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Benzodiazepine receptors in focal epilepsy with cortical dysgenesis: An 11 C‐flumazenil PET study
Author(s) -
Richardson M. P.,
Koepp M. J.,
Duncan J. S.,
Brooks D. J.,
Fish D. R.
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410400210
Subject(s) - flumazenil , statistical parametric mapping , magnetic resonance imaging , dysgenesis , temporal lobe , medicine , benzodiazepine , epilepsy , neuroscience , psychology , radiology , receptor , anatomy
Previous imaging studies using 11 C‐flumazenil in patients with mesial temporal lobe epilepsy and neocortical partial seizure disorders have found focal decreases in γ‐aminobutyric acid type A/benzodiazepine receptor binding. These studies used subjective visual assessment and a region of interest approach to quantitation. We performed three‐dimensional, 11 C‐flumazenil positron emission tomography in 12 patients with cortical dysgenesis identified by high‐resolution volumetric magnetic resonance imaging and in 26 normal subjects. Spectral analysis was used to produce a parametric image of 11 C‐flumazenil volume of distribution for each subjects. Using volumetric normalization and statistical parametric mapping, we compared the entire brain volume of each patient with the brains of the normal group to produce maps of regions of abnormal 11 C‐flumazenil binding which were then rendered into the volumetric magnetic resonance images. This allowed a correlation of structure and function to be made. Of the 12 patients, 10 showed at least one region of abnromal 11 C‐flumazenil binding; the abnormal regions were frequently more extensive than were the lesions seen with magnetic resonance imaging. 11 C‐Flumazenil binding abnormalities were frequently seen in regions of cortex that had a normal magnetic resonance appearance. Lesions were characterized by increases in γ‐aminobutyric acid type A/benzodiazepine receptor availability, and by the decreases found in previous studies. These findings have implications for the neurobiology of seizure disorders associated with cortical dysgenesis and for the management of such patients if surgery is contemplated.