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点燃式癫痫发作、发作后难治性、癫痫持续状态和电自我刺激。

Kindled epileptic seizures, postictal refractoriness, status epilepticus, and electrical self-stimulation.

作者信息

Herberg L J, Rose I C

机构信息

Institute of Neurology, London, UK.

出版信息

Neurosci Biobehav Rev. 1994 Fall;18(3):411-20. doi: 10.1016/0149-7634(94)90054-x.

DOI:10.1016/0149-7634(94)90054-x
PMID:7984359
Abstract

A single stimulus applied once daily to the limbic system commonly leads to convulsive seizures yet seizures are relatively infrequent during intracranial self-stimulation (ICSS), a procedure that involves many hundreds of similar stimuli. The present study examined the possible role of electrode site, interstimulus interval, afterdischarge and reinforcement thresholds and postictal refractoriness in accounting for this paradox. Electrode location was an overriding factor: seizures were never seen with hypothalamic implants posterior to the level of the ventromedial nucleus but were elicited by the majority of more rostral reward sites. Frequent repeated stimulation by ICSS did not in itself prevent subsequent kindling or reverse the effects of earlier kindling; on the contrary, seizures induced by ICSS showed a progressive increase in severity similar to the progression produced by conventional kindling. Individual convulsive seizures, as in previous studies, conferred transient protection against further seizures whether from ICSS or from kindling. More prolonged protection occassionally developed after repeated convulsive seizures: protection was accompanied by continuous EEG slow-waves corresponding in presentation to clinical petit mal status. Prolonged resistance to seizures has also been reported after tonic-clonic status epilepticus causing temporal lobe damage. The relative infrequency of seizures during ICSS ordinarily appears to depend on the siting of the electrodes, on distinct short- and long-term postictal refractory states, and on the rat learning to restrict stimulus input to subseizural levels.

摘要

每天对边缘系统施加一次单一刺激通常会导致惊厥性癫痫发作,但在颅内自我刺激(ICSS)过程中癫痫发作相对较少,该过程涉及数百次类似刺激。本研究探讨了电极位置、刺激间隔、放电后和强化阈值以及发作后不应期在解释这一矛盾现象中可能发挥的作用。电极位置是一个首要因素:在腹内侧核水平后方的下丘脑植入物从未引发癫痫发作,但大多数更靠前的奖赏位点会引发癫痫发作。ICSS频繁重复刺激本身并不能预防随后的点燃效应或逆转早期点燃效应的影响;相反,ICSS诱发的癫痫发作严重程度呈逐渐增加,类似于传统点燃效应产生的进展情况。与之前的研究一样,个体惊厥性癫痫发作会对进一步的癫痫发作产生短暂的保护作用,无论是来自ICSS还是点燃效应。在反复惊厥性癫痫发作后偶尔会出现更长时间的保护作用:这种保护作用伴随着持续的脑电图慢波,其表现与临床小发作状态相对应。在导致颞叶损伤的强直阵挛性癫痫持续状态后,也有关于对癫痫发作的长期抵抗的报道。ICSS期间癫痫发作相对较少通常似乎取决于电极的位置、不同的短期和长期发作后不应期状态,以及大鼠学会将刺激输入限制在亚癫痫发作水平。

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