[Brain contusion: morphology, pathogenesis and treatment].

Focal cerebral contusions can be dynamic and expansive, leading to a delayed neurological deterioration. In head--injured patients, the rise in intracranial pressure (ICP), subsequent to uncontrollable swelling, is the only and the most frequent cause of death. Studies show that brain swelling, after traumatic brain injury (TBI), is caused by brain edema rather than cerebral blood volume (CBV). CBV is reduced in proportion to cerebral blood flow (CBF) reduction, following a severe TBI. Cerebrovascular damages, leading to subsequent reductions in regional CBF, may play an important role in secondary cell damages following TBI. The histological examination revealed the formation of microthrombosis in the contused area, extending from the center to the peripheral areas within 6 hours after injury. In the pericontusional zone and surrounding parenchyma, vasoresponsivity may be nearly three times normal, which suggests hypersensitivity to hyperventilation and other phenomena. Glutamate is the most widely distributed excitatory neurotransmitter in the mammalian brain. However, when glutamate is present in excessive quantities, it may overactivate specific ion channels, especially the N-methyl-D-aspartate channel. A shift of potassium into the extracellular space will result in rapid swelling of astrocytes, which absorb quantities of potassium to preserve ionic homeostasis. This process may cause rapid cytotoxic edema, which is probably, a major factor in causation of posttraumatic raised ICP. The presence of a focal contusion and primary or secondary ischemic events were the clinical features most strongly correlated with high dialysate of glutamate. Raised ICP was significantly more common, and outcome was worse in patients with high levels of glutamate. Contusion is a key factor in the development of blood brain barrier (BBB) permeability. BBB endures at least 7 days post TBI. Biphasing opening of the BBB, following head trauma and a possible second wave of secondary brain damage, was confirmed. Brain tissue pO2 monitoring might become an important tool in the treatment regime for TBI patients. Histologically the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the cortical contusion and bilaterally in diffuse axonal injury. Aggressive, early hyperventilation after TBI augments neuronal death in CA3 hippocampus. Due to high mortality associated with such cerebral contusions, a standard practice has evolved into evacuating contusions in patients who had deterioration in the level of consciousness, lesions more than 30 sec and CT suggestion of raised ICP.