Cerebral Parenchymal Injuries

Parenchymal injuries are focal, diffuse, or both. Focal injuries—contusion and laceration—generally result from contact head injuries. Diffuse injuries result from acceleration of the head.

Contusions are bruises in the crest of the convolutions, characteristically, in the frontal and temporal figure 12.5

Acute contusion. A. Schematic drawing shows the sites of predilection of the contusions. B. Extensive subarachnoid hemorrhage and hemorrhagic necrosis of the frontoorbital and tem-poromesial cortex.

figure 12.6

Acute contre-coup contusion. A 47-year-old epileptic woman fell during a seizure and sustained a fracture of the left temporal bone. Two days later, she died. Right side of the brain shows extensive frontal and temporal hemorrhagic necrosis and multifocal subarachnoid hemorrhages.

figure 12.6

Acute contre-coup contusion. A 47-year-old epileptic woman fell during a seizure and sustained a fracture of the left temporal bone. Two days later, she died. Right side of the brain shows extensive frontal and temporal hemorrhagic necrosis and multifocal subarachnoid hemorrhages.

poles, orbital surfaces, and basal and lateral temporal regions. A stroke to a stationary head results in a "coup contusion" at the site of impact. When a moving head strikes a stationary object, the contusion is usually on the side opposite to the impact—a "contre-coup" contusion. Grossly, in acute contusions, the convolutions are hemorrhagic; in chronic contusions, they are yellow, depressed, soft, and necrotic. On cut section, the contusions are wedge-shaped cortical and subcortical defects with the apex toward the depth of the convolutions. The subcortical white matter is soft and, in severe cases, cavitated (Figs. 12.5 through 12.9). Histologically, the cortex in the crest of the convolutions is disrupted and partially missing. The margins of the defect contain fibrous astrocytes, macrophages, and hemosiderin pigments. The white matter is partially or completely demy-

elinated and, in severe cases, undergoes cystic necrosis that may extend deeply into the hemisphere.

Lacerations are tears in the dura, leptomeninges, and brain parenchyma caused by bony fragments or foreign bodies. Fracture dislocation of the base of the skull results in laceration of the brainstem and, in severe cases, pontomesencephalic or pontomedullary separations occur.

In diffuse axonal injuries (DAI), shearing of the axons results from movements of the brain during acceleration/deceleration of the head, as occurs in traffic accidents and falls and in shaken babies. The axonal disruption may continue even for a few hours after the accident.

In a few cases, the axonal injuries are grossly identified as minute hemorrhages in the dorsal aspect of the corpus callosum and fornices and the lateral aspect of the rostral brainstem. More often, however, they are discrete histologic findings diffusely distributed in the cerebral and cerebellar white matter and brainstem. They appear as eosinophilic and argyrophilic balls (blobs) of axoplasm extruded from the sheared ends of axons (Fig. 12.10). They can be identified a few hours after injury by using antibodies to amyloid precursor protein (APP), which accumulates in the disrupted axons (see Fig. 12.10). In the chronic stage, microglial clusters indicate the sites of axonal injuries.

DAIs are particularly important because they constitute the pathologic substrate of a broad spectrum of clinical symptoms that occur in the absence of a clinically or radiologically identifiable lesion.

Concussion is attributed to a transient biochemical dysfunction of the neurons that causes no structural alteration.

figure 12.5

Acute contusion. A. Schematic drawing shows the sites of predilection of the contusions. B. Extensive subarachnoid hemorrhage and hemorrhagic necrosis of the frontoorbital and tem-poromesial cortex.

figure 12.7

Subacute contusions. A. In lateral aspects of temporal and occipital lobes. B. Note the extensive necrosis and hemorrhagic discoloration of the hemispheric white matter.

figure 12.7

Subacute contusions. A. In lateral aspects of temporal and occipital lobes. B. Note the extensive necrosis and hemorrhagic discoloration of the hemispheric white matter.

figure 12.8

Chronic contusion. A. The fronto-orbital cortex is yellow, soft, and depressed. B. CT scan of orbital contusions in a different case. C. Transverse section shows wedge-shaped defects in fronto-orbital convolutions.

figure 12.8

Chronic contusion. A. The fronto-orbital cortex is yellow, soft, and depressed. B. CT scan of orbital contusions in a different case. C. Transverse section shows wedge-shaped defects in fronto-orbital convolutions.

