Özet:

Traumatic brain damage is one of the main causes of mortality and morbidity in individuals under the age of 45. More than these primary injuries that occur, it is essentially responsible for the secondary process, mortality and morbidity, which is initiated by this direct effect, and is also sensitive to therapeutic interventions. Both primary and secondary pathophysical processes lead to the release of cellular mediators (proinflammatory cytokins, prostaglandins, free radicals and complemants), the expression of the adezyon molecules, the chemotase and transmigration of defence and glial cells. The production and secretion of proinflammatory cytokines after traumatic brain damage has been shown in both human and experimental animal models. After trauma in the brain, the detection of interlökin 1, interlökin 6, tumor necrosis factor and high concentrations of cytokines from the central nervous system suggests that they play an important role in the pathological process that develops after trauma. Knowing the role these cytokines play in the damage process and developing the appropriate agents to stop this self-progressive process at a point, which means reducing neuronal damage, can save life in the head trauma.

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