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急性实验性诱导癫痫病灶发作间期棘波后的不应期。

Refractory periods following interictal spikes in acute experimentally induced epileptic foci.

作者信息

Dorn T, Witte O W

机构信息

Neurologische Klinik, Heinrich Heine Universität, Düsseldorf, Germany.

出版信息

Electroencephalogr Clin Neurophysiol. 1995 Jan;94(1):80-5. doi: 10.1016/0013-4694(94)00214-6.

DOI:10.1016/0013-4694(94)00214-6
PMID:7530642
Abstract

Under epileptic conditions, interictal epileptic events are followed by large inhibitions which prevent the transition to ictal discharges. In the present experiments the refractory period following interictal epileptic spikes was investigated in animal experiments. Interictal epileptic activity was elicited by application of penicillin onto the motor cortex of anesthetized rats. Interictal epileptic discharges were followed by an absolute refractory phase lasting 200-300 msec, in which no epileptic event could be elicited by epicortical stimulation. This was followed by a relative refractory period up to 900 msec after onset of the conditioning spike; spikes elicited with intervals between 300 and 900 msec were smaller than those with greater intervals and required higher stimulation intensities. This period ends by a sharp drop of threshold. In two-thirds of the experiments, spikes were favoured in intervals of 300-500 msec due to a sag of the threshold, which possibly indicates recurrent neuronal excitations. Stimulations with frequencies of about 1/sec favoured a transition from a pattern with spikes appearing in an irregular sequence every 2-3 sec, to a discharge pattern with spikes appearing with regular intervals of about 1 sec. This change of firing pattern was associated with a drop of the spike threshold. It is concluded that interictal epileptic events are followed by a refractory period comprising different components. Alterations of the neuronal inhibitions responsible for these refractory phases may be critical for the activity of the focus and may determine the transition from interictal to ictal discharges.

摘要

在癫痫状态下,发作间期癫痫事件之后会出现强烈抑制,从而阻止向发作期放电的转变。在本实验中,在动物实验中研究了发作间期癫痫棘波后的不应期。通过将青霉素应用于麻醉大鼠的运动皮层来诱发发作间期癫痫活动。发作间期癫痫放电之后是一个持续200 - 300毫秒的绝对不应期,在此期间,皮层刺激无法诱发癫痫事件。随后是一个相对不应期,在条件性棘波开始后长达900毫秒;间隔300至900毫秒诱发的棘波比间隔更长时诱发的棘波小,且需要更高的刺激强度。这个时期以阈值的急剧下降结束。在三分之二的实验中,由于阈值下降,间隔300 - 500毫秒时棘波更易出现,这可能表明存在神经元的反复兴奋。频率约为1次/秒的刺激有利于从每2 - 3秒不规则出现一次棘波的模式转变为约1秒规则间隔出现棘波的放电模式。这种放电模式的改变与棘波阈值的下降有关。得出的结论是,发作间期癫痫事件之后是一个包含不同成分的不应期。负责这些不应期的神经元抑制的改变可能对病灶的活动至关重要,并可能决定从发作间期向发作期放电的转变。

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