hemiplegia. Thalamic hemorrhage may pres-
ent with sensory phenomena, but often the
hemorrhage compresses ascending arousal
systems early so that loss of consciousness is
the primary presentation.
101
When the hem-
orrhage is into the caudal part of the thalamus,
such as the putamen, which overlies the pos-
terior commissure, the initial signs may be due
to dorsal midbrain compression or injury
102
(see page 110), with some combination of forced
downgaze and convergence (‘‘peering at the
tip of the nose’’), fixed pupils, and retractory
nystagmus. Another neuro-ophthalmologic pre-
sentation of thalamic hemorrhage was descri-
bed by Miller Fisher as ‘‘wrong-way eyes.’’
107
Whereas frontal lobe insults usually result in
deviation of the eyes toward the side of the le-
sion (i.e., paresis of gaze to the opposite side
of space), after thalamic hemorrhage (or occa-
sionally deep intraparenchymal hemorrhage
that damages the same pathways
108
) there may
be a paresis of gaze toward the side of the lesion
(see Chapter 3).
PATHOPHYSIOLOGY
Hemorrhages of the end artery type are often
called hypertensive hemorrhages, although they
may occur in other clinical settings. The reason
for the predilection of this class of artery for
both occlusion (lacunar infarction) and hemor-
rhage is not known. Miller Fisher attempted to
identify the arteries that had caused lacunar
infarctions in postmortem examination of the
brain.
109
He found an eosinophilic degenera-
tion of the wall of small penetrating arteries in
the region of the infarct and proposed that this
‘‘lipohyalinosis’’ was the cause of the infarction.
However, this description was based on a small
number of samples and did not give any insight
into the nature of the pathologic process. Given
the fact that such vessels typically take off at
a right angle from large cerebral arteries, one
might expect high sheering forces at the vessel
origin, so that high blood pressure or other ath-
erosclerotic risk factors might cause earlier or
more severe damage. However, the mechanism
for this phenomenon remains unclear.
End artery hemorrhages typically produce a
large hematoma with considerable local tissue
destruction and edema. Because much of the
clinical appearance is due to the mass effect,
which eventually is resorbed, the patient may
initially to be much more neurologically im-
paired than would be caused by a comparably
sized infarct. However, if the patient can be
supported through the initial event, recovery
is often much greater than might be initially an-
ticipated, and the hematoma is resorbed, leav-
ing a slit-like defect in the brain.
Amyloid angiopathy results from deposition
of beta-amyloid peptide in the walls of cerebral
blood vessels.
110
These deposits disrupt the
arterial elastic media resulting in predisposi-
tion to bleeding. Because amyloid deposits
occur along blood vessels as they penetrate the
ipsilateral peripheral facial palsy, and contralateral extensor plantar response.
Occasionally, course may proceed for 1 to 2 weeks. Spinal fluid bloody.
Acute cerebellar infarction
Mostly hypertensive, mostly males. Onset at any time. Vertigo, ataxia, nausea, dull
headache, nystagmus, dysarthria, ipsilateral dysmetria; 24 to 96 hours later:
drowsiness, miosis, ipsilateral gaze paresis and facial paresis, worsening ataxia,
extensor plantar responses. Coma, quadriplegia, and death may follow if not
decompressed. Spinal fluid sometimes microscopically bloody.
Acute subarachnoid hemorrhage
Awake at onset, sometimes hypertensive, sudden headache, often followed within
minutes by unconsciousness. Pupils small or unilaterally dilated. Subhyaloid
hemorrhages, hemiparesis or aphasia may or may not be present, hemisensory
changes rare. Neck stiff within 24 hours. Bloody spinal fluid.
Specific Causes of Structural Coma
139
cerebral cortex, the hemorrhages are typically
lobar (i.e., into a specific lobe of the cerebral
cortex).
111
The arteries that hemorrhage tend
to be small vessels, which seal spontaneously,
so that the patient usually survives but may have
multiple recurrences in later years.
