Mechanical loading of the brain will result in a variety of pathologies, including:

Diffuse axonal injury (DAI). Transmission of inertial energy in the form of angular acceleration or deceleration results in axonal disruption and immediate coma. CT is such cases is usually without significant intracranial injury but pathological injury indicates retraction balls. DAI is the most frequent finding in patients who die from severe head injury. DAI is seen in younger people, and is usually unassociated with high intracranial pressure [4]. Penetration of axolemma by Ca++ may activate the calpain cascade and disrupt the cytoskele-ton, causing chemical axotomy. Microdial-ysis studies have shown that the concentration of extracellular fluid glutamate in patients with DAI is lower than that encountered in sub-dural hematoma and cortical contusion [5].

Tissue tear hemorrhages (TTH).

Focal contusions.

Focal contusions are usually in the form of high-density lesions. Focal contusions do not occupy much space in the beginning but may blossom within days and cause significant intracranial hypertension. The extracellular concentration of glutamate is higher in patients with focal cortical damage than in patients with diffuse axonal injury.

Intracerebral hematomas. Intracerebral hematomas are usually in the form of parenchymal contusions. Delayed intracerebral hematomas could have traumatic aneurysms as the main source of bleeding.

Subdural hematomas. Up to 35-40% of patients with severe TBI have subdural hematomas (SDH). Transla-tional shifts of the hemispheres inside the cranium will result in rupture of cortical veins or arteries and bleeding in the sub-dural space. SDH could be considered as epiphenomena of underlying cortical injuries.

Epidural hematomas.

Depending on the type of the patient population studied, between 1 and 10% of patients with head injury will have epidural

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