157. Guillevin R, Vallee JN, Demeret S, et al. Cerebral
fat embolism: Usefulness of magnetic resonance
spectroscopy. Ann Neurol 57, 434–439, 2005.
158. Schoning M, Scheel P, Holzer M, et al. Volume
measurement of cerebral blood flow: assessment of
cerebral circulatory arrest. Transplantation 80 (3),
326–331, 2005.
159. Dominguez-Roldan JM, Garcia-Alfaro C, Jimenez-
Gonzalez PI, et al. Brain death due to supratentor-
ial masses: diagnosis using transcranial Doppler so-
nography. Transplant Proc 36 (10), 2898–2900, 2004.
160. Wojner-Alexandrov AW, Alexandrov AV, Rodriguez
D, et al. Houston paramedic and emergency stroke
treatment and outcomes study (HoPSTO). Stroke 36
(7), 1512–1518, 2005.
161. Panerai RB, Kerins V, Fan L, et al. Association
between dynamic cerebral autoregulation and mor-
tality in severe head injury. Br J Neurosurg 18 (5),
471–479, 2004.
162. Droste DW, Metz RJ. Clinical utility of echocontrast
agents in neurosonology. Neurol Res 26 (7), 754–
759, 2004.
163. Brenner RP. The interpretation of the EEG in
stupor and coma. Neurologist 11(5), 271–284, 2005.
164. Kaplan PW. Assessing the outcomes in patients with
nonconvulsive status epilepticus: nonconvulsive sta-
tus epilepticus is underdiagnosed, potentially over-
treated, and confounded by comorbidity. J Clin
Neurophysiol 16 (4), 341–352, discussion 353, 1999.
165. Brenner RP. Is it status? Epilepsia 43 (Suppl 3),
103–113, 2002.
166. Towne AR, Waterhouse EJ, Boggs JG, et al. Preva-
lence of nonconvulsive status epilepticus in coma-
tose patients. Neurology 54, 340–345, 2000.
167. Burneo JG, Knowlton RC, Gomez C, et al. Confir-
mation of nonconvulsive limbic status epilepticus
with the sodium amytal test. Epilepsia 44, 1122–
1126, 2003.
168. Kaplan PW. The clinical features, diagnosis, and
prognosis of nonconvulsive status epilepticus. Neu-
rologist 11(6), 348–361, 2005.
169. Fischer C, Luaute´ J, Adeleine P, et al. Predictive
value of sensory and cognitive evoked potentials for
awakening from coma. Neurology 63, 669–673, 2004.
Examination of the Comatose Patient
87
Chapter
3
Structural Causes of
Stupor and Coma
COMPRESSIVE LESIONS AS A CAUSE
OF COMA
COMPRESSIVE LESIONS MAY DIRECTLY
DISTORT THE AROUSAL SYSTEM
Compression at Different Levels
of the Central Nervous System Presents
in Distinct Ways
The Role of Increased Intracranial Pressure
in Coma
The Role of Vascular Factors and Cerebral
Edema in Mass Lesions
HERNIATION SYNDROMES:
INTRACRANIAL SHIFTS IN
THE PATHOGENESIS OF COMA
Anatomy of the Intracranial Compartments
Patterns of Brain Shifts That Contribute
to Coma
Clinical Findings in Uncal Herniation
Syndrome
Clinical Findings in Central Herniation
Syndrome
Clinical Findings in Dorsal Midbrain
Syndrome
Safety of Lumbar Puncture in Comatose
Patients
False Localizing Signs in the Diagnosis
of Structural Coma
DESTRUCTIVE LESIONS AS A CAUSE
OF COMA
DIFFUSE, BILATERAL CORTICAL
DESTRUCTION
DESTRUCTIVE DISEASE OF
THE DIENCEPHALON
DESTRUCTIVE LESIONS OF
THE BRAINSTEM
Two major classes of structural brain injuries
cause coma (Table 3–1): (1) Compressive lesions
may impair consciousness either by directly
compressing the ascending arousal system or
by distorting brain tissue so that it moves out
of position and secondarily compresses compo-
nents of the ascending arousal system or its
forebrain targets (see herniation syndromes,
page 95). These processes include a wide range
of space-occupying lesions such as tumor, he-
matoma, and abscess. (2) Destructive lesions
cause coma by direct damage to the ascending
arousal system or its forebrain targets. To cause
coma, lesions of the diencephalon or brainstem
must be bilateral, but can be quite focal if they
damage the ascending activating system near
the midline in the midbrain or caudal dien-
cephalon; cortical or subcortical damage must
be both bilateral and diffuse. Processes that
may cause these changes include tumor, hem-
orrhage, infarct, trauma, or infection. Both de-
structive and compressive lesions may cause
88
additional compression by producing brain
edema.
