Khm

Khm thn
thn kinh
kinh bnh
bnh nhn
nhn hn
hn m
m

TS. Cao Phi Phong.

2011

Cc cu hi t ra

How to evaluate this unresponsive pt?

What is the differential diagnoses?
What are the etiologies of coma?
What tests must be performed?
What neuroimaging to be obtained?
What therapies must be provided?

The
The RAS
RAS and
and Essential
Essential Neurotransmitters
Neurotransmitters

Epinephrine:
Locus Coeruleus
Serotonin:
Median Raphe
Acetylcholine:
Basal Nucleus

Nhn lc

RAS

RAS

Coma: Causes
>60% metabolic dysfunction
Drug poisonings
Metabolic
20% supratentorial mass lesions
Stroke
Hemorrhage
15% subtentorial mass lesions
<2% psychiatric causes of coma

Plum and Posner, 1980

Coma Etiologies
AEOIU-TIPS

A
E
I
O
U
T
I
P
S

alcohol, other toxins

endocrine
insulin (DM complications)
oxygen deficiency, opiates
uremia, renal disorders
trauma, temperature
infections
psychiatric, porphyria
space-occupying lesion, stroke, SAH

Toxic and Metabolic Causes of Coma

Toxins:
Lead, thallium, mushrooms, cyanide, methanol,
ethylene glycol, carbon monoxide
Drugs:
Sedatives, barbiturates, tranquilizers, alcohol,
opiates, paraldehyde, salicylates, psychotropics,
anticholinergics, amphetamines, lithium
Metabolic:
Hypoxia, hypercapnia,, disorders of sodium,
glucose, calcium, magnesium, Wernickes
encephalopathy, hepatic encephalopathy, uremia,
Addisonian crisis

Other Common Nonstructural Treatable

Causes of Coma

Nonconvulsive status epilepticus

Meningoencephalitis
Hypertensive encephalopathy
Hypothyroidism

Definition of Coma
Glasgow coma score of less than
10
Eyes closed unresponsiveness
@ Eye opening 1-4
@ Verbal 1-5
@ Motor 1-6

After ABCs stabilized. . .

Quickly investigate cause

DERM

D = Depth of coma

What does patient respond

to?
How does he respond?
AVPU
Glasgow Coma Scale

AVPU

GCS

(1)Coma, stupor, lethargy (hn m, l m

ng lm)
(a)Description * Depressed level of alertness *
For facilitating communication & enhancing
consistency
(b) Example * 'Patient was stuporous': provide
little information * 'Mr.Z lay motionless in
bed unless called loudly by name, when he
opened his eye briefly and looked to the
left. He failed to answer any questions or to
follow instructions' (ch th)

(2) Akinetic mutism

(a)Characteristics * State that seemingly
awake, but remains silent & motionless *
Only eye dart in direction of moving object *
Despite lack of movement, few motor signs
or movement
- Frontal release sign (sucking, grasp reflex)
- Move one side or one arm in stereotyped
fashion
-Pyramidal sign in paralyzed limb
Lao ti

(b) Lesion
- Bilateral frontal lesion (anterior
cingulate gyrus)
- Diencephalic-mesencephalic reticular
formation
- Globus pallidus or hypothalamus
- Common etiology --Anoxia, head
trauma, cerebral infarction, severe
acute hydrocaphalus,
Lao ti

(c) Differnetial diagnosis

Psychogenic (often catatonic) unresponsiveness
- Unless available history, may be difficult to
distinguish
- Signs favoring akinetic mutism: frontal
release sign, pyramidal sign: slow-wave
abnormality in EEG
- Signs favoring catatonia: normal EEG (often
desynchronized low-voltage fast activity)

Persistent vegetative state (PVS)

-Definition: vegetative state present 1
month after acute traumatic or
nontraumatic brain injury
- vegetative state lasting for at least 1
month in degenerative, metabolic,
developmental malformation

