LONG-TERM EFFECTS OF PILOCARPINE IN RATS - STRUCTURAL DAMAGE OF THE BRAIN TRIGGERS KINDLING AND SPONTANEOUS RECURRENT SEIZURES
LONG-TERM EFFECTS OF PILOCARPINE IN RATS - STRUCTURAL DAMAGE OF THE BRAIN TRIGGERS KINDLING AND SPONTANEOUS RECURRENT SEIZURES
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DOI：
10.1111/j.1528-1157.1991.tb05533.x
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发表时间：
1991-11-01
期刊：
影响因子：
5.6
通讯作者：
TURSKI, L
中科院分区：
文献类型：
--
作者：
CAVALHEIRO, EA;LEITE, JP;TURSKI, L
人类大脑的结构性损伤（围产期损伤、脑外伤、头部损伤、脑血管和退行性疾病、颅内肿瘤、代谢性疾病、毒素、药物诱导的癫痫发作）可能导致幸存者慢性癫痫。流行病学分析表明，在大脑暴露于损伤和癫痫发作之间存在相当大的时间延迟。这种癫痫发作通常是部分性或混合性的，可能在任何年龄发生，并且难以治疗。在全身给予胆碱能药物匹鲁卡品引发持续惊厥引起脑结构损伤的大鼠中，自发性癫痫发作可能在平均潜伏期14-15天后发生。自发性复发性惊厥的平均频率在数月内保持不变。这些抽搐的演变过程中，通过几个电图和行为阶段类似点燃。啮齿类动物也可通过反复全身给予惊厥药或反复电刺激敏感脑区诱发点燃。这些观察结果表明，大脑的结构性损伤可能导致大鼠自发复发性惊厥（慢性癫痫），点燃可能参与这种情况的演变。这一发现表明，点燃机制的基础上的发展癫痫灶的结构性脑损伤。这些机制可能与人类某些形式的癫痫的病因有关。
Structural damage of the human brain (perinatal damage, cerebral trauma, head injury, cerebrovascular and degenerative diseases, intracranial tumor, metabolic diseases, toxins, drug-induced seizures) may lead to chronic epilepsy in survivors. Epidemiologic analyses show that a considerable time-delay occurs between the exposure of the brain to injury and the appearance of seizures. Such seizures are usually partial or mixed, may develop at any age, and are difficult to treat. In rats subjected to structural damage of the brain induced by sustained convulsions triggered by systemic administration of the cholinergic agent pilocarpine, spontaneous seizures may develop after a mean latency of 14-15 days. The mean frequency of spontaneous recurrent convulsions remains constant for several months. Evolution of these convulsions proceeds through several electrographic and behavioral stages resembling kindling. Kindling may be otherwise induced in rodents by repeated systemic administration of convulsants or by repeated electrical stimulation of sensitive brain regions. These observations demonstrate that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling may be involved in the evolution of such a condition. This finding suggests that kindling mechanisms underlie the development of epileptic foci from structural brain lesions. Such mechanisms may be involved in the etiology of some forms of epilepsy in humans.