INTRACEREBRAL INFLAMMATORY RESPONSE TO EXPERIMENTAL BRAIN CONTUSION

The inflammatory reaction following experimental brain contusion was s tudied by immunohistochemistry in 22 rats during the first 16 days aft er trauma. An inflammatory mononuclear cell response was evident on da y 2, with a maximum on days 5-6 and signs remained still 16 days after the trauma. The lime course of the cellular infiltration adjacent to the lesion correlated with blood brain barrier dysfunction in the cont ralateral side of the traumatized hemisphere. The cellular infiltrate comprised NK cells, T-helper cells and T-cytotoxic suppressor cells as well as monocytes/macrophages. Most of the macrophages appeared to be activated by T-cells. Surprisingly, polymorphonuclear cells appeared less engaged than mononuclear cells in the inflammation. The demonstra tion of immunocompetent cells and the induction of MHC-1 and MHC-II an tigen provides a substrate for inflammatory reactions similar to those that cause neurological damage in inflammatory diseases such as viral infections, multiple sclerosis and experimental allergic encephalitis . Our observations indicate that the role of the inflammatory reaction s may have a role, hitherto neglected, in the pathogenesis of secondar y traumatic brain injury.