Lao ti

Features:
- lack of awareness of self & external stimuli
-

accompanied by sleep-wake cycle

preservation of vital vegetative function
no evidence of sustained, reproducible,
purposeful, voluntary behavior.
no evidence of language comprehension or
expression
bowel & bladder incontinence
variably preserved cranial nerve & spinal
reflexes
Lesion:
- severe or widespread cerebral hemispheric

(3) Locked-in syndrome

(a)Features
Mute, motionless
-

But, remain awake, alert, aware of self,

capable of perceiving sensory stimuli

Impaired horizontal eye movement (d/t

involvement of PPRF in pontine lesion)

Intact vertical eye movement or eyelid

movement (capable of response to
command)

(b) Lesion
- Pontine lesion
-

Basilar artery thrombosis /c ventral pontine

infarct, Pontine hemorrhage, pontine tumor.

Central pontine myelinolysis

Midbrain lesion (bilateral ventral region):

Bilateral ptosis & vertical, horizontal
ophthalmoplegia

Bilateral internal capsular lesion

Tentorial herniation, GBS, MG

Behavioral
Behavioral states
states confused
confused with
with coma
coma

1. Locked-in syndrome
2. Persistent vegetative state
3. Abulia (akinetic mutism )
4. Catatonia
5. Pseudocoma

Coma vs. Brain Death

Coma = sleep-like, unarousable

unconsciousness in a live person

Brain death = ambiguous term

death (necrosis) of the brain

death of the person (= death by neurological criteria)
statutory death in most countries and states, although
there is no consensus on the biological and
philosophical rationales for that equivalence

Coma
Coma vs.
vs. Brain
Brain Death
Death
Coma

Brain Death

Describes brain function at Permanent, irreversible

a moment in time (per se
lack of brain function
implies nothing re
reversibility or prognosis)
Loss of those brain
Loss of all brain functions
functions related to arousal
Midline brainstem or
Destruction (infarction/
diencephalic lesions
necrosis) of entire brain

Brain Death

(party line): BD = a state beyond coma =

death itself

(critics position): BD = a subset of coma =

very deep coma (in a live patient)
associated with no respiration or cranial
nerve reflexes

Brain Death Criteria

Three cardinal findings necessary for brain death:
Coma: no cerebral motor response to pain centrally or in
extremities
Absent brainstem reflexes
Pupillary responses
No ocular movement to VOR or caloric testing
No corneal or jaw reflex
No grimace to pain
No gag or cough response
Absent respiratory drive (including apnea test)
Diagnostic testing is not a substitute for these criteria

Brain Death Criteria: Apnea Testing

Numerous prerequisites including temperature, volume
status
Baseline PCO2 approximately 40
Pretreat with 100% O2
Disconnect ventilator for 8+ minutes and WATCH CLOSELY
FOR RESPIRATORY EFFORT
PCO2 at the end of the test much be >60 OR >20 points
above starting to have an interpretable result
Result is whether there was respiratory effort or not

Brain Death Criteria: 2nd Exam

Clinical evaluation 6 hours later recommended by AAN

to confirm irreversibility
Timing is somewhat arbitrary but should be adhered
to, especially in cases where there is some
uncertainty as to clinical situation
e.g., after cardiac arrest

Brain Death Criteria: Diagnostic Testing

Not necessary to establish brain death in the vast
majority of cases
Not a substitute for clinical exam
Tests not 100% sensitive or specific
Reserve for cases where entire exam cant be done,
for example:
Severe trauma including face
Preexisting pupillary abnormalities

Diagnostic Testing for Brain Death

Cerebral angiography
EEG
TCD
Technecium scan
SSEPs

Coma
Coma vs.
vs. Vegetative
Vegetative State
State
Coma
Sleep-like, unarousable
unresponsiveness (apart
from reflexes)
Midline brainstem or
diencephalic lesions
Does not remain coma
indefinitely; evolves to
awake ( degrees of
disability), VS or death

Vegetative State
Awake-like, arousable
unresponsiveness (apart
from reflexes)
Cortex and/or thalamic
lesions
Remains VS or evolves to
MCS or awake ( degrees
of disability)

