TEMPORAL-LOBE CENTRAL BENZODIAZEPINE BINDING IN UNILATERAL MESIAL TEMPORAL-LOBE EPILEPSY

PET-demonstrated decreases in [C-11]flumazenil binding occur in anteri or mesial temporal structures on the side of epileptogenesis in unilat eral mesial temporal lobe epilepsy. We performed quantitative autoradi ography on anterior mesial and lateral temporal specimens from 11 subj ects with unilateral mesial temporal lobe epilepsy and six neurologica lly normal controls to identify the predominant in vitro correlates of the decreased [C-11]flumazenil binding. In anterior mesial temporal r egions exhibiting the greatest neuronal cell loss, decreases in agonis t and antagonist binding to type 1 and 2 (central) benzodiazepine bind ing sites were highly correlated with neuronal cell counts. Cell loss and decreased binding were particularly prominent in the lateral porti on of hippocampal region CA1, adjacent to CA2. Lateral temporal centra l benzodiazepine binding was diffusely increased, achieving statistica l significance in cortical laminae V and VI. These findings suggest th at the predominant source of PET-demonstrated decreases in [C-11]fluma zenil binding in mesial temporal epilepsy is hippocampal sclerosis, ra ther than downregulation of central benzodiazepine binding sites on su rviving hippocampal neurone.