Page 834 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

820 C H A P T E R 22 Central Nervous System

CENTRAL NERVOUS SYSTEM TRAUMA A

Trauma to the brain and spinal cord is a significant cause B
of death and disability. The severity and site of injury affect
the outcome: injury of several cubic centimeters of brain Figure 22–12 Cerebral trauma. A, Acute contusions are present
parenchyma may be clinically silent (if in the frontal lobe), in both temporal lobes, with areas of hemorrhage and tissue disruption.
severely disabling (spinal cord), or fatal (involving the B, Remote contusions, seen as discolored yellow areas, are present on
brain stem). the inferior frontal surface of this brain.

A blow to the head may be penetrating or blunt; it may Old traumatic lesions have a characteristic macroscopic
cause an open or a closed injury. The magnitude and distri- appearance: They are depressed, retracted, yellowish brown
bution of resulting traumatic brain lesions depend on the patches involving the crests of gyri (Fig. 22–12, B). More
shape of the object causing the trauma, the force of impact, extensive hemorrhagic regions of brain trauma give rise to
and whether the head is in motion at the time of injury. larger cavitary lesions, which can resemble remote infarcts.
Severe brain damage can occur in the absence of external In sites of old contusions, gliosis and residual hemosiderin-
signs of head injury, and conversely, severe lacerations and laden macrophages predominate.
even skull fractures do not necessarily indicate damage to
the underlying brain. When the brain is damaged, the inju- Although contusions are more easily seen, trauma can also
ries may involve the parenchyma, the vasculature, or both. cause more subtle but widespread injury to axons within the
brain (called diffuse axonal injury), sometimes with dev-
Recent evidence suggests that repetitive episodes of astating consequences. The movement of one region of brain
trauma (such as occurs in athletes participating in contact relative to another is thought to disrupt axonal integrity and
sports) can lead to later development of neurodegenerative function. Angular acceleration, even in the absence of impact,
processes. In addition to a long-recognized association of may cause axonal injury as well as hemorrhage. As many as
trauma with the risk of Alzheimer disease, a distinct form 50% of patients who develop coma shortly after trauma are
of trauma-associated degeneration has been described, believed to have white matter damage and diffuse axonal
chronic traumatic encephalopathy, which is characterized by injury. Although these injuries may be widespread, the lesions
a unique pattern of intraneuronal tau protein inclusions usually are asymmetric and are most commonly found near
(described later). the angles of the lateral ventricles and in the brain stem. They
take the form of axonal swellings that appear within hours of
Traumatic Parenchymal Injuries the injury. These are best demonstrated with silver stains or
by immunohistochemical stains for axonal proteins.
When an object impacts the head, brain injury may occur
at the site of impact—a coup injury—or opposite the site of
impact on the other side of the brain—a contrecoup injury.
Both coup and contrecoup lesions are contusions, with
comparable gross and microscopic appearances. A contu-
sion is caused by rapid tissue displacement, disruption of
vascular channels, and subsequent hemorrhage, tissue
injury, and edema. Since they are closest to the skull, the
crests of the gyri are the part of the brain that is most sus-
ceptible to traumatic injury. Contusions are common in
regions of the brain overlying rough and irregular inner
skull surfaces, such as the orbitofrontal regions and the
temporal lobe tips. Penetration of the brain by a projectile
such as a bullet or a skull fragment from a fracture causes
a laceration, with tissue tearing, vascular disruption, and
hemorrhage.

MORPHOLOGY

On cross-section, contusions are wedge-shaped, with the
widest aspect closest to the point of impact (Fig. 22–12, A).
Within a few hours of injury, blood extravasates throughout
the involved tissue, across the width of the cerebral cortex,
and into the white matter and subarachnoid spaces. Although
functional effects are seen earlier, morphologic evidence of
injury in the neuronal cell body (nuclear pyknosis, cytoplasmic
eosinophilia, cellular disintegration) takes about 24 hours to
appear. The inflammatory response to the injured tissue
follows its usual course, with neutrophils preceding the
appearance of macrophages. In contrast with ischemic lesions,
in which the superficial layer of cortex may be preserved,
trauma affects the superficial layers most severely.