A. Concussion

Concussion is a transient acute unconsciousness due to head injury. It is of instantaneous onset and is manifested by neurological symptoms without much evidence of structural cerebral injury.

B. Contusions (areas of hemorrhagic necrosis)

1. Pathogenesis: Following head injury, the brain strikes supporting structures (tentorium and falx cerebri), and bony projections of skull, producing superficial bruising of gyral crests.

Contusions are present on the right frontal tip (left side of image) orbital surface.

2. Location: In general the most common sites are orbital surfaces, (inferior surface of frontal lobe) temporal lobes and occipital lobes. Contusions can be produced by rotation of the brain or by linear forces through the site of impact. The exact location may depend on conditions of the trauma. Contusions may be coup lesions (directly adjacent to the site of impact) or contrecoup lesions (on the opposite side of the brain from the impact). In the case of linear acceleration or deceleration injuries (i.e. a single blow to the unsupported head), contrecoup lesions are a common sequelae. A blow to the well supported head results in severe skull fractures, often with absence of coup and contre-coup lesions (the head does not accelerate or decelerate and the skull absorbs much of the force).

3. Pathology: In the most typical form of contusion, the summit of a cerebral gyrus is smashed, and the lesion has a wedge shape with its base toward the pia and the apex toward the white matter. All layers of cortex are regularly affected. In its early stage the hemorrhage remains bright red, and the surrounding brain tissue is edematous. When the lesion is older it becomes brick-red and finally golden orange-brown (due to deposition of hemosiderin), with a floor of glial tissue, covered by leptomeningeal fibrosis. The most chronic stage is sometimes called plaque jaune. Dura arachnoidal adhesions (meningocerebral cicatrix - scar involving meninges & cerebral cortex) later form on the surface, and frequently cause post-traumatic epilepsy.

C. Lacerations (rupture or tearing of brain tissue)

This physical disruption of tissue, often accompanied by contusions, is caused by a penetrating injury, e.g. by bony fragments or weapons. Meninges and cortex are both involved. The pattern of pathologic changes differs from that of contusion with respect to the increased amount of hemorrhage, more disruptive effect and the more obvious fibroblastic proliferation and scarring of meninges in lacerations.

D. Intracranial Hemorrhage

Pure intracerebral hemorrhage is rare in trauma. Hemorrhage is usually restricted to that associated with contusions or lacerations.

E. Diffuse Axonal Injury

Diffuse axonal injury is a major cause of prolonged traumatic coma. This type of lesion is present in 35% of head trauma deaths and is the most common cause of poor neurological outcome.

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