Farrell Jordan S, Wolff Marshal D, Teskey G Campbell
Hotchkiss Brain Institute, University of Calgary, Calgary, AB, T2N 4N1, Canada.
Adv Neurobiol. 2017;15:317-334. doi: 10.1007/978-3-319-57193-5_12.
Epilepsy is commonly associated with a number of neurodegenerative and pathological alterations in those areas of the brain that are involved in repeated electrographic seizures. These most prominently include neuron loss and an increase in astrocyte number and size but may also include enhanced blood-brain barrier permeability, the formation of new capillaries, axonal sprouting, and central inflammation. In animal models in which seizures are either repeatedly elicited or are self-generated, a similar set of neurodegenerative and pathological alterations in brain anatomy are observed. The primary causal agent responsible for these alterations may be the cascade of events that follow a seizure and lead to an hypoperfusion/hypoxic episode. While epilepsy has long and correctly been considered an electrical disorder, the vascular system likely plays an important causal role in the neurodegeneration and pathology that occur as a consequence of repeated seizures.
癫痫通常与大脑中参与反复脑电图发作的区域的一些神经退行性和病理改变有关。这些改变最显著的包括神经元丢失以及星形胶质细胞数量和大小的增加，但也可能包括血脑屏障通透性增强、新毛细血管形成、轴突发芽和中枢炎症。在反复诱发癫痫发作或癫痫发作自行产生的动物模型中，观察到大脑解剖结构中类似的一组神经退行性和病理改变。导致这些改变的主要致病因素可能是癫痫发作后随之而来并导致灌注不足/缺氧发作的一系列事件。虽然癫痫长期以来一直被正确地认为是一种电紊乱，但血管系统可能在反复癫痫发作导致的神经退行性变和病理过程中起重要的因果作用。
