Prevett M C, Lammertsma A A, Brooks D J, Cunningham V J, Fish D R, Duncan J S
MRC Cyclotron Unit, Hammersmith Hospital, London, England, U.K.
Epilepsia. 1995 Jun;36(6):592-9. doi: 10.1111/j.1528-1157.1995.tb02573.x.
The role of benzodiazepine (BZD)-gamma-aminobutyric acidA (GABAA) 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 GABAA receptor. Five patients with idiopathic generalized epilepsy (IGE) were studied at rest and during absence seizures with [11C]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 [11C]flumazenil binding. No evidence was found for a change in [11C]flumazenil binding with absence seizures. This result, together with those of a recent study showing no abnormality of [11C]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 GABAA receptor in the pathogenesis of absence seizures.
