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出生后早期持续存在的缺氧缺血性脑病可能导致大鼠永久性癫痫活动和皮质惊厥阈值改变。

Hypoxic-ischemic encephalopathy sustained in early postnatal life may result in permanent epileptic activity and an altered cortical convulsive threshold in rat.

作者信息

Romijn H J, Voskuyl R A, Coenen A M

机构信息

Netherlands Institute for Brain Research, Amsterdam.

出版信息

Epilepsy Res. 1994 Jan;17(1):31-42. doi: 10.1016/0920-1211(94)90077-9.

DOI:10.1016/0920-1211(94)90077-9
PMID:8174523
Abstract

The aim of this study was to investigate whether the rat cerebral cortex, damaged by hypoxia-ischemia in early postnatal life, would show an increased seizure susceptibility and/or spontaneous epileptic discharges in adulthood. To that end 12-13-day-old Wistar rat pups were unilaterally exposed to hypoxic-ischemic conditions. After a recovery period of about 2.5 months, recording and stimulation electrodes were permanently implanted over the left and right fronto-parietal neocortex. Long-term recording of baseline electrocortical activity showed that only those animals that had incurred severe brain damage, as was reflected by the presence of a cortical infarction, ran a high risk of developing permanent epileptic activity. With the aid of the stimulation electrodes the initial threshold for localized seizure activity was found to be the same for the experimental and non-treated groups. However, when the kindling-like decline of this threshold was assessed by repeated testing over a 2-week period, the infarcted animals tended to a more rapid decline but a higher stabilization level than the non-infarcted and control animals.

摘要

本研究的目的是调查出生后早期经历缺氧缺血性损伤的大鼠大脑皮层在成年后是否会表现出癫痫易感性增加和/或自发性癫痫放电。为此,将12 - 13日龄的Wistar大鼠幼崽单侧暴露于缺氧缺血环境。经过约2.5个月的恢复期后,将记录和刺激电极永久性植入左右额顶叶新皮层。对基线皮层电活动的长期记录表明,只有那些出现皮层梗死、遭受严重脑损伤的动物才有发生永久性癫痫活动的高风险。借助刺激电极发现,实验组和未治疗组的局部癫痫活动初始阈值相同。然而,当通过在2周内重复测试评估该阈值类似点燃的下降情况时,梗死动物的阈值下降往往比未梗死和对照动物更快,但稳定水平更高。

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