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Cerebral Contusions and Lacerations

Cerebral contusions are the most common of the

intraaxial injuries. True brain lacerations are
rare and typically occur only with severe (often
fatal) head injury.
Cerebral contusions are basically "brain
bruises". They evolve with time and often more
apparent on delayed scans than at the time of
initial imaging. Cerebral contusions are alsa
called gyral "crest" injury (2-57). The term
"gliding" contusion is sometimes used to
describe parasagital contusion.
Most cerebral contusions result from nonmissile or blunt head injury. Closed head injury
induces abrupt changes in angular momentum
and deceleration. The brain is suddenly and
forcibly impacted against an osseus ridge or the
hard, knife-like edges of the falx cerebri and
tentorium cerebelli. Less commonly, a
depressed skull fracture directly damages the
underlying brain.
LOCATION. Contusions are injuries of brain
surface that involve the gray matter and
contiguous subcortical white matter (2-57) (258) (2-59). They occur in very characteristic,
highly predictable locations. Nearly half involve
the temporal lobes. The temporal tips, as well as
the lateral and inferior surface and the
perisylvian gyri, are most commonly affected
(2-60). The inferior

(orbital) surface of the frontal lobes are also

frequently affected (2-61).
Convexity gyri, the dorsal corpus callosum
body, dorsolateral midbrain, and cerebelum are
less common sites of cerebral contusions. The
occipital poles are rarely involved even with
relatively severe closed head injury.
SIZE AND NUMBER. Cerebral contusions
vary in size from tiny lesions to large confluent
hematoma (2-59). They are almost always
multiple and often bilateral (2-62) contusions
that occur at 180 opposite the site of direct
impact (the "coup") are common and are called
"contre-coup" lesions.
GROSS PATHOLOGY. Contusions range in
appearance from small petechial to large
confluent hemorrhages. Cortical contusions are
usually associated with. traumatic subarachnoid
hemorrhage in adjacent sulci.


micro-hemorrhage rapidly form and coalesce
over time into more confluent hematomas.
Edema surrounding the hemorrhages develops.
Activations and proliferation of astrocytes
together with macrophage infiltration ensues.
Necrosis with neuronal loss and astrogliosis as
well as hemosiderin-laden macrophages are
present in subacute and chronic lesions.
Clinical Issues
Cerebral contusions account for approximatbely
half of all traumatic parenchymal lesions. They
occur at all ages, from infants to the elderly. The

pea age is from 15-24 years, and the M : F ratio

3 : 1.
PRESENTATION. Inital symptoms vary from
none to confusion, seizure or obtundation.
Compared to diffuse axonal injuries (see
below), cerebral contusions are less frequently
associated with immediate loss of consciousness
unless they extensive or occure with other
traumatic brain liesions (e.g. brainsterm trauma
or axonal injury).
deterioration is more common in older patients.
Patients with large contusions, initial low
Glasgow Coma Score (GCS), coagulopathy, and
presence of coexisting subdural hematoma are
prone to clinical deterioration. Those with small
contusions, good initial GCS, and absence of
clinical deterioration in the first 48 hours are
unlikely to require surgery.
Hematoma expansion requiring surgical
intervention occurs in approximately 20% of
conservatively managed patients. Patients with
unexplained clinical deterioration should have
repeat imaging.
TREATMENT OPTIONS. Treatment options
vary from conservative (observation with repeat
imaging if the patient deteriorates) to surgical
evacuation of large focal focal hematomas.
Craniectomy is perfomed in patients with severe
brain swelling to present fatal brain herniation.
GENERAL FEATURES. With time, cortical
contusions become more apparent on imaging
studies. Radiologic progression is the rule, not
the exception. Nearly half of all patients show
increase in lesion size and number over the first
24-48 hours. In the absence of clinical

deterioration, though, the relevance

documenting this progression is debutable.


CT FINDINGS. Initial scans obtained soon

after a closed head injury may be normal. The
most frequent abnormality is the presence of
petechial hemorrhages along gyral crest
immediately adjacent to the calvaria (2-63). A
mixture of petechial hemorrhages surrounding
by patchy illdefined hypodense areas of edema
is common.
Lesions "blooming" over time is frequent and is
seen with progressive increase in hemorrhages,
edema, and many effect. Small lesion may
coalesce' formng larger focal hematomas.
Developement of new lesions that were not
present on initial is also common.
MR FINDINGS. MR is much more sensitive
that CT in detecting cerebral contusions but is
rarely obtained in the acte stage of traumatic
brain injury. T1 scans may show only mild
inhomogeneous isointensites and mass effect.

T2 scans show patchy hyperintense area

(edema) surrounding hypointense foci of
hemorrhage (2-64A).
FLAIR scan are most sensitive for detecting
cortical edema and associated traumatic
subarachnoid hemorrhages, both of which
appear as hyperintense foci on FLAIR. T2*
(GRE' SWI) is the most sensitive sequence for
imaging parenchymal hemorrhages. Significant
"blooming" is typical in acute lesions (2-64B).
Hemorrhagic contusions follow the expected
evolution of parenchymal hematomas, with T1
shortening developing over time. Atrophy,
demyelination, and microglial scarring are seen
on FLAIR and T2W1. Parenchymal volume loss
with ventricular enlargement and sulcal
prominsence is common.

DWI in patients with cortical contusions shows

diffuse restriction in areas of cell death. DTI
may disclose coexisting white matter damage in
minor head trauma even when standars MR
sequences are normal.

Severe corical contusion with confluent

hematomas may be difficult to distinguish from
brain laceration on imaging studies. Brain
laceration occurs when severe trauma disrupts
the pia and literally tears the under apart.

Differential Diagnosis

A "burst lobe" is the most severe manifestation

of frank brain laceration (2-65) (2-66). Here the
affected lobe is grossly disruptes, with large
hematoma formation and adjacent traumatic
subarachnoid hemorrhage. In some cases,
especially those with depressed skull fracture,
the arachnoid is also lacerated and hemorrhage
from the burst lobe extends to communicate
directly with the subdural space, forming a
coexisting subdural hematoma.

The major diffrential diagnosis of cortical

contusions Diffuse Axonal Injury (DAI). Both
cerebral contusions and DAI are often present in
patients who have sustained moderate to severe
head injury. Contusions tend to be superficial,
located along gyral crests. DAI is most
commonly found in the corona radiata and along
compact white matter tracts such as the internal
capsule and corpus callosum.