HISTO-PATHOLOGY OF THE FERRIC-INDUCED CHRONIC EPILEPTIC FOCUS IN CAT - GOLGI-STUDY
HISTO-PATHOLOGY OF THE FERRIC-INDUCED CHRONIC EPILEPTIC FOCUS IN CAT - GOLGI-STUDY
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DOI：
10.1016/0014-4886(79)90075-x
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发表时间：
1979-01-01
影响因子：
5.3
通讯作者：
WILLMORE, LJ
中科院分区：
文献类型：
--
作者：
REID, SA;SYPERT, GW;WILLMORE, LJ
通过软膜下注射饱和FeCl 3溶液，使5只猫慢性癫痫。注射后6周，皮质电图记录显示注射区域出现局灶性癫痫样尖峰。在注射生理盐水的对照组中未观察到该结果。使用Nissl和Golgi-Cox技术对癫痫病灶进行的组织学分析显示，高尔基体浸渍的神经元减少，星形胶质细胞增生，树突棘丢失，树突分支减少和树突静脉曲张。这些与人类致痫灶的病理学发现相似。这些结果，结合经常观察到的含铁血黄素沉着症在人类致痫灶的地区，牵连释放的Fe从外渗的血液元素作为一个可能的病因机制。FeCl 3实验致痫灶在电生理学和组织病理学方面准确模拟了人类临床实体（创伤后癫痫）。
Five cats were rendered chronically epileptic via subpial injection of saturated FeCl3 solution. Six weeks postinjection, electrocorticographic recording demonstrated focal epileptiform spiking in the region of the injection. This finding was not observed in saline-injected controls. Histopathological analysis of the epileptic focus using Nissl and Golgi-Cox techniques revealed depopulation of Golgi-impregnated neurons, astrocytic gliosis, loss of dendritic spines, decreased dendritic branching and dendritic varicosities. These are similar to the pathological findings which were described for human epileptogenic foci. These results, in combination with the frequent observation of hemosiderosis in regions of human epileptogenic foci, implicate the release of Fe from extravasated blood elements as a possible etiologic mechanism. The FeCl3 experimental epileptogenic focus accurately models the human clinical entity (postraumatic epilepsy) with respect to both electrophysiology and histopathology.