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Pathology of Traumatic Brain Injury

The anatomical alterations are macroscopic or microscopic, depending on the mechanism and the forces involved. The patient who has a mild trauma may not present any anatomical damage. The severity and consequences of clinical manifestations vary enormously. Trauma is generally categorized as open or closed.

Open head trauma involves penetration of the scalp and skull (and usually the meninges and underlying brain tissue). They are usually due to a projectile or a sharp object, but a fracture of the skull with underlying laceration due to a strong direct impact is also considered an open trauma.

Usually, blunt head trauma occurs when the head is bumped, hit with an object, or violently shaken, causing the brain to accelerate and decelerate rapidly. Acceleration or deceleration can injure the tissue at the point of impact (blow), on the opposite side (kickback), or diffusely; the frontal and temporal lobes are particularly vulnerable to this type of injury. Axons and/or blood vessels can be sheared or torn, resulting in diffuse axonal injury. Injured blood vessels cause blood loss, causing bruising, subarachnoid or intracerebral hemorrhages and

Concussion ( see also Sports Concussion ) is defined as a transient, reversible, traumatic alteration in mental status (eg, loss of consciousness or memory, confusion) that lasts seconds or minutes and, by arbitrary definition ,.

Structural brain damage and severe neurological sequelae are not part of concussion, although temporary disability may be due to symptoms, such as nausea, headache, dizziness, memory impairment and difficulty concentrating (syndrome post concussion) which usually disappear within a few weeks. However, it is believed that the multiplication of concussions can lead to chronic traumatic encephalopathy , which results in severe brain dysfunction.

Brain bruises

Contusions (brain bruises) can occur after blunt or open trauma and can affect many brain functions, depending on the size of the bruise and its topography. Larger bruises can lead to extensive cerebral edema and increased intracranial pressure. Bruising can worsen over the hours and days following the initial injury and cause neurological deterioration; surgery may be needed.

Diffuse axonal injury

Diffuse axonal injury occurs when rotational deceleration induces shear forces that result in widespread and diffuse disruption of axonal fibers and myelin sheaths. Some diffuse axonal damage may also be due to minor head injuries. Large anatomic lesions are not part of diffuse axonal lesions, but small white matter petechial hemorrhages are often seen on CT and histopathology.

Diffuse axonal damage is sometimes clinically defined as loss of consciousness lasting > 6 hours in the absence of specific focal damage.

Lesional edema often increases intracranial pressure, which induces various manifestations .

Diffuse axonal damage is the damage usually seen in shaken baby syndrome (Silverman syndrome).

Hematomas (collections of blood in or around the brain) can occur in open or closed wounds and can be

Subdural

Subarachnoid hemorrhage (bleeding into the subarachnoid space) is common in traumatic brain injury, although the appearance on CT is usually not the same as that of aneurysmal subarachnoid hemorrhage. Blood from a subarachnoid hemorrhage does not appear as a discrete hematoma

A subdural hematoma is the presence of blood between the dura mater and the arachnoid. Acute subdural hematomas result from laceration of cortical veins or avulsion of anastomotic veins between the cortex and the dural sinuses.

Acute subdural hematomas often occur in patients with the following disorders

Head trauma caused by a fall or road accident

Underlying brain contusions

Contralateral epidural hematoma

Compression of the brain by the hematoma and swelling of the brain due to edema or hyperemia (increased blood flow due to engorgement of blood vessels) can increase intracranial pressure. When both compression and swelling occur together, mortality and morbidity can be high.

A chronic subdural hematoma can develop and gradually become symptomatic several weeks after the trauma. Chronic subdural hematomas are more common in alcoholic and elderly patients (especially on antiplatelet or anticoagulant drugs or who have cerebral atrophy). Elderly patients may view the head injury as unimportant or even forget about it. Unlike acute subdural hematoma, edema and increased intracranial pressure are rare.

Extradural hematomas are collections of blood located between the cranium and the dura and are less common than subdural hematomas. Extradural hematomas are usually due to arterial hemorrhage, usually from damage to the middle meningeal artery due to temporal bone fracture. Without intervention, a patient with an arterial or large epidural hematoma can rapidly deteriorate and the patient may die. Small venous extradural hematomas are rarely fatal.

Intracerebral hematomas are collections of blood in the brain. In trauma, they result from the coalescence of bruises. The mechanism by which one or more bruises form a hematoma is not well defined. Increased intracranial pressure, entrapment, and signs of brainstem involvement may develop, particularly with temporal or cerebellar hematomas .

Cranial fractures

Penetrating injuries by definition involve a fracture. Blunt trauma can also lead to cranial fractures, which are linear, embarassed, or comminuted. The presence of a fracture suggests that a significant force was involved in the injury.

Most patients with simple linear fractures and no neurological involvement are not at high risk for brain damage, but patients with any fracture associated with neurological impairment are at increased risk for intracranial hematoma.

Skull fractures that involve special risks include

Brain function can be immediately impaired by direct damage (eg, crushing, laceration) to brain tissue. Further damage may occur soon after the cascade of events triggered by the initial trauma.

Any type of traumatic brain injury can lead to edema of the injured tissues. The cranial vault is dimensionally fixed (constrained by the skull) and filled with incompressible CSF and minimally compressible brain tissue;

 

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