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Benzodiazepine‐GABA A Receptors in Idiopathic Generalized Epilepsy Measured with [ 11 C]Flumazenil and Positron Emission Tomography
Author(s) -
Prevett Martin C.,
Lammertsma Adriaan A.,
Brooks David J.,
Bartenstein Peter A.,
Patsalos Philip N.,
Fish David R.,
Duncan John S.
Publication year - 1995
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1995.tb00969.x
Subject(s) - flumazenil , benzodiazepine , positron emission tomography , medicine , epilepsy , juvenile myoclonic epilepsy , antagonist , gabaa receptor , endocrinology , receptor , neuroscience , psychology , nuclear medicine
Summary The neurochemical basis of absence seizures and the mechanism of their suppression by valproate (VPA) are uncertain. We used positron emission tomography (PET) to determine whether an abnormality of [ 11 C]flumazenil binding to benzodiazepine (BZD)‐GABA A receptors exists in patients with childhood and juvenile absence epilepsy and to examine the effects of VPA on [ 11 C] flumazenil binding. The regional cerebral volume of distribution ( V d ) of [ 11 C]flumazenil in patients not treated with VPA was not different from that in normal controls; V d was lower in patients treated with VPA, and the number of receptors available for binding was significantly reduced in such patients as compared with normal controls. There was no evidence of a primary abnormality of the BZD‐GABA, receptor in childhood and juvenile absence epilepsy (CAE/JAE), but the data suggest that treatment with VPA is associated with a reduction in [ 11 C]flumazenil binding that may be relevant to its mode of action in CAE/JAE.