112
Acute
onset of focal hemispheric signs and a head-
ache are the most common presentation. As
with end artery hemorrhages, the severity of
the initial presentation often is misleading, and
as the hemorrhage is resorbed, there may be
much greater return of function than in a pa-
tient with a similarly placed infarction. Gradi-
ent echo MRI may reveal additional areas of
small, subclinical cortical and subcortical hem-
orrhage.
113
Mycotic aneurysms are typically seen in the
setting of a patient who has subacute bacterial
endocarditis.
114
Infected emboli that reach the
brain lodge in small penetrating arteries in the
white matter just deep to the cerebral cortex.
The wall of the blood vessel is colonized by
bacteria, resulting in aneurysmal dilation sev-
eral millimeters in diameter. These aneurysms,
which may be visualized on cerebral angiog-
raphy, may be multiple. Because there may
be multiple mycotic aneurysms, and to elimi-
nate an arteriovenous malformation or saccular
aneurysm as the source, an angiogram is gener-
ally necessary. Unruptured mycotic aneurysms
are treated by antibiotics, but ruptured aneu-
rysms may require endovascular or open surgi-
cal intervention.
115
Vascular malformations may occur in any
location in the brain. They range from small
cavernous angiomas to large arteriovenous mal-
formations that are life threatening. MRI iden-
tifies many more cavernous angiomas than are
seen on conventional arteriography or CT scan-
ning. The abnormal vessels in these malfor-
mations are thin-walled, low-pressure and low-
flow venous channels. As a result, cavernous
angiomas bleed easily, but rarely are life threat-
ening. Cavernous angiomas of the brainstem
may cause coma if they hemorrhage and have
a tendency to rebleed.
116
They can often be re-
moved successfully.
117
Radiosurgery may also
reduce the risk of hemorrhage, but can cause
local edema or even hemorrhage acutely.
118,119
Complex
arteriovenous
malformations
(AVMs) contain large arterial feeding vessels
and are often devastating when they bleed.
120
Although somewhat less likely to cause im-
mediate death than are saccular aneurysms,
arteriovenous malformations may be much
harder to treat and bleeding may recur multi-
ple times with gradually worsening outcome.
AVMs may also cause symptoms by inducing
epilepsy, or by causing a vascular steal from
surrounding brain. AVMs that come to atten-
tion without hemorrhage have about a 2% to
4% per year chance of bleeding, but those that
have previously bled have a much higher risk.
AVMs are typically treated by a combination of
endovascular occlusion of the arterial supply
followed, if necessary, by surgery, although
radiosurgery may also shrink AVMs in inac-
cessible regions.
Hemorrhage into a tumor typically occurs in
the setting of a patient with known metasta-
tic cancer. However, in some cases, the hem-
orrhage may be the first sign of the tumor. A
higher percentage of metastatic melanoma, thy-
roid carcinoma, renal cell carcinoma, and germ
cell tumors hemorrhage than is true for other
tumor types, but lung cancer is so much more
common than these tumors that it is the sin-
gle most common cause of hemorrhage into
a tumor.
121
Primary brain tumors, particularly
oligodendrogliomas, may also present with a
hemorrhage into the tumor. Because it is often
difficult to see contrast enhancement of the
tumor amidst the initial blood on MRI or CT
scan, it is generally necessary to reimage the
brain several weeks later, when the acute blood
has been resorbed, if no cause of the hemor-
rhage is seen on initial imaging.
Intracerebral Tumors
Both primary and metastatic tumors may in-
vade the brain, resulting in impairment of con-
sciousness.
121,122
Primary tumors are typically
either gliomas or primary CNS lymphomas,
whereas metastatic tumors may come from
many types of systemic cancer. Certain prin-
ciples apply broadly across these classes of
tumors.
Gliomas include both astrocytic tumors and
oligodendrogliomas.
122
Astrocytic tumors typ-
ically invade the substance of the brain, and
in extreme cases (gliomatosis cerebri), may dif-
fusely infiltrate the entire brain.
123
Oligoden-
drogliomas typically are slower growing, and
may contain calcifications visible on CT or MRI.
140
Plum and Posner’s Diagnosis of Stupor and Coma