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目的建立外伤性癫痫模型,观察症状、脑电图(EEG)和病理改变,探讨病理及致痫机制。方法立体定向注射不同剂量氯化亚铁(FeCl2)于大鼠右侧运动皮层或杏仁体致痫,设立正常对照组、生理盐水对照组。连续30 d行为学评分、EEG记录,HE染色、普鲁士蓝和腾氏蓝反应及Nissl染色行病理学观察。结果 1 000 nmol氯化亚铁皮层注射后平均经过(60±18)s的潜伏期,大鼠EEG表现出多种形式的癫痫样放电波形,大鼠症状及EEG呈典型癫痫变化,该组模型成功率87．5％,其行为学评分与对照组及其他各组之间比较有显著性差异(P<0．01)。氯化亚铁皮层注射组大体外观见右额叶萎缩,明显棕黄色,为含铁血黄素沉着。氯化亚铁右杏仁体注射组亦可见边缘系统含铁血黄素沉着。普鲁士蓝和腾氏蓝反应证实含铁化合物的沉积。皮层及杏仁体氯化亚铁注射部位、实验侧海马CA3区神经元减少,核固缩,胶质增生明显。结论含铁化合物在大鼠的皮层和边缘结构的沉积可以导致慢性的、自发性发作的癫痫灶形成。皮层注射1 000 nmol氯化亚铁建立的外伤性癫痫动物模型比杏仁体注射铁离子建立的模型更接近人类的外伤性癫痫临床与病理改变。
Objective To establish a traumatic epilepsy model and observe the symptoms, electroencephalogram (EEG) and pathological changes to explore the pathology and mechanism of epilepsy. Methods Stereotaxic injection of different doses of ferrous chloride (FeCl2) induced epilepsy in the right motor cortex or amygdala in rats, and normal control group and normal saline control group were established. Behavioral scores of 30 consecutive days, EEG recording, HE staining, Prussian blue and Teng blue reaction and Nissl staining were observed. Results After a mean incubation period of (60 ± 18) s, the EEG of 1 000 nmol cortical chloride injection showed various forms of epileptiform discharge waveform. The symptoms of rats and the typical epilepsy of EEG were successful. The model was successful The rate of 87.5%, the behavioral score and the control group and other groups were significantly different (P <0.01). Ferrous chloride cortical injection group generally see the right frontal lobe atrophy, obviously brown yellow, hemosiderin. Ferrous chloride right amygdaloid injection group also showed the limbic hemosiderin. Prussian blue and Teng blue reaction confirmed the deposition of iron compounds. Cortical and amygdala ferrous chloride injection site, experimental side of the hippocampal CA3 area neurons decreased, nuclear pyknosis, glial proliferation significantly. Conclusion The deposition of iron-containing compounds in rat cortical and limbic structures can lead to the development of a chronic, spontaneous seizure of epileptic foci. Traumatic epilepsy animal model established by cortical injection of 1 000 nmol ferrous chloride was more close to the clinical and pathological changes of human traumatic epilepsy than the model of amygdala injection of iron ions.