figure 12.9

Histology of contusions. A. Acute contusion shows subarachnoid and cortical pericapillary hemorrhages. Pallor of staining of the adjacent convolution is likely from ischemic-hypoxic injury (HE). B. Chronic contusion shows disruption of the cortical ribbon in the crest of convolutions. The subcortical white matter is partially demyel inated (LFB-Eosin) and shows. C. large bizarre-shaped astrocytes (HE). D. Wedge-shaped cortical defect. The residual tissue and walls of the defect consist of a loose glial-mesodermal meshwork and collections of hemosid-erin pigments (HE).

figure 12.10

Shearing axonal injury. A 40-year old man survived 6 days following a head injury from a fall. Corpus callosum shows

(A) injured axons staining positively for P-amyloid precursor protein (P-APP) (immunostain). Hemisphere white matter shows

(B) axonal spheroids (Holmes stain). C. Axonal spheroids are present in medullary pyramids (HE).

figure 12.10

Shearing axonal injury. A 40-year old man survived 6 days following a head injury from a fall. Corpus callosum shows

(A) injured axons staining positively for P-amyloid precursor protein (P-APP) (immunostain). Hemisphere white matter shows

(B) axonal spheroids (Holmes stain). C. Axonal spheroids are present in medullary pyramids (HE).

table 12.2.

Neuropathology of the Battered Child

Skull fracture Subdural hematoma Parenchymal hematoma Cerebral contusion Axonal shearing injury Retinal hemorrhage

figure 12.11

Shrapnel injury. A 68-year-old man had, at age 23, sustained shrapnel injury to his left forehead. The lateral aspect of the left frontal lobe contains a large, round cortical and white matter defect with irregular margins.

Injuries in Children

The types of injuries observed in battered children are summarized in Table 12.2.

figure 12.11

Shrapnel injury. A 68-year-old man had, at age 23, sustained shrapnel injury to his left forehead. The lateral aspect of the left frontal lobe contains a large, round cortical and white matter defect with irregular margins.

MISSILE HEAD INJURIES

Missile injuries, caused by bullets and shrapnel, are either penetrating or perforating injuries (Fig. 12.11). In the former, the missile remains in the cranial cavity; in the latter, it traverses it. The exit wound is larger than the entrance wound. Both injuries carry a high risk of infection.

SECONDARY INJURIES

Acute cerebral injuries are apt to induce vascular/circulatory disorders and cerebral edema and are potential sources of infection.

Vascular/Circulatory Disorders

Vasodilatation is due to impaired autoregulation. In ischemic-hypoxic encephalopathy, the lesions vary from discrete ischemic neuronal necrosis to multiple focal and laminar neuronal losses, preferentially in the hippocampus, cerebral cortex, basal ganglia, and cerebellar cortex. Less common ischemic complications are multiple focal or diffuse white matter degenerations.

Edema

Diffuse vasogenic edema results from an increased permeability of the capillary endothelium and an escape of protein and fluid into the white matter. An increase in brain volume and gradual rise of ICP decrease the cerebral perfusion pressure, leading to global ischemia and eventually to brain death.

Local edema, confined to a hematoma or a parenchymal lesion, when severe, presents a life-threatening situation. It leads to herniations and subsequent brain-stem and medullary compression.

Infection at the site of a penetrating injury is a potential source of meningitis and abscesses.

CLINICAL PRESENTATION OF CEREBRAL INJURIES

The clinical presentation of head injuries depends on the type, location, and extent of the pathologic lesions and also on the presence of any secondary injury.

Acute Injury

Alterations of consciousness and neurologic deficits are the distinguishing clinical features of acute cerebral injuries. Concussion, the mildest injury, with no structural alteration, causes a loss of consciousness that usually lasts from seconds to a few minutes at most. Moderate and severe structural injuries cause a depression of consciousness ranging from drowsiness and obtundation to deep coma that may last from hours or days to months, even years.

The level of consciousness is determined using the Glasgow Coma Scale (GCS). The GCS assesses the patient's eye blinking and motor and verbal responses to stimuli. Scores of 15 to 13 indicate mild injuries, and scores below 8, severe injuries.

Among diagnostic tests, computed tomography (CT) scan is the method of choice to demonstrate hemorrhages. Acute epidural hematoma between the skull and the dura appears as an extra-axial hyperdense bioconvex lesion, whereas subdural hematoma between the dura and the cerebral cortex is crescent-shaped (see Fig. 12.2). Magnetic resonance imaging (MRI) demonstrates axonal injuries as tiny hemorrhages in the callo-sum and rostral brainstem. The determination of specific brain proteins (S-100 protein, neuron specific enolase [NSE], and glial fibrillary acidic protein [GFAP]) in the table 12.3.

