CHAPTER3
Table 3-3. Glasgow Coma Scale.
Motor
Score EyeOpening Vtrbal Response Response
None None None
Extension
2 Topain Vocal but notverbal
3 Tovoice Verbalbut not Flexion
conversational
4
5
Spontaneous Conversational but
disoriented
Oriented
Withdraws
from pain
localizes pain
6 Obeys
commands
AdJpred from Teasdale G. Jenneu B. Assessment of coma and
1mp.Nea consc1ousness.Apract1calscale. Lancer. 1974;2:81-84.
Glasgow Coma Scale
The .rupillar ·· ere mm·ement, and motor responses
descnbed carher are sometimes translated to a numerical
scale so that changes in the examination (and thus th
numen.ca Iscore) may be more easily noticed over time ande
compared between different examiners (Table 3-3).
PATHOPHYSIOLOGICASSESSMENT
! h e mos.t important step in e\·aluating a comatose patient
IS to deode whether the cause is a structural brain lesion
(for which emergency neurosurgical intervention may be
reqUired ) or a diffuse disorder caused by a metabolic dis
turban ce, meningitis, or seizures (for which immediate
medical treatment may be needed).
Supratentorial Structural Lesions
When coma results from a supratentorial mass lesion, the
history and physical findings early in the course usually
point to dysfunction of one cerebral hemisphere. Symptoms
and signs include contralateral hemiparesis, contralateral
hemisensory loss, aphasia (with dominant, usually left,
hemisphere lesions), and agnosia (indifference to or denial
of the deficit, with injury to the nondominant hemisphere).
As the mass expands (commonly from associated
edema), the patient becomes increasingly lethargic due to
compression of the contralateral hemisphere or thalamus.
Stupor progresses to coma, but findings on examination
often remain asymmetric. With rostral- caudal (down
ward) progression of brain injury, the thalamu s, midbrain,
pons, and medulla become sequentially involved, and the
neurologic examination reveal s dysfunction at successively
lower anatomic levels (see Figure 3-2). This segmental pat
tern of rostral-caudal involvement strongly supports the
Lateral ......
_ c . ...
ventricles (J) - .
r.\;a
Uncus '
>I @ p ) l r: - - cerebeu;
Tentorium
Cerebellar tonsil / ?
Brainstem
I
A F•'gure3-4. Anatomic basis of herniar
An :x anding supratentorial mass lesionron syndromes
bram trssue to be displaced into d' may cause ·
c an a Jacent ·
ompartment, resulting in (1) cingulat h .'n racranial
under the falx, (2) downward transte e .ernratron
herniation, (3) uncal herniation o orral (central)
tentorium, or (4) cerebellar ton 'llverht e d e of the
c sr ar ernratron ·
,oramen magnum. Coma and ultimate! Into the
when (2), (3), or (4) produces brainstemy death re ult
compressron.
diagnosis
. I hof a. supratentorial mass with d ownward tr
tentona e• rmation (Figure 3-4) and dI.Ctates the needancs.
neurosurgical intervention. At th f 11 tor
'db . I e u y develop d
m1 . ram eve] (midsized, unreactive pupils) hances e
I .h ' c of
sur:lva Wit out severe neurologic impairment d
drapidly,
fi especially
. . in adults. Once the pont ·me lecrelase
eve of
ys un1ctiOn IS reached (unreactive pupils •and absent hon.-
zonta eye movements), a fatal outcome is inevitable
Supratentorial mass lesions may cause herniation.ofth
medial portion of the temporal lobe (the uncus) over th;
edge of he cerebellar tentorium (see Figure 3-4). This
exerts direct pressure on the upper brainstem and
produces signs of oculomotor (III) nerve and midbrain
compression, such as ipsilateral pupillary dilatation and
impaired adduction of the eye (uncal syndrome) , which
may precede loss of consciousness. Neurosurgica l decom·
pression must occur early in the course of oculomotor (III)
nerve involvement if functional recovery is to occur.
Subtentorial Structural Lesions
Coma of sudden onset with focal signs of brainstem dys
function strongly suggests a subtentorial structural lesion.
Abnormal pupillary function and impaired eye movement
are the findings most suggestive of a subtentorial structual
lesion, especially if these abnormalities are asymmetnc.
Midbrain lesions cause Joss of pupillary function: th;
upils are midsized (approximately 5 mm in diam · eteinr)faarnc-
P
unreacti ve to light. Pontine hemorrhage, pontme b Jlar
tion ' or compression of the pons by adjacent cere e.115
· · t puP ·
hemorrhage or infarction produces pmpom
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