Proposed
Proposed Alternative
Alternative
Terminologies
Terminologies
Vegetative State
Coma vigil
Post-coma
unresponsiveness
Post-coma
unawareness

Min. Cons. State

Severe disability
Minimally responsive
state

Vegetative State Terminology

Persistent VS = VS lasting 1 month (=
has persisted until now; per se implies
nothing re future)

Permanent VS = 3 months (anoxic

etiology); 12 months (traumatic etiology)

(= statistical prediction: very likely to
remain unchanged indefinitely into the
future)

E = Eyes

Pupils
Pupils equal, dilated, constricted,
Responsive to light?
How?

E = Eyes
Pupils
@ Size - mid, dilated or constricted
measurement - e.g. 4 mm
@ Shape - round, oval, pontine
@ Equality - equal in size
@ Symmetry - equal in reaction/
response
@ Response to light
Yes or No
How ?

Sympathetic
Sympathetic &
& parasympathetic
parasympathetic innervation
innervation
1)Sympathetic innervation
* Ipsilateral hypothalamus, lateral
tegmentum of brainstem
- intermediolateral gray matter of C8T2 cord segment
- superior cervical ganglion, carotid
plexus
- ophthalmic branch of trigeminal N,
reaching pupil through long ciliary nerve

Sympathetic
Sympathetic &
& parasympathetic
parasympathetic innervation
innervation
2) Parasympathetic innervation
* Edinger-Westphal subNu. 3rd N, ciliary
ganglion, pupil
* Ciliary ganglion: located on temporal
side of ophthalmic A
* Pupillomotor fiber
-Peripheral location (superficially
dorsally in 3rd N), immediate internal
to epineurium

1. Afferent input: optic nerve, optic chiasm,

optic tract, and projections into the
midbrain tectum
2. Efferent fibers: the Edinger-Westphal
nucleus and oculomotor nerve.
3. Abnormalities in pupil size and reactivity
- structural damage between the
thalamus and pons,
- warning sign brainstem herniation,
- differentiate structural causes of coma
from metabolic causes.

1. Thalamic lesions: small, reactive pupils:

diencephalic pupils. (toxic-metabolic)
2. Hypothalamic lesions: or lesions elsewhere
along the sympathetic pathway: Horner's
syndrome
3. Midbrain lesions: three types of pupillary
abnormality, depending on where the lesion
occurs
- Dorsal tectal lesions: midposition eyes,
fixed to light but react to accommodation,
(impossible to test in the comatose patient)

- Nuclear midbrain lesions: affect both

sympathetic and parasympathetic
pathways: fixed, irregular midposition pupils
3. Lesions of the third nerve: wide pupillary
dilation, unresponsive to light
4. Pontine lesions: interrupt sympathetic
pathways: small, pinpoint pupils, remain
reactive.
5. Lesions above the thalamus and below the
pons: pupillary function intact, except for
Horner's syndrome in medullary or cervical
spinal cord lesions.

- Asymmetry in pupillary size or reactivity,

even of minor degree, is important
- Asymmetry of pupil size may be due to
dilation (mydriasis) of one pupil, third nerve
palsy, or contraction (miosis) of the other,
Horner's syndrome
- A sluggishly reactive pupil may be one of
the first signs of uncal herniation

Khm ng t

aniosocoria

Anisocoria
1. Cu hoi u tin: which side is the
problem?
- Examine pupils in light
Larger pupil does not constrict as wel
- Examine pupils in the dark
Smaller pupil does not dilate as well
2. Cu hoi th 2: is the anisocoria nonneurologic?

Neurologic Anisocoria
Pupillary size determined by balance between
sympathetic and parasympathetic tone

Sympathetic Fibers
- radial dilators
(anisocoria greater in
darkness)
1.
2.

