BENZODIAZEPINE RECEPTORS IN FOCAL EPILEPSY WITH CORTICAL DYSGENESIS -AN C-11 FLUMAZENIL PET STUDY

Previous imaging studies using C-11-flumazenil in patients with mesial temporal lobe epilepsy and neocortical partial seizure disorders have found focal decreases in gamma-aminobutyric acid type A/benzodiazepin e receptor binding. These studies used subjective visual assessment an d a region of interest approach to quantitation. We performed three-di mensional, C-11-flumazenil positron emission tomography in 12 patients with cortical dysgenesis identified by high-resolution volumetric mag netic resonance imaging and in 26 normal subjects. Spectral analysis w as used to produce a parametric image of C-11-flumazenil volume of dis tribution for each subject. Using volumetric normalization and statist ical parametric mapping, we compared the entire brain volume of each p atient with the brains of the normal group to produce maps of regions of abnormal C-11-flumazenil binding which were then rendered into the volumetric magnetic resonance images. This allowed a correlation of st ructure and function to be made. Of the 12 patients, 10 showed at leas t one region of abnormal C-11-flumazenil binding; the abnormal regions were frequently more extensive than were the lesions seen with magnet ic resonance imaging. C-11-Flumazenil binding abnormalities were frequ ently seen in regions of cortex that had a normal magnetic resonance a ppearance. Lesions were characterized by increases in gamma-aminobutyr ic acid type A/benzodiazepine receptor availability, and by the decrea ses found in previous studies. These findings have implications for th e neurobiology of seizure disorders associated with cortical dysgenesi s and for the management of such patients if surgery is contemplated.