Koepp M J, Richardson M P, Brooks D J, Duncan J S
MRC Cyclotron Unit Hammersmith Hospital, London, UK.
Lancet. 1998 Sep 19;352(9132):952-5. doi: 10.1016/s0140-6736(97)09077-6.
Studies in animals implicate endogenous release of opioid peptides as a mechanism for terminating partial and generalised seizures. To localise dynamic changes in opioid neurotransmission associated with partial seizures and higher cognitive function, we investigated the release of endogenous opioids in patients with reading-induced seizures compared with healthy controls.
Five patients who had reading epilepsy and six controls had 11C-diprenorphine (DPN) positron-emission-tomography (PET) scans while reading a string of symbols (baseline) or a scientific paper (activation). Statistical parametric mapping was used to find areas with differences in opioid-receptor binding.
On activation scans mean 11C-DPN binding to opioid receptors was significantly lower (p<0.05 corrected for multiple non-independent comparisons) in the left parieto-temporo-occipital cortex (Brodmann area 37) in reading-epilepsy patients compared with controls.
These findings suggest that opioid-like substances are involved in the termination of reading-induced seizures.
动物研究表明内源性阿片肽释放是终止部分性和全身性癫痫发作的一种机制。为了定位与部分性癫痫发作和更高认知功能相关的阿片类神经传递的动态变化，我们对阅读性癫痫患者与健康对照者内源性阿片类物质的释放情况进行了研究。
5名患有阅读性癫痫的患者和6名对照者在阅读一串符号（基线）或一篇科学论文（激活）时接受了11C-二丙诺啡（DPN）正电子发射断层扫描（PET）。采用统计参数映射来寻找阿片受体结合存在差异的区域。
在激活扫描中，与对照者相比，阅读性癫痫患者左侧顶颞枕叶皮质（布罗德曼区37）中11C-DPN与阿片受体的平均结合显著降低（经多次非独立比较校正后p<0.05）。
这些发现表明阿片样物质参与了阅读性癫痫发作的终止。