Sequelae of Traumatic Cerebral Injuries

Somatic complaints Cranial nerve deficits Seizures

Motor, sensory deficits Language impairment Normal-pressure hydrocephalus Diabetes insipidus

Inappropriate antidiuretic hormone (ADH) secretion

Affective, behavioral changes

Personality changes

Cognitive decline

Dementia serum may provide prognostic information. High concentrations of these proteins suggest severe brain damage and poor outcome.

Sequelae of Cerebral Injuries

An estimated 10% of head injuries are fatal. Infants and young children suffering from shaken baby syndrome have a high mortality rate, averaging 20% to 25%.

In survivors, the outcome varies widely from complete recovery to a prolonged coma or a persistent vegetative state. Between these extremes, a variety of neurologic and psychiatric symptoms may occur, some permanent and some reversible. Gradual recovery of consciousness is usually associated with amnesia and confusion of variable duration. Retrograde amnesia refers to memory loss for events that occurred before the trauma, and anterograde amnesia for events that occurred after awakening.

The major sequelae of moderate and severe cerebral injuries are seizures; normal-pressure hydrocephalus; variable neurologic deficits; hypothalamic-endocrine dysfunction; cognitive decline, ranging from memory impairment to dementia; and behavioral and affective changes (Table 12.3). Children present with learning disabilities and behavioral changes.

Concussion often is followed by headaches, dizziness, tinnitus, memory impairment, and fatigue. Skull fractures may injure cranial nerves 1, 3, 7, and 8.

SPINAL CORD INJURIES

The major causes of spinal cord injuries are fracture dislocation, subluxation from sudden flexion or hyperextension of the spinal column, and prolapsed intervertebral disc. These injuries occur in traffic and sports-related accidents, falls, and diving in shallow water. Penetrating injuries are caused by stabbing, gunshots, and missiles.

Compression, contusion, laceration, hemorrhage (hematomyelia), and complete transection from crush injury are major pathologic changes (Figs. 12.12 and 12.13). Extensive parenchymal necrosis, edema, hemorrhage, and axonal disruption with retraction balls characterize the acute stage of severe injuries. In the chronic stage, a mesoglial scar develops and wallerian degeneration takes place in the descending and ascending fiber

figure 12.12

Transverse section of the spinal cord showing total necrosis and hemorrhages in a 27-year-old man involved in an automobile accident (HE).

figure 12.12

Transverse section of the spinal cord showing total necrosis and hemorrhages in a 27-year-old man involved in an automobile accident (HE).

tracts. In some cases, a cavity remains after the removal of tissue debris (posttraumatic syringomyelia). Schwann cell proliferation in the damaged nerve roots produces traumatic neurinomas.

The clinical course and outcome vary with the extent and anatomic level of the lesions. About 40% of patients with severe injuries die within 24 hours of the accident. Acute injuries cause a spinal shock with paralysis, anesthesia, and loss of reflexes below the level of the lesion, and loss of autonomic and sphincter functions. The spinal shock, gradually resolves, within 3 to 4 weeks. The return of functions depends on the extent of the lesions. Complete transection of the spinal cord results in loss of motor, sensory, and autonomic functions below the lesion. Incomplete transection produces various spinal cord syndromes, which often are not sharply defined. Minor injuries produce spinal cord concussion, in which the neurologic deficits resolve within minutes or hours.

OTHER INJURIES Vascular Injuries

Vascular injuries, occurring alone or in conjunction with cerebral injuries, are arteriovenous fistula, dissection of carotid and vertebral arteries, arterial and venous thrombosis, and pseudoaneurysm. Carotid-cavernous fistula results from the laceration of the internal carotid artery within the cavernous sinus by skull fracture or penetrating missile. Dissection of the cervical arteries is caused by a fracture of the cervical spine or by spinal

figure 12.14

Fat embolization to the brain. A 77-year-old woman fell and fractured her femur. Within a few hours, she had lost consciousness and, 3 days later, she died. A. Fat emboli occlude distended capillaries in the cerebral hemispheric white matter (oil-red-O stain). B. Pericapillary ball hemorrhage and (C) microinfarct in the white matter (HE).

manipulative therapy. Hemorrhagic or thrombotic occlusion of the dissected artery carries the risk of cerebral infarction.

Pituitary necrosis and hemorrhage results from injury to the pituitary stalk.

In subdural hygroma, an accumulation of CSF in the subdural space results from tearing of the arachnoid.

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