FUNCTIONAL MAPPING OF THE LATE STAGES OF STATUS EPILEPTICUS IN THE LITHIUM PILOCARPINE MODEL IN RAT - A (14)C-2-DEOXYGLUCOSE STUDY
FUNCTIONAL MAPPING OF THE LATE STAGES OF STATUS EPILEPTICUS IN THE LITHIUM PILOCARPINE MODEL IN RAT - A (14)C-2-DEOXYGLUCOSE STUDY
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DOI：
10.1016/0306-4522(94)00377-h
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发表时间：
1995-02-01
期刊：
影响因子：
3.3
通讯作者：
TREIMAN, DM
中科院分区：
文献类型：
--
作者：
HANDFORTH, A;TREIMAN, DM
匹鲁卡品给药氯化锂预处理的大鼠最初的结果在离散惊厥发作，每一个行为和脑电图终止，然后发展到惊厥活动与起伏的行为和电图的严重程度，最后，一个连续的惊厥状态envelope，与连续快速尖峰电图。这一阶段不会无限期地持续下去，但随后会发生戏剧性的电描记变化，成为周期性癫痫样放电。本研究的目的是确定与C-14-2-脱氧葡萄糖的功能映射技术发生在癫痫发作的解剖基板在此过渡期间和之后的变化，以便能够推断潜在的机制。与早期和晚期连续快速尖峰相关的行为包括头部抽搐;相应的脱氧葡萄糖放射自显影显示大多数前脑区域中存在高浓度葡萄糖利用;小脑脑干正常。在2-3小时的状态下，快速尖峰被平坦的时期打断;周期性复合波很快主导了脑电图。行为学上，惊厥严重程度增加。尽管这一戏剧性的电图演变，发生在一般性前脑代谢过度活化的变化不大，除了齿状回/顶盖前/上级丘复合体显示出显着增加的活动。脱氧葡萄糖的研究，在后期阶段的周期性癫痫样放电建立了一个序列的进一步变化。在晚期周期性放电与阵挛痉挛，在4小时后进入状态，广义前脑过度激活仍然盛行，但程度较低，比早期周期性放电与阵挛痉挛。在更晚的阶段，晚周期性放电，微妙的惊厥，放射自显影显示收缩的神经元激活的解剖基板：超激活丢失的大部分新皮层和丘脑，在尾部嗅觉结构，皮质杏仁核，和内嗅区，但保留在枕叶皮层和许多边缘系统领域。在最后一个阶段，晚周期性放电，电气，不相关的惊厥行为，放射自显影显示残留的激活只有阿蒙的角，相反，前脑显示低于正常的葡萄糖utilization.These结果表明，在癫痫持续状态的后期阶段，从快速尖峰周期性复合物的过渡是不相关的减少癫痫发作解剖基板。周期性癫痫样放电的电描记实体在解剖学或行为学上不是同质的，而是通过连续的阶段进行的，其特征在于最初在全身性癫痫激活的前脑内葡萄糖利用的减少，然后癫痫发作解剖基质的收缩。可能的机制过渡到周期性的配合物进行了讨论。
Pilocarpine administration to lithium chloride-pretreated rats results initially in discrete convulsive seizures, each behaviorally and electroencephalographically terminated, which then progress to convulsive activity with waxing-and-waning behavioral and electrographic severity; finally, a continuous convulsive state ensues, associated electrographically with continuous fast spiking. This stage does not last indefinitely but is followed by a dramatic electrographic change to periodic epileptiform discharges. The purpose of the present study was to determine with the C-14-2-deoxyglucose functional mapping technique what changes occur in the seizure anatomic substrate during and after this transition, in order to enable inferences about underlying mechanisms. Behavior associated with early and late continuous fast spiking consisted of head twitching; corresponding deoxyglucose autoradiographs displayed seizure-induced intense glucose utilization in most forebrain areas; extranigral brainstem was normal. At 2-3 h of status, fast spiking became interrupted by flat periods; periodic complexes soon dominated the electroencephalogram. Behaviorally, convulsive severity increased. Despite this dramatic electrographic evolution, little change in generalized forebrain metabolic hyperactivation occurred, except that the zona incerta/pretectal/superior colliculus complex displayed markedly increased activity. Deoxyglucose studies in late stages of periodic epileptiform discharges established a sequence of further changes. In late periodic discharges with clonic jerks, at 4 h after status entry, generalized forebrain hyperactivation still prevailed, but to a lesser degree than in early periodic discharges with clonic jerks. At a still later stage, late periodic discharges, subtle convulsive, autoradiographs revealed constriction of the seizure-activated anatomic substrate: hyperactivation was lost in most of neocortex and thalamus, and in caudal olfactory structures, cortical amygdala, and entorhinal areas, but retained in deep occipital cortex and many limbic areas. In the last stage, late periodic discharges, electrical, not associated with convulsive behavior, autoradiographs revealed residual activation in only Ammon's horn; in contrast, much of the forebrain displayed below-normal glucose utilization.These results demonstrate that in the later stages of status epilepticus, the transition from fast spiking to periodic complexes is not associated with a reduction in the seizure anatomic substrate. The electrographic entity of periodic epileptiform discharges is not anatomically or behaviorally homogeneous, but proceeds through successive stages characterized initially by a reduction of glucose utilization within generalized seizure-activated forebrain, then a contraction of the seizure anatomic substrate. Possible mechanisms underlying the transition to periodic complexes are discussed.