CHAPTER 3

Table 3-3. Glasgow Coma Scale. Lateral _c . .........

r. \
ventricles (J) - .
Motor
Score Eye Opening Vtrbal Response Response
None None None
Uncus '
2 To pain Vocal but not verbal Extension

;a I
3 To voice Verbal but not Flexion
conversational r:-- Tentorium
cerebeu;
>I
4 Spontaneous Conversational but Withdraws
disoriented from pain
5 Oriented localizes pain
Cerebellar tonsil /?
Obeys Brainstem
6 A F•'gure 3-4. Anatomic basis of herniar
commands
An :x anding supratentorial mass lesionron syndromes
AdJpr ed from Teasdale G. Jenneu B. Assessment of coma bram trssue to be displaced into d' may cause ·
c an a Jacent ·
and ompartment, resulting in (1) cingulat h .'n racranial
1mp.Nea consc1ou sness.A pract 1cal scale. Lancer. 1974;2:81-84. 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 ·
Glasgow Coma Scale ,oramen magnum. Coma and ultimate! Into the
when (2), (3), or (4) produces brainstemy death reult
compressron.
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 diagno s is of a supratentorial mass with d
. I e tentona. I eh rmation
. ownward
(Figure 3-4) and d I.Ct ates tr
numen ca score) may be more easily noticed over time and • the
compared between different examiners (Table 3-3). needanc s. neurosurgical intervention. At11 th f
tor
PATH OPHYSIOLOGIC ASSESSMENT m1'db ram e u y hdeveloped
. Ieve] (midsized, unreactive pupils)
. I .h ' cances of
sur:lva Wit out severe neurologic impairment d
!he mos.t important step in e\·aluating a comatose rapidly, especially in adults. Once the pont · lecrel ase
d fi . . me eve of
patient
IS to deode whether the cause is a structural brain lesion ysun ctiOn IS reached (unreactive pupils •and absent hon.-
(for which emergency neurosurgical intervention may be 1
zonta eye movements), a fatal outcome is inevitable
reqUired ) or a diffuse disorder caused by a metabolic dis Supratentorial mass lesions may cause herniation .ofth
turban ce, meningitis, or seizures (for which immediate medial portion of the temporal lobe (the uncus) over th;
medical treatment may be needed). edge of he cerebellar tentorium (see Figure 3-4). This
exerts direct pressure on the upper brain stem and
Supratentorial Structural Lesions produces signs of oculomotor (III) nerve and midbrain
compression, such as ipsilateral pupillary dilatation and
When coma results from a supratentorial mass lesion, the impaired adduction of the eye (uncal syndrome) , which
history and physi cal findings early in the course usually may precede loss of consciousness. Neurosurgica l decom
point to dysfunction of one cerebral hemisphere. Symptoms · pression must occur early in the course of oculomotor
and signs include contral ateral hemiparesis, contralateral (III) nerve involvement if functional recovery is to occur.
hemisensory loss, aphasia (with dominant, usually left,
hemisphere lesions), and agnosia (indifference to or denial Subtentorial Structural Lesions
of the deficit, with injury to the nondominant hemisphere).
As the mass expands (commonly from associated Coma of sudden onset with focal signs of brainstem dys
function strongly suggests a subtentorial structural lesion.
edema), the patient becomes increasingly lethargic due to
Abnormal pupill ary function and impaired eye movement
compression of the contralateral hemisphere or thalamus.
are the findings most suggestive of a subtentorial structual
Stupor progresses to coma, but findings on examination
lesion, especially if these abnormalities are asymmetnc.
often remain asymmetric. With rostral-caudal (down
Midbrain lesions cause Joss of pupillary function:
ward) progression of brain injury, the thalamu s, midbrain , th;
pons, and medulla become sequentially involved, and the
neurologic examination reveal s dysfunction at successively upils are midsized (approximately 5 mm in diam
P r) a n unreacti
ete ve to light. Pontine hemorrhage,·
lower anatomic levels (see Figure 3-2). This segmental pat in fa r c-
tern of rostral-caudal involvement strongly supports the pontme b Jlar tion or compression of the pons by adja
15
cent ' cere e .
· · t puP 1 ·
hemorrhage or infarction produ ces
pmpom
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