Parasympathetic Fibers
- circular sphincter
- ciliary muscles
(anisocoria greater in
light)

1.
Horners syndrome
Aberrant regeneration 2.
3.

III nerve palsy

Adies tonic pupil
Pharmacologic

ng t hippus

@ ng t p ng i xng no gia bnh thng

@ Normal pupils + Absent Dolls Metabolic / Sedatives
@ Fixed Mid position pupil Focal Midbrain Lesion
@ Pinpoint Reactive Pontine Damage / Opiate /
Hydrocephalus / Thalamic Hemorrhage
@ Unil / Dil / Fixed Uncal Herniation - same/opposite
@ Bil / Dil / Fixed Central Herniation / Hypoxia /
Atropine or Barbiturate Poisoning / Mydriatics
@ Bu dc khng ng tm - Early midbrain / III n
Compression
@ Unil / Small (Horner) Large Cerebral Hemorrhage
Affecting Thalamus

E = Eyes

Ocular
Ocular Motility
Motility

cerebrum, cerebellum, and brainstem

Evaluation of ocular motility:
(1) observation of the resting position of
the eyes, including eye deviation;
(2) notation of spontaneous eye
movements.
(3) testing of reflex ocular movements.

E = Eyes

Ocular
Ocular Motility
Motility

Abnormalities in Resting Position

Eye
Deviation

conjugate
dysconjugate

1. Conjugate lateral eye deviation

@ ipsilateral lesion
@ contralateral lesion
2. Downward deviation of the eyes
@ Brainstem lesions (most often from
tectal compression), hepatic coma.
@ Thalamic and subthalamic lesions:
downward and inward
3. upward eye deviation
@ Sleep, seizure, syncope, CheyneStokes, hemorrhage vermis, brainstem
ischemia or encephalitis

E = Eyes

Ocular Motility

1. Potine conjugate gaze palsy

2. Internuclear ophthalmoplegia(INO)
3. One-and-a-half syndrome
4. Paralytic pontine exotropia

Paralytic pontine
exotropia
(Acute 1 syndrome)
Phi

L ngoi
Phi

tri

4. Skew deviation
@ posterior fossa lesion (brainstem or
cerebellar)
@ Dysconjugate vertical eye position
may sometimes occur in the absence of
a brainstem lesion in the obtunded
patient.

4. Skew deviation
- vertical ocular deviation, not due to a
cranial nerve palsy, orbital lesion, or
strabismus
- disturbed supranuclear input to the
third and fourth cranial nerve nuclei.
- unilateral damage to the otolith-ocular
pathways or the pathways mediating
the VOR.

E = Eyes

Ocular Motility

Spontaneous Eye Movements

1. Roving eye movements
- slow, conjugate, lateral to-and-fro
- brainstem is intact
- metabolic or toxic cause or bilateral
lesions above the brainstem (may be ocular
palsies or internuclear ophthalmoplegia )

Lu ong

E = Eyes

Ocular Motility

Spontaneous Eye Movements

2. Nystagmus (irritative or
epileptogenic supratentorial focus)
- manifestations of seizures
(eye, eyelid, face, jaw, or tongue )
- EEG

E = Eyes

Ocular Motility

Spontaneous Eye Movements

3. Spontaneous conjugate vertical
eye movements (nhieu loai phan
biet: velocities of their downward and
upward phases)

- Ocular bobbing: rapid downward

jerks of both eyes, followed by a slow
return to the midposition. - Typycal form :
paralysis of both reflex and spontaneous horizontal
eye movements.

E = Eyes

Ocular Motility

-Monocular or paretic bobbing:

bobbing occurs when
a coexisting ocular motor palsy alters the
appearance of typical bobbing
(atypical bobbing: all other variations of
bobbing that cannot be explained by an ocular
palsy superimposed on typical bobbing).
Ocular bobbing khi nhn ben con.
Bobbing ien hnh khong ac trng
ton thng cau nao cap. Bobbing
khong ien hnh khi thieu oxy va

E = Eyes

Ocular Motility

- Ocular dipping (inverse ocular bobbing ):

initial slow downward phase is followed by a
relatively rapid return, reflex horizontal eye
movements are preserved (diffuse cerebral
damage)

*slow initial downward phase, followed by a

rapid return that carries the eyes past the
midposition into full upward gaze. Then the
eyes slowly return to the midposition
nonlocalizing.

