CHRONIC ENCEPHALITIS ASSOCIATED WITH EPILEPSY - IMMUNOHISTOCHEMICAL AND ULTRASTRUCTURAL STUDIES

Chronic encephalitis has been recognized as a cause of epilepsy since the work of Rasmussen et al. in the late 1950s. Despite this, few immu nohistochemical studies of the affected brain tissue have been attempt ed. We have studied specimens of brain tissue from seven patients with this condition who underwent therapeutic multilobar cortical resectio n or hemispherectomy. Immunohistochemical studies were carried out usi ng antibodies to glial fibrillary acidic protein (GFAP), proliferating cell nuclear antigen (PCNA, PC10), T lymphocytes (UCHL-1), B lymphocy tes (L26), macrophages and microglia (HAM-56), and major histocompatib ility complex molecules (LN3 and beta(2)-microglobulin), Additionally, the results of preliminary immunohistochemical and ultrastructural in vestigation of possible immune complex deposition in blood vessel wall s of affected brain tissue are presented. The pattern of GFAP immunore activity suggested a patchy and/or laminar disease process in most pat ients. GFAP immunoreactive cells were especially prominent around micr ovessels in some cases, suggesting an abnormality of the blood-brain b arrier. Both microglial nodules and perivascular collections of inflam matory cells, seen to a variable extent in all cases, contained abunda nt cells immunolabelled with UCHL-1, LN3 and beta(2)-microglobulin. L2 6-labelled B lymphocytes were extremely sparse. Anti-PCNA frequently l abelled microvascular endothelial cells, rare pericytes and occasional cells with microglial/macrophage morphology. The data suggest that ch ronic encephalitis found in patients with epilepsy results from patchy but widespread parenchymal brain injury, in the course of which cells of both microglial and lymphocyte series accumulate or proliferate wi thin brain. Despite the lack of clear evidence of a causal viral patho gen from other studies, the predominant T cell lymphocytic infiltrate is consistent with a viral cause for this disorder. However, autoimmun e factors (possibly triggered by viral infection) may contribute to th e extensive neuropathological abnormalities. Very preliminary results using anti-IgG immunocytochemistry showed that in Rasmussen's encephal itis brain there was scattered labelling of neuronal cell bodies and s ome microvessels. Ultrastructural examination of brain tissue from one patient also showed unusual electron-dense material in microvascular endothelial basement membranes.