Normal

Central
hyperventilation

Ataxic

Gasping

Figure 3-5. Ventilatory patterns in coma. Cheyne

Stokes respiration and central hyperventilation are
seen with metabolic disturbances and with structural
lesions at a variety of sites in the brain. They are
therefore not useful for anatomic localization of
disorders producing coma. Ataxic and gasping
ventilatory patterns are most commonly seen with
pontomedullary lesions.
Scanned by CamScan
 Brains . :11 lt·sions may also be associated with conjugate
gaze devic_ticn away from the side of the lesion (and
toward a hemiparesis) (see Figure 7-17), or disconjugate eye
move ments such as· internuclear
ophthalmoplegia (selective impairment of eye
adduction). Motor responses are gener ally not helpful in
separating subtentorial from supratento rial lesions.
Ventilatory patterns associated with subtentorial lesions are
abnormal but variable and may be ataxic or gasp ing (Figure
3-5). Because the fully developed syndrome of
transtentorial herniation from a supratentorial mass is
characterized by extensive brainstem dysfunction, its
differentiation from a primary subtentorial process may be
impossible except by history.

Diffuse Encephalopathies
Diffuse encephalopathies that result in coma (sometimes
· termed metabolic coma) include not only metabolic disor
ders such as hypoglycemia and drug intoxication, but other
processes that affect the brain diffusely, such as meningitis,
subarachnoid hemorrhage, and seizures.
. The clinical presentation of diffuse encephalopathy
18
distinct from that of a mass lesion. There are usually no
focal signs, such as hemiparesis, hemisensory loss, or
aphasia,
h
 and-.except i some cases of subarachnoid hemorrhage
consciOusness 1s lost only gradually, typically after a
period of progressive somnolence or agitated delirium.
A symmetric neurologic examination is the rule,
although hypoglycemia, hyperosmolar nonketotic hyper
glycemia, and hepatic encephalopathy may sometimes be
accompanied by focal signs, such as hemiparesis, which
may alternate from side to side. Asterixis, myoclonus, and
tremor preceding coma are important clues that suggest
metabolic disease. Symmetric decorticate or decerebrate
posturing can be seen with hepatic, uremic, anoxic, hypo
glycemic, or sedative drug-induced coma.
Reactive pupils in the presence of otherwise impaired
brainstem function is the hallmark of metabolic encepha
lopathy. Although coma with intact pupillary reaction can
also be seen early in transtentorial herniation (see
Figure 3-2), the latter is associated with asymmetric neuro
logic fmdings, such as hemiparesis. A few metabolic
causes of coma can also impair pupillary light reflexes,
including massive barbiturate overdose with apnea and
hypotension, acute anoxia, marked hypothermia,
anticholinergic poi soning (large pupils), and opioid
overdose (pinpoint pupils), but even in these settings,
completely unreactive pupils are uncommon .
Ventilatory patterns in metabolic coma vary widely (see
Figure 3-5), but measuring arterial blood gases and pH
may help to establish an etiologic diagnosis. Arterial blood
gas abnormalities in coma are outlined in Table 3-2.

Summary
The relationship between neurologic signs and the patho
physiology of coma is summarized in Table 3-4.
Examining pupil size and reactivity and testing reflex eye
movements and the motor response to pain help
determine whether brain function is disrupted at a
discrete anatomic level (structural lesion) or in a diffuse
manner (metabolic coma).
Supratentorial structural lesions compromise the brain
in an orderly way, producing dysfunction at progressively
lower anatomic levels. In patients with metabolic coma,
such localization is not possible, and scattered, anatomi
cally inconsistent findings may be seen. An impressive
example of the anatomically discordant findings character
istic of metabolic coma is the retention of pupillary
reactivity in the face of otherwise depressed brainstem
functions including paralysis of eye movements,
respiratory depres sion, flaccid muscle tone, and
unresponsiveness to painful stimuli-after sedative drug
overdose. The same degree of low brainstem dysfunction
produced by a supratentorial mass lesion would first
compromise the more rostrally situated midbrain
structures that mediate pupillary reac tivity before
affecting the lower brainstem centers.

Edlow JA, Rabinstein A, Traub SJ, Wijdicks EF. Diagnosis of

reversible causes of coma. Lancet.2014;in press.
 c
Figure 7-17. Disorders of gaze associated with hemispheric and brainstem lesions. (A) Destructive lesion in
the frontal lobe of the right cerebral hemisphere.(B) Seizure arising from the frontal lobe of the right cerebral
hemi sphere. (C) Destructive lesion in the right pons. Arrows indicate the direction of gaze preference (away from
the hemiparetic side in (A) and toward the convulsing or hemiparetic side in [B] and [C]).