Prevett M C, Lammertsma A A, Brooks D J, Bartenstein P A, Patsalos P N, Fish D R, Duncan J S
MRC Cyclotron Unit, Hammersmith Hospital, London, England.
Epilepsia. 1995 Feb;36(2):113-21. doi: 10.1111/j.1528-1157.1995.tb00969.x.
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 [11C]flumazenil binding to benzodiazepine (BZD)-GABAA receptors exists in patients with childhood and juvenile absence epilepsy and to examine the effects of VPA on [11C]flumazenil binding. The regional cerebral volume of distribution (Vd) of [11C]flumazenil in patients not treated with VPA was not different from that in normal controls; Vd 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-GABAA receptor in childhood and juvenile absence epilepsy (CAE/JAE), but the data suggest that treatment with VPA is associated with a reduction in [11C]flumazenil binding that may be relevant to its mode of action in CAE/JAE.
失神发作的神经化学基础及其被丙戊酸盐（VPA）抑制的机制尚不清楚。我们使用正电子发射断层扫描（PET）来确定儿童和青少年失神癫痫患者是否存在[11C]氟马西尼与苯二氮䓬（BZD）-GABAA受体结合异常，并研究VPA对[11C]氟马西尼结合的影响。未接受VPA治疗的患者中[11C]氟马西尼的区域脑分布容积（Vd）与正常对照组无差异；接受VPA治疗的患者Vd较低，与正常对照组相比，此类患者中可用于结合的受体数量显著减少。没有证据表明儿童和青少年失神癫痫（CAE/JAE）中存在BZD-GABAA受体原发性异常，但数据表明，VPA治疗与[11C]氟马西尼结合减少有关，这可能与其在CAE/JAE中的作用方式有关。