E = Eyes

Ocular Motility

Spontaneous Eye Movements

4. Vertical nystagmus: abnormal pursuit or
vestibular system (slow deviation of the eyes: the
primary position, with a rapid, immediate return to
the primary position )
@Ocular-palatal myoclonus: damage to the lower
brainstem (Guillain-Mollaret triangle , cerebellar
dentate, red nucleus, and inferior olive)
@Ocular flutter: back-to-back saccades horizontal

E = Eyes

Ocular Motility

Reflex Ocular Movements

@oculocephalic reflex (doll's eye
phenomenon)
@ vestibulo-oculogyric reflex, by
caloric (thermal) testing.
doll's eye phenomenon and doll's eye
maneuver =oculocephalic reflex,
COWS (cold opposite, warm same) fast phases

NP
NP nhit
nhit

Chiu di chuyn
dng ni dch

NP nc nng

NP nc lnh

R = Respiratory pattern
@ Rate?
@ Unusually deep or shallow?
@ Altered pattern?
1. Cheyne-Stokes respiration
2. central neurogenic hyperventilation
3. apneustic breathing
4. cluster breathing
5. ataxic respiration

R = Respiratory pattern
Cheyne-Stokes respiration
@ bilateral hemispheric or diencephalic
insults or upper pons .
@ pupillary size, and heart rhythm may vary
during Cheyne-Stokes respiration
@Two breathing patterns similar
- Short-cycle periodic breathing
- Biot's breathing

R = Respiratory pattern
Central neurogenic respiration
@ central tegmental pontine lesions just
ventral to the aqueduct or fourth ventricle
@ differentiated: reactive hyperventilation
(metabolic abnormalities of hypoxemia
secondary)
@ Hyperpnea cannot ascribe CNS lesion
when arterial oxygen pressure < 70-80 mm
Hg or carbon dioxide pressure > 40 mm Hg.

R = Respiratory pattern
@ Kussmaul breathing :deep,
regular respiration ( metabolic
acidosis )
@Apneustic breathing: prolonged
inspiratory gasp with a pause at full
inspiration. Lesions: dorsolateral
lower half of the pons

R = Respiratory pattern
@ Cluster breathing: high medullary
damage, periodic respirations:
irregular in frequency and amplitude,
with variable pauses between clusters
of breaths.
@Ataxic breathing: irregular rate &
rhythm, medullary lesions
*Ataxic respiration and bilateral sixth nerve palsy may
be a warning sign of brainstem compression

Cheyne-Stocks

Central Neurogenic Hyperventilation

Apneustic

Cluster
Ataxic

Cac kieu roi loan nhp th phoi

hp vi sang thng benh ly cua
nao
A-Th Cheyne-Stokes : ton thng lan
toa nao trc
B- Th tang thong kh do than kinh:
ton thng phan bung thap nao
gia en cong Sylvius va bung
tren cau nao en nao that 4.
C- Ngng th keo dai cuoi ky ht
vao: ton thng phan mai lng ben
phan uoi va gia cau nao
D- Th tng cum: ton thng phan

Abnormal breathing patterns in coma

Cheynes - Stokes
Central Neurogenic

Midbrain

Apneustic
Pons

Ataxic

Medulla
ARAS

 CheyneStokes respiration:
(hyperpnoea alternates with apneas) is
commonly found in comatose patients,
often with cerebral disease, but is
relatively non-specific.
Rapid, regular respiration is also
common in comatose patients and is
often found with pneumonia or acidosis.

