C h a p t e r 3 7
Disorders of Brain Function
925
there are focal symptoms related to the area of the brain
involved. These symptoms can include ipsilateral pupil
dilation and contralateral (opposite side) hemiparesis
from uncal herniation. If the hematoma is not removed,
the condition progresses, with increased ICP, tentorial
herniation, and death. The prognosis is excellent, how-
ever, if the hematoma is removed before loss of con-
sciousness occurs.
Subdural Hematoma.
A subdural hematoma develops
in the area between the dura and the arachnoid (sub-
dural space) and usually is the result of a tear in the
small bridging veins that connect veins on the surface
of the cortex to dural sinuses. The bridging veins pass
from the pial vessels through the CSF-filled subarach-
noid space, penetrate the arachnoid and the dura, and
empty into the intradural sinuses.
1,4,7
These veins are
readily snapped in head injury when the brain moves
suddenly in relation to the cranium (Fig. 37-8). Bleeding
can occur between the dura and arachnoid (i.e., sub-
dural hematoma) or into the CSF-filled subarachnoid
space (i.e., subarachnoid hematoma).
The venous source of bleeding in a subdural hema-
toma develops more slowly than the arterial bleeding in
an epidural hematoma. Subdural hematomas are clas-
sified as acute, subacute, or chronic. This classification
system is based on the approximate time before the
appearance of symptoms. Symptoms of acute hematoma
are seen within 24 hours of the injury, whereas subacute
hematoma does not produce symptoms until 2 to 10 days
after injury. Symptoms of chronic subdural hematoma
may not arise until several weeks after the injury.
Acute subdural hematomas progress rapidly and have
a high mortality rate because of the severe secondary
injuries related to edema and increased ICP. The high
mortality rate has been associated with uncontrolled
ICP increase, loss of consciousness, decerebrate postur-
ing (see Fig. 37-4B), and delay in surgical removal of
the hematoma. The clinical picture is similar to that of
epidural hematoma, except that there usually is no lucid
interval. By contrast, in subacute subdural hematoma,
there may be a period of improvement in the level of
consciousness and neurologic symptoms, only to be fol-
lowed by deterioration if the hematoma is not removed.
Symptoms of chronic subdural hematoma develop
weeks after a head injury, so much later that the person
may not remember having had a head injury. Chronic
subdural hematoma is more common in older persons
because brain atrophy causes the brain to shrink away
from the dura and stretch fragile bridging veins. When
these veins rupture, there is slow seepage of blood into
the subdural space. Fibroblastic activity causes the
hematoma to become encapsulated. The sanguinous
(blood fluid) in this encapsulated mass, with its high
concentration of osmotically-active particles, draws
fluid from the surrounding subarachnoid space, causing
the hematoma to expand and exert pressure on the sur-
rounding brain tissue. In some instances, the clinical pic-
ture is less defined, with the most prominent symptom
being a decreasing level of consciousness, as manifested
by drowsiness, confusion, headache, and apathy
Traumatic Intracerebral Hematomas.
Traumatic
intracerebral hematomas may be single or multiple. They
can occur in any lobe of the brain but are most com-
mon in the frontal or temporal lobes, related to the bony
prominences on the inner skull surface (Fig. 37-9). They
may occur in association with the severe motion that
the brain undergoes during head injury, or a contusion
can coalesce into a hematoma. Intracerebral hematomas
occur more frequently in older persons and alcoholics,
whose cerebral vessels are more friable.
Epidural
hematoma
Anterior
Posterior
Intracerebral
hematoma
Subdural
hematoma
FIGURE 37-7.
Location of epidural, subdural, and intracerebral
hematomas.
Outer
membrane
Subdural
hematoma
Inner
membrane
Dura
Arachnoid
Severance of
bridging veins
Sagittal sinus
Bridging
vein
FIGURE 37-8.
Mechanism of bleeding in subdural
hematoma. (FromTrojanowski JQ.The central nervous
system. In: Rubin E, Gorstein F, Rubin R, et al; eds. Rubin’s
Pathology: Clinicopathologic Foundations of Medicine. 4th
ed. Philadelphia, PA: Lippincott Williams &Wilkins; 2005:1430.
Courtesy of Dmitri Karetnikov, artist.)