Most compressive lesions are treated surgi-
cally, whereas destructive lesions are generally
treated medically. This chapter describes the
pathophysiology and general approach to pa-
tients with structural lesions of the brain, first
considering compressive and then destructive
lesions. Chapter 4 deals with some of the spe-
cific causes of coma outlined in Table 3–1.
Chapter 2 has described some of the phys-
ical findings that distinguish structural from
nonstructural causes of stupor and coma. The
physician must first decide whether the patient
is indeed stuporous or comatose, distinguish-
ing those patients who are not in coma but suf-
fer from abulia, akinetic mutism, psychologic
unresponsiveness, or the locked-in state from
those truly stuporous or comatose (see Chap-
ter 1). This is usually relatively easily done dur-
ing the course of the initial examination. More
difficult is distinguishing structural from met-
abolic causes of stupor or coma. As indicated
in Chapter 2, if the structural cause of coma
involves the ascending arousal system in the
brainstem, the presence of focal findings usu-
ally makes the distinction between metabolic
and structural coma easy. However, when the
structural disease involves the cerebral cortex
diffusely or the diencephalon bilaterally, focal
signs are often absent and it may be difficult to
distinguish structural from metabolic coma.
Compressive lesions that initially do not cause
focal signs eventually do so, but by then coma
may be irreversible. Thus, if there is any ques-
tion about the distinction between structural
and metabolic coma, immediately after stabi-
lizing the patient, an imaging study (usually a
computed tomography [CT] scan but, if avail-
able, a magnetic resonance imaging [MRI]
scan) must be obtained to rule out a mass le-
sion that may be surgically remediable. Identi-
fying surgically remediable lesions that have
not yet caused focal findings gives the physi-
cian time to stabilize the patient and investi-
gate other additional nonstructural causes of
coma. The time, however, is short and should
be counted in minutes rather than hours or
days. If focal findings are already present, ef-
forts to decrease intracranial pressure (ICP),
including hyperventilation and hyperosmolar
agents and often administration of corticoste-
roids (Chapter 7), should be instituted before
sending the patient for imaging.
COMPRESSIVE LESIONS AS
A CAUSE OF COMA
Compressive lesions may impair consciousness
in a number of critical ways: (1) by directly dis-
torting the arousal system or its forebrain tar-
gets; (2) by increasing ICP diffusely to the point
of impairing global cerebral blood flow; (3)
by distorting tissue to the point of causing lo-
cal ischemia; (4) by causing edema, thus fur-
ther distorting neural tissue; or (5) by causing
tissue shifts (herniations). Understanding the
Table 3–1 Sites and Representative Causes of Structural Lesions
That Can Cause Coma
Compressive
Destructive
Cerebral
Cerebral hemisphere
Bilateral subdural hematomas
Cortex (e.g., acute anoxic injury)
Diencephalon
Subcortical white matter
(e.g., delayed anoxic injury)
Thalamus (e.g., hemorrhage)
Hypothalamus (e.g., pituitary tumor)
Diencephalon
Brainstem
Thalamus (e.g., infarct)
Midbrain (e.g., uncal herniation)
Brainstem
Cerebellum (e.g., tumor,
hemorrhage, abscess)
Midbrain, pons (e.g., infarct)
Structural Causes of Stupor and Coma
89