PINEAL TUMORS
The pineal gland is technically outside the brain,
sitting in the subdural space overlying the pre-
tectal area and rostral midbrain. Tumors of the
pineal gland commonly compress the dorsal sur-
face of the midbrain, causing Parinaud’s syn-
drome (loss of upward gaze, large poorly reactive
pupils, and retractory convergence nystagmus),
which points to the diagnosis. The tumor may
also compress the cerebral aqueduct, causing hy-
drocephalus; typically this only alters conscious-
ness when increased intracranial pressure from
hydrocephalus causes plateau waves (see page
93) or if there is sudden hemorrhage into the
pineal tumor (pineal apoplexy).
55
CT or MRI will
demonstrate both the tumor and the hydroceph-
alus and can detect hemorrhage into the tumor.
SUBARACHNOID LESIONS
Like epidural, dural, and subdural lesions,
subarachnoid lesions are outside of the brain
itself. Unlike epidural or dural lesions, alter-
ations of consciousness resulting from sub-
arachnoid lesions are not usually the result of
a mass effect, but occur when hemorrhage,
tumor, or infection either compress, infiltrate,
or cause inflammation of blood vessels in the
subarachnoid space that supply the brain, or
alter CSF absorptive pathways, thus causing hy-
drocephalus. Thus, strictly speaking, in some
cases the damage done by these lesions may be
more ‘‘metabolic’’ than structural. On the other
hand, subarachnoid hemorrhage and bacterial
meningitis are among the most acute emergen-
cies encountered in evaluating comatose pa-
tients, and for that reason this class of disorders
is considered here.
Subarachnoid Hemorrhage
Subarachnoid hemorrhage, in which there is
little if any intraparenchymal component, is
usually due to a rupture of a saccular aneurysm,
although it can also occur when a superficial
arteriovenous malformation ruptures. Saccular
aneurysms occur throughout life, generally at
branch points of large cerebral arteries, such as
the origin of the anterior communicating ar-
tery from the anterior cerebral artery; the ori-
gin of the posterior communicating artery from
the posterior cerebral artery; the origin of the
posterior cerebral artery from the basilar ar-
tery; or the origin of the middle cerebral artery
from the internal carotid artery. Microscopic
examination discloses an incomplete elastic me-
dia, which results in an aneurysmal dilation that
may enlarge with time. Aneurysms are found
with increasing frequency with age.
Aneurysms are typically silent until they
hemorrhage. Some ruptures are presaged by
a severe headache, a so-called sentinel head-
ache,
56,57
presumably resulting from sudden
dilation or leakage of blood from the aneurysm.
The frequency of sentinel headaches varies in
different series from 0% to 40%. Giant aneu-
rysms of the internal carotid artery sometimes
occur in the region of the cavernous sinus, and
these may present as a mass lesion causing
impairment of the cranial nerves of the cav-
ernous sinus (III, IV, VI, and V
1
) or by com-
pressing the frontal lobes. Occasionally an an-
eurysm of the posterior communicating artery
compresses the adjacent third nerve causing
ipsilateral pupillary dilation. For this reason,
new onset of anisocoria even in an awake pa-
tient is considered a medical emergency until
the possibility of a posterior communicating ar-
tery aneurysm is eliminated.
Unfortunately, most aneurysms are not ap-
parent until they bleed. The classic presentation
of a subarachnoid hemorrhage is the sudden
onset of the worst headache of the patient’s life.
However, many other types of headaches may
present in this way (e.g., ‘‘thunderclap head-
ache’’),
58
so it is often necessary to rule out
subarachnoid hemorrhage in the emergency
department. If the hemorrhage is sufficiently
large, the sudden pressure wave, as intracranial
pressure approximates arterial pressure, may
result in impaired cerebral blood flow and loss
of consciousness. About 12% of patients with
subarachnoid hemorrhage die before reaching
medical care.
59
At the other end of the spec-
trum, if the leak is small or seals rapidly, there
may be little in the way of neurologic signs. The
most important finding is impairment of con-
sciousness. The symptoms may vary from mild
dullness to confusion to stupor or coma. The
cause of the behavioral impairment after sub-
arachnoid hemorrhage is not well understood.
It is believed that the blood excites an inflam-
matory response with cytokine expression that
may diffusely impair brain metabolism as well
as cause brain edema. Parenchymal signs are
Specific Causes of Structural Coma
129
often lacking unless a jet of blood from the rup-
tured aneurysm has damaged the brain.
Patient 4–2
An 18-year-old woman was brought to the emer-
gency department by her sister because she had
been confused and forgetful for 2 days. She did not
offer a history of headache, but upon being asked,
the patient did admit that she had one. On ex-
amination the neck was stiff, but the neurologic
examination showed only lethargy and inatten-
tion. A CT scan disclosed a subarachnoid hemor-
rhage, with blood collection around the circle of
Willis on the right side. Lumbar puncture yielded
bloody fluid, with 23,000 red blood cells and 500
white blood cells. Cultures were negative. A ce-
rebral angiogram demonstrated a saccular aneu-
rysm at the junction of the internal carotid and
middle cerebral arteries on the right.
CT scans are highly sensitive to subarach-
noid blood, making the diagnosis in more than
95% of cases if done within 12 hours
60
(Figure
4–4). MRI fluid-attenuated inversion recovery
(FLAIR) sequences may be more sensitive,
61,62
but in a patient with a suspected subarachnoid
hemorrhage if the CT is negative, a lumbar
puncture is mandatory.
57,62,63
As lumbar punc-
ture itself may introduce blood into the CSF,
the analysis of blood in the CSF is of great
importance. Signs that suggest that the blood
was present before the tap include the persis-
tence of the same number of red cells in tubes
1 and 4, or the presence of crenated red blood
cells and/or xanthochromia if the hemorrhage
is at least several hours old. Spectrophotome-
try of CSF is available in some institutions.
64
Another alternative is to centrifuge the CSF
and test the supernate with a urine dipstick
for blood. If the bleeding preceded the tap by
at least 6 hours, it is likely that there will be
blood breakdown products in the CSF, which
can be visualized on the dipstick.
Figure 4–4. A 66-year-old man was brought to the Emergency Department after sudden onset of a severe global headache
with nausea and vomiting. His legs collapsed under him. CT scan (A) showed blood in the cisterns surrounding the circle of
Willis at the base of the brain, with blood extending into the interhemispheric fissure at the midline, and the right Sylvian
fissure (arrow). A CT angiogram (B) showed that the anterior cerebral arteries were fused from the anterior communicating
artery up to a bifurcation point, at which a large saccular aneurysm was noted (arrow). ACA, anterior cerebral artery; LVA,
left vertebral artery; RMCA, right middle cerebral artery.
130
Plum and Posner’s Diagnosis of Stupor and Coma