particularly


important in helping to identify those lesions
that may affect the ARAS, explain the
reason of coma
GENERAL ORGANIZATION
OF THE NERVOUS SYSTEM

Afferent

Efferent
BRAINSTEM FUNCTION
Assessment of brainstem function via reflexes
 Pupillary reaction (CN 2,3)
 Corneal reflex ( CN 5,7)
 Oculocephalic/caloric (CN 3.4.6.8)
 Gag Reflex (CN 9,10)
PUPILLARY REACTION
 = PUPIL REFLEX / LIGHT REFLEX
 Pupillary respon to light stimulus
 Afferent : optic nerve (CN 2)  tectum
 Efferent : parasympathetics via
occulomotor (CN 3) → m. constrictor pupil
 Abnormal response:
lesion on afferent & efferent pathways
Midbrain integrity/tectum
Gb pupillary reflex
PUPILLARY REACTION
 Normal pupils : 3-4 mm in diameter & equal
bilaterally, constrict briskly & symmetrically in
response to light
 Fixed dilated pupils : > 7 mm in diameter and
fixed (nonreactive to light)
compression of the oculomotor (III) cranial nerve
anywhere along its course from the midbrain to
the orbit
Anticholinergic or symphatomimetic drug
intoxication
The most common cause : transtentorial
herniation of the medial temporal lobe from a
supratentorial mass
PUPILLARY REACTION
 Pinpoint pupils (1-1,5 mm in diameter)
Focal damaged at pontine level
Opioid overdose
Organophospate poisoning
Miotic eye drops
 Asymetric pupils (anisocoria) with
difference ≥ 1 mm
Structural lession affecting the mid brain or
oculomotor nerve
QUESTION
 IF YOU FLASH THE LIGHT ON THE
RIGHT PUPIL , and:
Right pupil did not constrict, and neither left
pupil
 THEN YOU FLASH THE LIGHT ON
THE LEFT PUPIL, and:
Left pupil constrict , and either right pupil

WHERE IS THE LESION ??


ANSWER
 DEFECT ON RIGHT AFFERENT
PATHWAY (Right Optic nerve)
 Gb pupillary reflex
CORNEAL REFLEX
 Afferent : trigeminal nerve
(N. V)
 Efferent :
Facial nerve (eye closure)–
N. VII
 To test pontine integrity
REFLEX EYE
MOVEMENT
Oculocephalic reflex = doll’s head maneuver
○ stimulating the vestibular system by passive
head rotation
Oculovestibular reflex = caloric test
○ Stimulus cold/warm water irrigation againts
the tympanic membrane
OCULOCEPHALIC
RESPONSE
When the head or body moves
unexpectedly, reflex movements of the
head and eye muscles compensate and
maintain fixation on the visual target.
This compensatory  vestibulo-ocular
reflex

Lateral gaze centers : in the paramedian


pontine reticular formation (PPRF)
Move head passively and observe motion of the eyes. The eyes
should move conjugately in the direction opposite to the
movement. An abnormal response (absent or assymmetric)
implies brainstem disease. Do not perform when neck instability
is suspected
CALORIC TEST
 by instilling 50-200 ml of ice cold water
into the external auditory meatus.

 A dysconjugate response or no
response indicates braistem damage
Caloric response: if doll’s eye movement are absent proceed to calorics. Ice cold water
applied to the tympanic membrane normally elicits a slow conjugate deviation to the
irrigated side. Absence indicates brainstem disease. Caloric testing is more sensitive
than the oculocephalic response. Check the tympanic membrane is intact before
testing
RESPIRATION
 Cheyne Stokes Respiration
 after bilateral hemispheric dysfunction
 Regularly alternating periods of hyperpneu and apneu
 Frequently obseved in metabolic coma
 Central Neurogenic hyperventilation
 Extreme hyperventilation  diencephalic, midbrain
 Cluster Breathing
 Short-cycle CRS (more irreguler)
 Apneustic breathing Low pontine
 Pauses of several seconds in full inspiration) damage
 Ataxic → irreguler, medullary damage, preterminal
MOTOR RESPONSE TO PAIN
Localize the stimulus
A decorticate response to pain (flexion of the
arm at the elbow, adduction at the shoulder,
extension of the leg and ankle)
A decerebrate response to pain (extension
at the elbow, internal rotation at the shoulder
& forearm, leg extension)
Asymmetric posturing
○ Facial weakness
○ Limb weakness
MOTOR RESPONSE TO PAIN
MOTOR RESPONSE TO PAIN
MOTOR RESPONSE TO PAIN
 Tone & reflex
 Plantar response : Babinski
Neurological sign in coma
with downward transtentorial herniation

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