Evaluation of Patients in

Coma

Liam Durcan MD FRCPC

Department of Neurology
and Neurosurgery
What We’ll Cover

Basic definitions
Key exam points
Epidemiology of Coma
Coma mimics
What we won’t talk about

Brain death/ chronic vegetative state

toxidromes
really complex neuroanatomy
Exhaustive lists of causes
Basic Resuscitative Care
Definitions

Coma: “Unarousable unresponsiveness in

which the subjects lie with eyes closed”
Plum and Posner- Diagnosis of Stupor and
Coma
Other terms: obtundation, stupor
fallen out of favour because of imprecision
descriptive methods favoured
Consciousness

Two components of conscious behavior

content- the sum of cognitive and affective
function
arousal- appearance of wakefulness
Content depends on arousal but normal
arousal does not guarantee normal
content
Really Simple
Neuroanatomy

Arousal: where is it localized?

Ascending Reticular Activating System
(ARAS) ‘core of the brainstem’
receives input from numerous somatic
afferents
projects to midline thalamic nuclei (which are
in a circuit with cortical structures) and the
limbic system
ARAS

ARAS acts as a gating system, increasing

or decreasing thalamic inhibitory influence
on the cortex
alters effect of sensory stimuli ascending
alters descending cortical stimulation
Demands of Arousal

Function of ARAS-Thalamic-Cortical
system depends on:
anatomic integrity of structures
metabolic integrity (circulatory integrity)
communicative integrity (neurotransmitter
function)
Coma Fact Number One

Coma implies dysfunction of:

ARAS or
Both hemi-cortices
Anatomically, this means
central brainstem structures (bilaterally) from
caudal medulla to rostral midbrain
both hemispheres
Epidemiology of Coma

Plum and Posner 1982

500 consecutive cases of coma
101 supratentorial (44/101 ICH)
65 subtentorial lesions (40/65 brainstem infarcts)
326 diffuse or metabolic brain dysfunction
• 149 drug intoxication
Clues from History

Onset of symptoms
sudden onset
fluctuations
Associated neurologic symptoms
Medications
Neurologic Exam

Cornerstone of assessment
Descriptive, systematic
Reference point for serial assessment
Exam goals

Primary CNS event versus secondary

Implications:
short and long-term outcome
investigations
Breathing

Abnormalities of respiration can help

localize but almost always in the context
of other signs
Central-reflex Hyperpnea (midbrain-
hypothalamus)
Apneustic, cluster, Ataxic (Lower pons)
Loss of automatic breathing (medulla)
Cranial Nerve Exam

Systematic assessment of brainstem

function via reflexes
Cranial Nerve Exam
Pupillary light response (CN 2-3)
Occulocephalic/calorics (CN 3,4,6,8)
Corneal reflex (CN 5,7)
Gag refelx (CN 9,10)
.Pupillary Light Responses

Afferent Limb: Optic Nerve

Efferent Limb: Parasympathetics via
occulomotor
Midbrain integrity/ tectum
Uncal Herniation (3rd nerve dysfunction)
Pupillary resistance to insult
Pupillary Light Responses

Be aware of drug effects

Systemic and Local
Avoid ‘PERLA’
State size, before and after light stimulation
Specify right and left
Pupils: Localizing Value

Pons-pinpoint pupils
Symp. Dysfinction plus parasymp.irritation
Midbrain-Large fixed pupils unresponsive
to light, hippus
Horner’s- symp.dysfunction
Unilateral dilation- parasymp. Dysfunction
usually due to 3rd nerve lesion
Ciliospinal Reflex

1-2 mm pupillary dilatation evoked by

noxious cutaneous stimulation
More prominent in sleep or coma than
during wakefulness
Test integrity of symp.pathways in
comatose patients
Not particularly useful in evaluating
brainstem function
Corneal Reflex

Afferent: Trigeminal Nerve

Efferent: Third Nerve (Bell’s Phenomenon
and Facial Nerve (Eye closure)
Tests dorsal midbrain (Bell’s) and pontine
integrity (Eye closure)
Eye Movements

Before maneuvers attempted note resting

position
Midline
Deviation suggests frontal/pontine damage
Conjugate
Dysconjugance suggests CN abn.
Moving
Roving, dipping, bobbing
Occulocephalic/ Calorics

Same reflex elicited differently

Afferent: Eighth nerve
Efferent: 3,4,6 via MLF and PPRF
Occulocephalics may also involve
proprioceptive afferents from the neck
Occulcephalic Reflex

Brisk rotation of head with eyes held open

Watch for contraversive movements
Next:
Flexion: eyes deviate up and eyelids open
(doll’s head phenomenon)
Extension:eyes deviate downward
Caloric reflex

Ensure TM integrity
Elevation of head to 30 degrees (so that
lateral semicircular canal is vertical)
Instillation of up to 120 ml of ice water
Awake: deviation toward,nystagmus away
Comatose: deviation toward
Wait 5 minutes, do other ear
Calorics

Watch for conjugance of deviation

To test vertical eye movements
Both ears, cold water-downward gaze
Both ears, warm water-upward gaze
Gag Reflex

Afferent: Glossopharyngeal
Efferent: Vagus
Taken in context of other findings
Motor Exam

Assess tone, presence of asterixis

Response to painful stimuli
none
abnormal flexor
abnormal extensor
normal localization/withdrawal
Avoid use of decerebrate/ decorticate
Reflexes

Brainstem
Deep tendon
Biceps, brachioradialis, triceps
Patellar, Achilles
Plantar Responses
Superficial skin
Abdominal, cresmasteric
Uncal herniaiton

Expanding lesions in lateral middle fossa

Compression of hippocampal gyrus over
free edge of tentorium
Three stages described
Early third nerve
Late third nerve
Midbrain-Upper pons stage
Goals in Emergency

Primary Neurological Process?

evidence of raised ICP
focal findings, especially that implicate
brainstem structures
Secondary Processes
signs of infection, toxic/metabolic processes
relative lack of focality
Coma Mimics

Akinetic mutism
‘Locked-in’ syndrome
Catatonia
Conversion reactions
Akinetic Mutism

Silent, immobile but alert appearing

Usually due to lesion in bilateral mesial
frontal lobes, bilateral thalamic lesions or
lesions in peri-aqueductal grey
(brainstem)
“Locked-In’ Syndrome

Infarction of basis pontis (all descending

motor fibers to body and face)
May spare eye-movements
Often spares eye-opening
EEG is normal or shows alpha activity
Catatonia

Symptom complex associated with severe

psychiatric disease with:
stupor, excitement, mutism, posturing
can also be seen in organic brain diease:
encephalitis, toxic and drug-induced
psychosis
Conversion reactions

Fairly rare
Occulocephalics may or may not be
present
The presence of nystagmus with cold
water calorics indicates the patient is
physiologically awake
EEG used to confirm normal activity