Nevertheless, if prompt antibiotic therapy is be-
gun and the patient shows any signs of increased
ICP, it is probably wise to use dexamethasone.
96
CT scans may show pus in the subarachnoid
space as hypodense CSF with enlargement of
sulci, but in the absence of prior scans in the
same patient, this is often difficult to inter-
pret. Meningeal enhancement usually does not
occur until several days after the onset of in-
fection. Cortical infarction, which may be due
to inflammation and occlusion either of pene-
trating arteries or cortical veins, also tends to
occur late. The MRI scan is much more sen-
sitive for showing the changes indicated above
but may be entirely normal in patients with
acute meningitis (Table 4–5).
97
INTRACEREBRAL MASSES
Intracerebral masses by nature tend to include
both destructive and compressive elements.
However, in many cases, the damage from the
mass effect far exceeds the damage from dis-
ruption of local neurons and white matter.
Hence, we have included this class of lesions
with compressive processes.
Intracerebral Hemorrhage
Intracerebral hemorrhage may result from a
variety of pathologic processes that affect the
blood vessels. These include rupture of deep
Table 4–5 Imaging Findings in Acute Meningitis
Finding
CT*
MR*
Sensitivity
Sulcal dilation
Hypodense CSF;
enlargement of sulci
T1WI: Hypointense
CSF in sulci
MR>CT
T2WI: Hyperintense
CSF in sulci
Leptomeningeal
enhancement
CE: Increase in density
of subarachnoid space
T1WI, CE: Marked increase
in signal intensity
MR>CT
Ischemic cortical
infarction
Hypodense cortical mass
effect
T1WI: Hypointense cortex;
mass effect
MR>CT
secondary to
vasculitis
CE: Subacute increase
in density (enhancement)
T2WI: Hyperintense cortex,
mass effect
FLAIR: Hyperintense cortex,
mass effect
CE: Subacute enhancement;
hyperintense on T1WI
DWI: Bright (white)
ADC: Dark (black)
Subdural collections
Hypodense peripheral CSF
plus density collection
T1WI: Hypointense
peripheral collection
MR>CT
CE: Hygroma, no; empyema,
yes
T2WI: Hyperintense
peripheral collection
FLAIR: hygroma, hypointense;
empyema, variable
CE: Hygroma, no; empyema, yes
DWI: Hydroma, dark;
empyema, bright
ADC: Hygroma, bright;
empyema, dark
ADC, apparent diffusion coefficient map; CE, contrast enhanced; CSF, cerebrospinal fluid; CT, computed tomography;
DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; MR, magnetic resonance; T1WI, T1-
weighted image; T2WI, T2-weighted image.
*Intensity relative to normal brain ±.
From Zimmerman et al.,
98
with permission.
Specific Causes of Structural Coma
135
cerebral end arteries, trauma, rupture of an ar-
teriovenous malformation, rupture of a mycotic
aneurysm, amyloid angiopathy, or hemorrhage
into a tumor. Rupture of a saccular aneurysm
can also cause an intraparenchymal hematoma,
but the picture is generally dominated by the
presence of subarachnoid blood. In contrast,
despite their differing pathophysiology, the
signs and symptoms of primary intracerebral
hemorrhages are due to the compressive ef-
fects of the hematoma, and thus are more alike
than different, depending more on location
than on the underlying pathologic process.
Spontaneous supratentorial intracerebral hem-
orrhages are therefore usually classified as lo-
bar or deep, with the latter sometimes extend-
ing intraventricularly.
Lobar hemorrhages can occur anywhere in
the cerebral hemispheres, and may involve one
or multiple lobes (Figure 4–6A). As compared
to deeper hemorrhages, patients with lobar
hemorrhages are older, less likely to be male,
and less likely to be hypertensive. Severe head-
ache is a characteristic of lobar hemorrhages.
Focal neurologic deficits occur in almost 90%
of patients and vary somewhat depending on
the site of the hemorrhage. About half the pa-
tients have a decreased level of conscious-
ness and 20% are in a coma when admitted.
99
Seizures are a common occurrence and may be
nonconvulsive (see page 281), so that electro-
encephalographic (EEG) evaluation is valuable
if there is impairment of consciousness.
Deep hemorrhages in the supratentorial re-
gion include those into the basal ganglia, inter-
nal capsule, and thalamus. Hemorrhages into
the pons and cerebellum are discussed in the
section on infratentorial hemorrhages. Chung
and colleagues divided patients with striato-
capsular hemorrhages into six groups with vary-
ing clinical findings and prognoses.
100
These
included posterolateral (33%), affecting pri-
marily the posterior portion of the putamen;
massive (24%), involving the entire striatal
capsular region but occasionally sparing the
caudate nucleus and the anterior rim of the
internal capsule; lateral (21%), located be-
tween the external capsule and insular cortex;
anterior (11%), involving the caudate nucleus;
middle (7%), involving the globus pallidus in
the middle portion of the medial putamen; and
posterior medial (4%), localized to the anterior
half of the posterior rim of the internal cap-
sule. Consciousness was only rarely impaired
in anterior and posterior medial lesions, but
was impaired in about one-third of patients
Figure 4–6. Computed tomography scans from two patients with intracerebral hemorrhages. (A) shows a large hemor-
rhage into the right parieto-occipital lobe in a 77-year-old woman who was previously healthy and presented with difficulty
walking and a headache. Examination showed left-sided neglect. She took 325 mg aspirin at home on the advice of her
primary care doctor because she suspected a stroke. The hematoma ruptured into the lateral ventricle. (B) shows a right
thalamocapsular hemorrhage in a 60-year-old man with a history of hypertension who was not being treated at the time of
the hemorrhage. He presented with headache, left-sided weakness and sensory loss, and some left-sided inattention.
136
Plum and Posner’s Diagnosis of Stupor and Coma