Jobe Phillip C, Browning Ronald A
University of Illinois College of Medicine, Peoria, IL, USA.
Epilepsy Behav. 2005 Dec;7(4):602-19. doi: 10.1016/j.yebeh.2005.07.014. Epub 2005 Oct 5.
Contrary to existing evidence, convulsant liability of the antidepressants has been attributed to noradrenergic and serotonergic increments. This is a classic case of confusing treatment effects with the manifestations of illness. In fact, the remarkable anticonvulsant effectiveness of antidepressant-induced noradrenergic and serotonergic activation has been ignored. Some antidepressant drugs such as the specific serotonin reuptake inhibitor (SSRI) fluoxetine may be devoid of convulsant liability entirely, while having distinct anticonvulsant properties. Some authorities advance the notion that the seizure predisposition of patients with epilepsy increases risks for antidepressant-induced seizures. However, evidence does not support this contention. Instead, data increasingly support the concept that noradrenergic and serotonergic deficiencies contribute to seizure predisposition. Indeed, the antidepressants have the potential to overcome seizure predisposition in epilepsy. Whereas therapeutic doses of antidepressants elevate noradrenergic and serotonergic transmission, larger doses can activate other biological processes that may be convulsant.
与现有证据相反，抗抑郁药的惊厥易感性一直被归因于去甲肾上腺素能和5-羟色胺能的增加。这是一个将治疗效果与疾病表现相混淆的典型案例。事实上，抗抑郁药诱导的去甲肾上腺素能和5-羟色胺能激活所具有的显著抗惊厥效果一直被忽视。一些抗抑郁药物，如特异性5-羟色胺再摄取抑制剂（SSRI）氟西汀，可能完全没有惊厥易感性，同时却具有明显的抗惊厥特性。一些权威人士提出，癫痫患者的癫痫发作易感性会增加抗抑郁药诱发癫痫的风险。然而，证据并不支持这一观点。相反，越来越多的数据支持这样一种观点，即去甲肾上腺素能和5-羟色胺能缺乏会导致癫痫发作易感性。的确，抗抑郁药有潜力克服癫痫中的癫痫发作易感性。虽然治疗剂量的抗抑郁药会提高去甲肾上腺素能和5-羟色胺能传递，但更大剂量可能会激活其他可能导致惊厥的生物学过程。
