Department of Psychiatry & Human Behavior, University of Mississippi Medical Center, Jackson, MS 39216, USA.
J ECT. 2010 Dec;26(4):253-8. doi: 10.1097/YCT.0b013e3181fbf96d.
Catatonia has been rediscovered over the last 2 decades as a unique syndrome that consists of specific motor signs with a characteristic and uniform response to benzodiazepines and electroconvulsive therapy. Further inquiry into its developmental, environmental, psychological, and biological underpinnings is warranted. In this review, medical catatonia models of motor circuitry dysfunction, abnormal neurotransmitters, epilepsy, genetic risk factors, endocrine dysfunction, and immune abnormalities are discussed. Developmental, environmental, and psychological risk factors for catatonia are currently unknown. The following hypotheses need to be tested: neuroleptic malignant syndrome is a drug-induced form of malignant catatonia; Prader-Willi syndrome is a clinical GABAergic genetic-endocrine model of catatonia; Kleine-Levin syndrome represents a periodic form of adolescent catatonia; and anti-N-methyl-d-aspartate receptor encephalitis is an autoimmune type of catatonia.
过去 20 年来，人们重新发现了紧张症，它是一种独特的综合征，由特定的运动体征组成，对苯二氮䓬类药物和电惊厥疗法有特征性和一致的反应。进一步探究其发展、环境、心理和生物学基础是有必要的。在这篇综述中，讨论了运动回路功能障碍、神经递质异常、癫痫、遗传风险因素、内分泌功能障碍和免疫异常等医学紧张症模型。目前尚不清楚紧张症的发展、环境和心理风险因素。以下假设需要进行测试：神经阻滞剂恶性综合征是一种药物引起的恶性紧张症；普拉德-威利综合征是紧张症的一种临床 GABA 能遗传-内分泌模型；克莱因-莱文综合征代表青少年紧张症的周期性形式；抗 N-甲基-D-天冬氨酸受体脑炎是一种自身免疫性紧张症。
