PARVALBUMIN AND CALBINDIN-D28K IMMUNOCYTOCHEMISTRY IN HUMAN NEOCORTICAL EPILEPTIC FOCI

Serial sections of cortical resection of 30 patients suffering from dr ug-resistant epilepsy were processed for parvalbumin and calbindin-D28 k immunocytochemistry to determine local circuit neuron populations. O ur findings indicate that there is not a simple mechanism to explain n eocortical epileptic foci. On the basis of the present results it can be suggested that: (1) reduced percentage of local circuit neurons in the vicinity of neoplasms may account for a decreased intracortical in hibition. (2) Abnormal morphology and distribution of local circuit ne urons may result in abnormal cortical inhibition in patients with foca l cortical dysplasia, and, probably, in other focal migrational disord ers, including neuronal nests in the white matter. (3) Increased perce ntages of immunoreactive local circuit neurons and fibers in focal neo cortical necrosis (cavernous angiomas), diffuse hypoxic encephalopathy , and hippocampus in patients with temporal lobe epilepsy due to mesia l sclerosis, may play a role in epilepsy. These neurons can be activat ed by reduced excitatory inputs, or they may establish abnormal synapt ic contacts with other inhibitory neurons. (4) Lack of consistent morp hologic abnormalities in the neocortex of patients with temporal lobe epilepsy, and in patients with cryptogenetic frontal lobe epilepsy, su ggests that electrically abnormal neocortical foci in these cases are probably epiphenomena.