 Central neurogenic hyperventilation

Brainstem tegmentum (mostly tumors):
PO2, PCO2, and
Respiratory alkalosis in the absence of
any evidence of pulmonary disease
Sometimes complicates hepatic encephalopathy

1- Apneustic breathing:
Brainstem lesions: Pons may also give with
a pause at full inspiration
2- Ataxic:
Medullary lesions: irregular respiration with
random deep and shallow breaths

Odour of breath
Acetone: DKA
Fetor Hepaticus(mi hi ca gan): in hepatic
coma
Urineferous odour: in uremic coma
Alcohol odour: in alcohol intoxication

M = Motor Function
@ Evidence of paralysis?
@ Movement on stimulation?
@ How?
1. Decerebrate posturing
2. Decorticate posturing
3. Unilateral decerebrate or decorticate
postures

M = Motor Function
Adventitious movements
@ Myoclonic jerking: anoxic
encephalopathy or other metabolic
comas, such as hepatic
encephalopathy.
@ Rhythmic myoclonus: brainstem
injury
@Cerebellar fits : tonsillar herniation
(opisthotonos, respiratory rate slowing and irregularity,
Ngau nhien cn,
and pupillary dilation )

DIFFERENTIAL
DIFFERENTIAL DIAGNOSIS
DIAGNOSIS
Differentiate metabolic or toxic causes
from structural lesions
1. State of consciousness.
2. Respiration.
3. Funduscopic examination
4. Pupil size

DIFFERENTIAL
DIFFERENTIAL DIAGNOSIS
DIAGNOSIS
5. Pupil reactivity
6. Ocular motility.
7. Spontaneous eye movements.
8. Reflex eye movements.
9. Adventitious movement
10.Muscle tone.

DIFFERENTIAL
DIFFERENTIAL DIAGNOSIS
DIAGNOSIS
Differentiating Psychiatric Coma
and Pseudocoma
@ Examinations of the eyelid, pupil,
adventitious eye movements, and
vestibulo-oculogyric reflex by cold
caloric testing

Chn on cht no

The role of EEG in diagnosis

@ Differentiates coma from psychogenic
unresponsiveness
@ Identifies non convulsive status epilepticus
@ Bilateral delta indicates the patient is either
deeply asleep or unconscious
@ A normal EEG rules out metabolic brain
disease as a cause of coma.

The role of EEG in diagnosis

@ A normal EEG in delerium
strongly suggests an alcohol or drug
withdrawal state
@ The degree of slowing usually
reflects the severity of the metabolic
encephalopathy

The role of EEG in diagnosis

@ In diffuse metabolic encephalopathy
the EEG is usually more sensitive than
the clinical assessment with slowing still
present when the patient has returned
to clinical normality

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Five Grades
Grade 1. Near normal
@ Excellent prognosis unless
locked inor alpha pattern coma

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Five Grades
Grade 2. Theta dominant
@ If reactive the prognosis is very
good If nonreactive survival is usually
accompanied by neurological
sequelae

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Five Grades
Grade 3. Delta dominant
@If reactive the prognosis can be
good
@If non-reactive the prognosis is
grave provided drugs and
hypothermia excluded

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Five Grades
Grade 4. Burst suppression & continuous
bilateral periodic sharp waves
@ Prognosis grave if drugs and
hypothermia excluded
@ Often associated with clinical
myoclonus.

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Grade 5. Isoelectric
Prognosis grave if drugs and
hypothermia excluded

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Rare Variants
Alpha pattern coma
@ Anterior predominance
@ Unreactive alpha frequency
activity.
@ Rare survivors but only if brain
stem reflexes intact.

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Rare Variants
Theta pattern coma
@ Usually elderly
@ 5 Hz theta with low amplitude
burst suppression morphology
@ Grave prognosis

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

Rare Variants
Spindle coma
@Usually head injury, rarely anoxic
injury
@ resembles stage II sleep
@ prognostically benign.

The
The role
role of
of EEG
EEG in
in prognosis
prognosis of
of anoxic
anoxic cerebral
cerebral injury
injury

@ The difficult group are grade II

nonreactives and grade III. These
are also the most common groups.
@ SEPs are useful to further define
the prognosis in these groups.

