Lesions of acetylcholine neurons in refractory epilepsy.
Lesions of acetylcholine neurons in refractory epilepsy.
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DOI：
10.5402/2012/404263
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Kodama T
中科院分区：
文献类型：
--
作者：
Hayashi M;Nakajima K;Miyata R;Tanuma N;Kodama T
我们研究了难治性癫痫患者的脑干病变，包括West综合征（WS）、Lennox-Gastaut综合征（LGS）和齿状核红核苍白球路易体萎缩（DRPLA）。脚桥被盖核（PPN）中的乙酰胆碱能神经元（AchNs）参与智力发育，神经元烟碱乙酰胆碱受体的破坏可导致癫痫。为了研究AchNs病变在难治性癫痫中的参与，我们对有WS和/或LGS既往史的尸检病例和显示进行性肌阵挛性癫痫的DRPLA病例的PPN中AchNs进行了免疫组化分析。此外，我们进行了初步的定量水平的乙酰胆碱，神经肽和单胺代谢产物的患者的脑脊液（CSF）的WS和良性惊厥与轻度胃肠炎（CwG）。在PPN分析中，WS/LGS和WS病例的神经元总数和AchNs数量减少，而DRPLA病例显示AchNs数量和百分比减少。在CSF分析中，WS患者表现出抑制性神经肽水平降低，而CwG患者表现出乙酰胆碱水平升高和5-羟色胺代谢物水平降低。这些数据表明，在WS和DRPLA的AchNs病变的可能参与。
We have examined brainstem lesions in patients with refractory epilepsy disorders, including West syndrome (WS), Lennox-Gastaut syndrome (LGS), and dentatorubral-pallidoluysian atrophy (DRPLA). Acetylcholinergic neurons (AchNs) in the pedunculopontine tegmental nucleus (PPN) are involved in mental development, and disruption of neuronal nicotinic acetylcholine receptors can lead to epilepsy. In order to investigate the involvement of lesions of AchNs in refractory epilepsy, we performed immunohistochemical analyses of AchNs in the PPN in autopsy cases who had a past history of WS and/or LGS and in DRPLA cases who showed progressive myoclonic epilepsy. In addition, we performed a preliminary quantification of the levels of acetylcholine, neuropeptides, and monoamine metabolites in the cerebrospinal fluid (CSF) of patients with WS and benign convulsions associated with mild gastroenteritis (CwG). In the PPN analysis, the total number of neurons and the number of AchNs were reduced in WS/LGS and WS cases, while DRPLA cases showed a decrease in the number and percentage of AchNs. In the CSF analysis, WS patients demonstrated a reduction in the levels of inhibitory neuropeptides, while CwG patients showed increased levels of acetylcholine and decreased levels of serotonin metabolites. These data suggest the possible involvement of lesions of AchNs in WS and DRPLA.