Coma

Question 1

What is a coma?

Answer 1

 Clinical syndrome of altered
consciousness
 Unresponsive patient who cannot be
aroused
 Inability to arouse the patient
distinguishes coma from other
syndromes of altered consciousness
where the primary deficit is lack of
awareness
 Coma is not an etiologic diagnosis

Question 2

level of consciousness

Answer 2

 Many terms are used to describe
patients who have altered
consciousness but are not in deep coma
 Stupor, lethargy, and drowsiness are all
relatively non-specific terms (no measurable way to distinguish them)
 Sleep is a physiologic loss of
consciousness with distinct stages
recognized on EEG
 Sleep is distinguished from coma by the
ability to arouse the patient

Question 3

anatomy of alertness

Answer 3

 Maintenance of consciousness requires interaction
between ARAS (ascending reticular activating system) and cerebral hemispheres (cortex)
 ARAS is located in the paramedian tegmentum of
the upper pons and the midbrain
 ARAS projects through the posterior hypothalamus
to the thalamic reticular formation
 Thalamus projects diffusely to most of the cortex
 The MLF (medial longitudinal fasiculus) and the CN III and IV nuclei lie within the
area of the ARAS in the pons and midbrain

Question 4

localization of coma

Answer 4

 Brainstem lesions involving the ARAS
- Frequently have other brainstem findings to
assist in localization
 Bilateral hemispheric lesions can
transiently cause coma
- Usually involve mesial frontal region
 Large unilateral hemispheric lesions
- Mass effect causing secondary dysfunction of
the non-lesional hemisphere
- Transient unresponsiveness can be seen even
in the absence of mass effect

Question 5

coma mimics

Answer 5

• akinetic mutism
• locked in syndrome
• persistent vegetative state
• brain death

Question 6

akinetic mutism

Answer 6

 Patient appears to be awake
 Lies motionless and silent
 May track movement with the eyes - horizontal roving eye movements (not seen in locked in)
 Does not follow commands
 Should have no significant loss of descending motor
pathways, although can be seen in hemiplegic
patients
 Caused by lesions of bilateral frontal lobes (anterior
cingulate), globus pallidi, or rostral ARAS (thalamus,
hypothalamus, upper midbrain)
 Etiologies include anoxia, head trauma, stroke,
acute hydrocephalus, tumour

Question 7

locked in syndrome

Answer 7

 De-efferented state due to extensive
destruction of the ventral pons (afferent pathways are fine but efferent are not)
 Patient is mute and motionless
 Patient is awake, alert, aware, and capable
of sensation
 Communication may be preserved through
eyelid blinking and vertical eye movements
 Most commonly due to basilar artery
thrombosis

Question 8

persistent vegetative state

Answer 8

 Usually seen in patients following a period of
coma
 Intact sleep-wake cycles
 Complete lack of awareness of self or
environment
 Preservation of vegetative function (cardiac,
respiratory, blood pressure)
 No sustained, reproducible, purposeful or
voluntary behavioural response to visual,
auditory, tactile, or noxious stimuli
 Cranial nerve and spinal reflexes may be intact
 Bowel and bladder incontinence

Question 9

brain death

Answer 9

 Brain death = death (legally)
 Total and irreversible loss of function of the
cerebrum and brainstem
 Must be demonstrated in the absence of
hypothermia, CNS depressants, metabolic
disturbance (nothing that can cause issues with reflexes and influence exam)

Question 10

neurologic exam of the comatose patient

Answer 10

 Level of responsiveness/arousal
 Cranial nerves
 II & III (pupils and fundi)
 III, IV & VI (eye movements; oculocephalic
response)
 V & VII (corneal reflex, facial movements)
 VI & VIII (vestibulo-ocular reflex – VOR;
caloric testing)
 IX & X (gag, cough, respiration)
 Motor & sensory (spontaneous and
induced limb movements)
 Muscle stretch reflexes
 Babinski response

Question 11

respiratory patterns - cheyne stokes

Answer 11

Cheyne-Stokes respiration
 Brief periods of hyperpnea alternating with
shorter periods of apnea
 Pathologic post-hyperventialation apnea due to
blunting of response to CO2 levels
 May be due to bithalamic dysfunction, but can
be from any bilateral lesions from the cerebral
hemispheres to the upper pons
 Often seen in metabolic disturbances such as
uremia, diffuse anoxia, heart failure
 May be seen in elderly during sleep or normal
individuals at high altitude

Question 12

resp patterns - rostral

Answer 12

 Rostral → caudal brainstem patterns of respiration
(may not be as localizing as presented in texts)
 Hyperventilation from brainstem injury
○ Lesions in midbrain or pons
○ Hypoxia despite increased respiratory rate
 Apneustic breathing
○ Long inspiratory pauses
○ Lateral tegmentum of lower pons
 Cluster breathing
○ Low pontine or high medulla lesions
 Ataxic breathing
○ Completely irregular pattern of breathing
○ Damage to dorsomedial medulla
○ Heralds complete respiratory failure

Question 13

pupils

Answer 13

 Pupillary light reflex is very resistant to metabolic
dysfunction
 Abnormalities, especially when asymmetric, often
suggest midbrain pathology
 Beware toxins or drugs which can affect pupillary
response
 Diencephalic– small, reactive
 Midbrain – midposition, fixed, may have hippus
 Pons – pinpoint (disruption of descending
sympathetics), technically reactive
 Lateral pons, medulla or ventrolateral cervical cord –
Horner’s syndrome
 ** Third nerve compression ** - dilated pupil due to
unopposed sympathetic innervation

Question 14

motor activity of the limbs

Answer 14

 Posturing (not really localizing):
 Decorticate
○ Adduction of the shoulder and arm
○ Flexion of the elbow
○ Pronation and flexion of the wrist
○ Legs remain extended at hip and knee
 Decerebrate
○ Extension and pronation of the arms
○ Plantar flexion of the foot

Question 15

eye movements

Answer 15

 There is a laundry list of spontaneous
abnormal eye movements reputed to
have some localizing value, although
they frequently do not
** Understand the technique and
interpretation of cold caloric testing in
the comatose patient **