Gale K
Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007.
J Clin Neurophysiol. 1992 Apr;9(2):264-77. doi: 10.1097/00004691-199204010-00007.
Convulsive seizures in animal models usually involve one or more of the following components: (1) limbic motor seizures, (2) explosive running-bouncing clonic seizures, and (3) tonic extensor seizures. Each of these components depends on specific and experimentally separable anatomic substrates. Limbic motor seizures depend on forebrain structures for their initiation and propagation, with the prepiriform, piriform, and entorhinal cortices playing a prominent role in conjunction with hippocampus, amygdala, substantia innominata, and mediodorsal thalamus. In contrast, seizures involving running-bouncing clonus or tonic extension depend on neural substrates in the brainstem and do not appear to require the integrity of the forebrain for their development or expression. The inferior colliculus is a region from which running-bouncing seizures can be elicited by chemical or electrical stimulation. Tonic extensor seizures depend on the integrity of the nucleus reticularis pontis oralis, but a specific locus responsible for triggering these seizures has yet to be identified. Under conditions of chronic or repeated seizure activity over prolonged time periods, seizures evoked from the hindbrain can recruit forebrain circuits; conversely, repeated stimulation of forebrain limbic circuits (e.g., kindling) can modify susceptibility to brainstem convulsions. These long-term alterations may result from changes in the activity of seizure "gating" pathways, which are circuits that influence seizure susceptibility by modulating the threshold for the initiation and/or propagation of the seizures. In general, these pathways are not part of any core seizure propagation pathway per se. In many cases, the gating substrates are relatively nonselective as to the type of seizure they can influence. In this category, the substantia nigra and its related circuits within the basal ganglia serve a prominent role. In addition, ascending noradrenergic projections have been implicated in the regulation of seizure threshold. Other gating mechanisms involve thalamic circuitry and pathways originating in cerebellum.
(1) 边缘性运动性癫痫发作，(2) 爆发性奔跑-跳跃阵挛性癫痫发作，以及 (3) 强直性伸展性癫痫发作。这些组成部分中的每一个都依赖于特定的、实验上可分离的解剖学基质。边缘性运动性癫痫发作的起始和传播依赖于前脑结构，梨状前皮质、梨状皮质和内嗅皮质与海马体、杏仁核、无名质和丘脑背内侧核一起发挥着重要作用。相比之下，涉及奔跑-跳跃阵挛或强直性伸展的癫痫发作依赖于脑干中的神经基质，其发展或表现似乎不需要前脑的完整性。下丘是一个通过化学或电刺激可引发奔跑-跳跃性癫痫发作的区域。强直性伸展性癫痫发作依赖于脑桥嘴侧网状核的完整性，但尚未确定引发这些癫痫发作的具体部位。在长期慢性或反复癫痫活动的情况下，后脑海马引发的癫痫发作可募集前脑回路；相反，反复刺激前脑边缘回路（如点燃）可改变对脑干惊厥的易感性。这些长期改变可能是由于癫痫“门控”通路活动的变化所致，这些通路是通过调节癫痫发作起始和/或传播的阈值来影响癫痫易感性的回路。一般来说，这些通路本身并非任何核心癫痫传播通路的一部分。在许多情况下，门控基质对它们能够影响的癫痫发作类型相对不具选择性。在这方面，黑质及其在基底神经节内的相关回路发挥着重要作用。此外，去甲肾上腺素能上行投射与癫痫阈值的调节有关。其他门控机制涉及丘脑回路和起源于小脑的通路。
