Specificity of seizure genesis during electroconvulsive therapy and modified pentylenetetrazole kindling

V. L. Kozlovskii, D. N. Kosterin, O. V. Lepik, M. Yu. Popov
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Abstract

Comparison of the development of chemically induced seizures in the experiment with the change in convulsive thresholds during electroconvulsive therapy (ECT) has demonstrated that repeated ‘chemical’ seizures can initiate the development of the kindling phenomenon, but regular ECT from the first to the 14th session most likely cause an increase in convulsive thresholds. However, the repeated ECT over 15 sessions is associated with a rapid decrease in the threshold current dose and probable dysregulation of endogenous anticonvulsant mechanisms, with the risk of the development of uncontrolled paroxysmal conditions and the risk of organic CNS lesions. The mechanisms of the convulsive action of ECT and pentylenetetrazolinduced kindling are fundamentally different. Differences in the pathogenesis of systemic convulsive reactions determine the divergent change in seizure thresholds during ECT and pentylenetetrazol stimulations.
电惊厥治疗和改良戊四唑点燃期间癫痫发生的特异性
实验中化学诱发癫痫发作的发展与电惊厥治疗(ECT)期间惊厥阈值的变化的比较表明,重复的“化学”癫痫发作可以启动引燃现象的发展,但从第一次到第14次的常规ECT最有可能导致惊厥阈值的增加。然而,超过15次的重复ECT与阈值电流剂量的快速下降和内源性抗惊厥机制的可能失调有关,具有发展为不受控制的发作性疾病的风险和有机中枢神经系统病变的风险。电痉挛作用的机制和戊四唑诱发的引燃是根本不同的。全身惊厥反应发病机制的差异决定了ECT和戊四唑刺激时癫痫发作阈值的不同变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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