Abstract：
Serotonin (5-HT) syndrome (SS) consists of changes in mental status as well as autonomic and neuromuscular changes. Though not well understood, serotonergic pathways have been implicated in the mechanism of action of electroconvulsive therapy (ECT). Ketamine has been used as an induction agent in ECT and as therapy for treatment-resistant depression. Utilizing a case report and literature review, we explored the underlying serotonergic mechanisms of ECT and ketamine by which a syndrome of serotonin toxicity may be precipitated. We describe the case of a 72-year-old woman who developed recurrent SS on 2 occasions in similar circumstances involving the administration of ketamine for ECT. In our literature review, we found 5 cases in which SS was associated with ECT and 1 case linking ketamine to SS. There is emerging evidence that the mechanism of ECT involves 5-HT1A and 5-HT2A receptors, the same receptors that are involved in SS. ECT can transiently increase the permeability of the blood-brain barrier, leading to increased levels of antidepressants in the brain. ECT can, therefore, enhance 5-HT transmission and the likelihood of SS in the presence of serotonergic agents. The effect of ketamine on 5-HT transmission is mediated by the glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Ketamine increases α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid activity in the medial prefrontal cortex, which leads to downstream 5-HT release through glutamate. Through this mechanism, ketamine can increase 5-HT transmission, leading to SS. To our knowledge, this is the only case report of recurrent SS with concurrent use of ECT and ketamine. As ketamine is frequently used in ECT and many patients undergoing ECT are on serotonergic medications, it is important to recognize ketamine as a potential risk factor for SS. There is no evidence for added efficacy when combining ECT and ketamine. Thus, one should proceed with caution when combining these treatments. The burgeoning use of ketamine in ambulatory settings makes it necessary to elucidate the risks, which we discuss further. More research is needed into the mechanisms of ketamine and ECT, specifically how the combination of these treatments influence 5-HT levels.
摘要：
5-羟色胺（5-HT）综合征（SS）包括精神状态的变化以及自主神经和神经肌肉的变化。虽然不是很了解，血清素能途径与电惊厥治疗（ECT）的作用机制有关。氯胺酮已在ECT中用作诱导剂，并用作治疗难治性抑郁症的疗法。利用病例报告和文献综述，我们探讨了ECT和氯胺酮的潜在5-羟色胺能机制,由此可能导致5-羟色胺毒性综合征.我们描述了一名72岁女性的病例，该女性在类似情况下2次复发SS，涉及使用氯胺酮进行ECT。在我们的文献综述中，我们发现5例SS与ECT相关，1例氯胺酮与SS相关。有新的证据表明，ECT的机制涉及5-HT1A和5-HT2A受体，参与SS的相同受体。ECT可以短暂增加血脑屏障的通透性，导致大脑中抗抑郁药水平升高。ECT可以，因此,在5-羟色胺能药物的存在下，增强5-HT传递和SS的可能性。氯胺酮对5-HT传播的影响是由谷氨酸α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体介导的。氯胺酮增加内侧前额叶皮质中的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸活性，这导致下游5-HT通过谷氨酸释放。通过这种机制,氯胺酮可以增加5-HT的传播，导致SS。据我们所知,这是唯一一例复发性SS同时使用ECT和氯胺酮的病例报告.由于氯胺酮经常用于ECT，许多接受ECT的患者正在服用5-羟色胺能药物，重要的是认识到氯胺酮是SS的潜在危险因素。当结合ECT和氯胺酮时,没有增加功效的证据。因此，结合这些治疗方法时，应谨慎行事。氯胺酮在非卧床环境中的迅速使用使得有必要阐明风险，我们进一步讨论。需要对氯胺酮和ECT的机制进行更多的研究，特别是这些治疗的组合如何影响5-HT水平。