The
The role
role of
of EEG
EEG in
in prognosis
prognosis in
in severe
severe head
head injury
injury

@EEG is considerably more limited in

prognostication in severe head injury.
@Reactivity may be the most useful
parameter for classifying outcome into
good vs bad
@ Good being moderately disabled
or better
@ Bad being worse than moderately
disabled.

Reactivity can be
@ Attenuation
@ Paradoxical (high amplitude slow
waves)
@ Doubtful/Uncertain
@ absent.
- 90 + % of patients with preserved reactivity of either
type have goodoutcomes
- 90 +% of patients with absent reactivity have bad
outcomes.
- 20 +% have uncertain reactivity & 70+ % of these
have good outcomes

The
The role
role of
of SEPs
SEPs in
in anoxic
anoxic cerebral
cerebral injury
injury and
and
severe
severe head
head injury
injury

@ The bilateral absent of the

thalamo-cortical wave forms (N19,
N20, N1)signifies that the patient will
not recover to better than
PVS.100% specificity
@ However sensitivity is low (20-30
%).
@Hence the interest in the N70

N70
@ Madl et al
Of 113 patients with a bilateral N70 peak
latency >130 msec or absent all but one had
a poor outcome
Sensitivity of 94% and specificity of 97%
@ Sherman et al
Using a bilateral N70 peak latency > 176
msec all had a poor outcome
Sensitivity 78% and specificity of 100

Coma Prognostication
Gauging coma:
History
Exam
Ancillary studies

History cannot accurately predict outcome

of coma.

Coma Prognostication
Ancillary studies cannot accurately
ascertain coma emergence
Exception:
SSEPs performed days 1-3 after coma.
Absence of cortical response shows poor
prognosis.

Coma Prognosis
Exam
Glascow coma score (eye opening, motor
response, verbal response)
rather useless
Motor:
Command>purposeful>flexor>extensor>flaccid
Cranial nerves: present>absent
Roving eye movements > no spontaneous

Coma Prognosis: Take Home

(its bad when)
First 24hr post circulatory arrest:
myoclonus status epilepticus
Or by day 3:
no corneals, or
absent pupillary reaction, or
motor response is extensor or worse

PROGNOSIS
outcome in any comatose patient cannot be predicted
with 100% certainty unless that patient meets the criteria
for brain death
subcategories:
drug-induced
Nontraumatic
traumatic coma

Drug-induced coma usually is reversible unless the

patient has not had appropriate systemic support whiIe
comatose and has sustained secondary injury from
hypoperfusion, hypoxia, or lack of other necessary
metabolic substrates

Nontraumatic Coma
Only about 15% of patients in nontraumatic coma make a satisfactory
recovery
Functional recovery is related to the cause of coma.
Diseases causing structural damage, such as cerebrovascular
disease including subarachnoid hemorrhage, carry the worst
prognosis
coma from hypoxia-ischemia due to such causes as cardiac arrest
has an intermediate prognosis
coma due to hepatic encephalopathy and other metabolic causes has
the best ultimate outcome
Age does not appear to be predictive of recovery
The longer a coma lasts, the less likely the patient is to regain
independent functioning.

Nontraumatic Coma
patients with nontraumatic coma who have not
regained awareness by the end of 1 month are
unlikely to do so. Even if they do regain
consciousness, they have practically no chance
of achieving an independent existence
poor neurological outcome: within 3 days of
coma
The absence of pupillary light responses
The absence of motor responses to pain
low Glasgow Coma scores (less than 5)

Traumatic Coma
The prognosis for traumatic coma differs from
that for nontraumatic coma in many ways
First, many patients with head trauma are young
Second, prolonged coma of up to several months
does not preclude a satisfactory outcome in traumatic
coma
Third, in relationship to their initial degree of
neurological abnormality, traumatic coma patients do
better than nontraumatic coma patients

Traumatic Coma
early predictors of the outcome of posttraumatic coma include
patient's age
motor response
pupillary reactivity
depth and duration of coma
The prognosis worsens with increasing age
little influence on the outcome
Cause of injury
skull fracture
lateralization of damage to one hemisphere
extracranial injury