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下丘的电诱发癫痫发作:癫痫起源的潜在部位?

Electrically elicited seizures from the inferior colliculus: a potential site for the genesis of epilepsy?

作者信息

McCown T J, Greenwood R S, Frye G D, Breese G R

出版信息

Exp Neurol. 1984 Dec;86(3):527-42. doi: 10.1016/0014-4886(84)90087-6.

Abstract

Most electrically induced seizures involve forebrain structures, such as the amygdala or frontal cortex, but the following studies characterized a specific anatomic site in the inferior colliculus which generated seizure-like behavior after a single, low current electrical stimulation. When a bipolar electrode was implanted into the dorsomedial aspect of the inferior colliculus, low stimulation currents (120 to 200 microA, 30 Hz) produced wild running behavior which outlasted the stimulation by 4 to 10 s. This wild running behavior was directly correlated with local afterdischarge in the inferior colliculus, while no changes were found in the EEG activity in the cortex or hippocampus. Though the threshold current necessary to invoke the wild running seizures remained stable for long periods of time, the presentation of two stimulations a day for 2 weeks caused a progressive increase in the duration of poststimulus wild running. In the last days of the chronic stimulations, some forelimb tonus or myoclonic jerks followed the wild running seizures. These latter behaviors were correlated with local afterdischarges at the electrode tips in the inferior colliculus and spiking EEG activity in the frontal cortex. Pharmacologically, haloperidol, phenobarbital, carbamazepine, and ethosuximide proved ineffective in attenuating the seizures, whereas phenytoin, sodium valproate, and chlordiazepoxide attenuated the seizures. These findings are discussed in relation to the genesis of epilepsy in humans.

摘要

大多数电诱导癫痫发作涉及前脑结构,如杏仁核或额叶皮质,但以下研究描述了下丘中的一个特定解剖部位,在单次低电流电刺激后会产生类似癫痫发作的行为。当将双极电极植入下丘的背内侧时,低刺激电流(120至200微安,30赫兹)会产生狂奔行为,这种行为在刺激结束后持续4至10秒。这种狂奔行为与下丘中的局部放电直接相关,而在皮质或海马的脑电图活动中未发现变化。尽管引发狂奔性癫痫发作所需的阈值电流在很长一段时间内保持稳定,但每天进行两次刺激,持续2周,会导致刺激后狂奔持续时间逐渐增加。在慢性刺激的最后几天,一些前肢强直或肌阵挛性抽搐跟随狂奔性癫痫发作。这些后期行为与下丘电极尖端的局部放电以及额叶皮质的尖峰脑电图活动相关。在药理学上,氟哌啶醇、苯巴比妥、卡马西平和乙琥胺在减轻癫痫发作方面无效,而苯妥英钠、丙戊酸钠和氯氮卓可减轻癫痫发作。结合人类癫痫的发生对这些发现进行了讨论。

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