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NEUROLOGY 1995;45:934-941
© 1995 American Academy of Neurology

Temporal lobe central benzodiazepine binding in unilateral mesial temporal lobe epilepsy

D. E. Burdette, MD, S. Y. Sakurai, PhD, T. R. Henry, MD, D. A. Ross, MD, P. B. Pennell, MD, K. A. Frey, MD, PhD, J. C. Sackellares, MD and R. L. Albin, MD

From the Departments of Neurology (Drs. Burdette, Sakurai, Henry, Pennell, Frey, Sackellares, and Albin) and Internal Medicine (Dr. Frey) and the Section of Neurosurgery (Dr. Ross), University of Michigan, Ann Arbor, MI; the Department of Clinical Neuroscience (Dr. Burdette), USAF Medical Center, Wright-Patterson AFB, Dayton, OH; and the Neurology Service (Dr. Sackellares), VA Medical Center, Gainesville, FL.

Article abstract—PET-demonstrated decreases in [11C]flumazenil binding occur in anterior mesial temporal structures on the side of epileptogenesis in unilateral mesial temporal lobe epilepsy. We performed quantitative autoradiog-raphy on anterior mesial and lateral temporal specimens from 11 subjects with unilateral mesial temporal lobe epilepsy and six neurologically normal controls to identify the predominant in vitro correlates of the decreased [11C]flumazenil binding. In anterior mesial temporal regions exhibiting the greatest neuronal cell loss, decreases in agonist and antagonist binding to type 1 and 2 (central) benzodiazepine binding sites were highly correlated with neuronal cell counts. Cell loss and decreased binding were particularly prominent in the lateral portion of hippocampal region CA1, adjacent to CA2. Lateral temporal central benzodiazepine binding was diffusely increased, achieving statistical significance in cortical laminae V and VI. These findings suggest that the predominant source of PET-demonstrated decreases in [11C]flumazenil binding in mesial temporal epilepsy is hippocampal sclerosis, rather than down-regulation of central benzodiazepine binding sites on surviving hippocampal neurons.




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