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Benzodiazepine‐GABA A Receptor Binding During Absence Seizures
Author(s) -
Prevett Martin C.,
Lammertsma Adriaan A.,
Brooks David J.,
Cunningham Vincent J.,
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.tb02573.x
Subject(s) - flumazenil , benzodiazepine , epilepsy , juvenile myoclonic epilepsy , medicine , generalized epilepsy , ictal , pathogenesis , antagonist , endocrinology , gabaa receptor , anesthesia , receptor , neuroscience , psychology
Summary: The role of benzodiazepine (BZD)‐γ‐aminobutyric acid, (GABA) receptors in the pathogenesis of absence seizures is uncertain. In this study, we examined the effect of absence seizures on the binding of flumazenil to the BZD binding site of the GABA, receptor. Five patients with idiopathic generalized epilepsy (IGE) were studied at rest and during absence seizures with [ 11 C]flumazenil and positron emission tomography (PET). Normalized regional cerebral time‐activity curves from the resting and ictal scans were compared with each other and with computed simulations showing the effects of changes in cerebral blood flow (CBF) and [ 11 Clfluma‐zenil binding. No evidence was found for a change in [ 11 C]flumazenil binding with absence seizures. This result, together with those of a recent study showing no abnormality of [ 11 C]flumazenil binding interictally in patients with childhood and juvenile absence epilepsy (JAE) does not support a primary role for the BZD binding site of the GABA, receptor in the pathogenesis of absence seizures.