School of Psychiatry and Clinical Neurosciences, University of Western Australia, Graylands Hospital, Mount Claremont, Perth, Australia.
J Clin Psychopharmacol. 2010 Feb;30(1):3-10. doi: 10.1097/JCP.0b013e3181c9bfe6.
Neuroleptic-induced catatonia (NIC), manifested in an extrapyramidal-catatonic syndrome, has been sporadically reported in the literature. Confusion surrounds its relationship to neuroleptic malignant syndrome (NMS) and extrapyramidal reactions to neuroleptics. This study examined (a) its clinical presentation and response to benzodiazepines, (b) the hypothesis that NIC and NMS are on the same spectrum with a continuum of symptom progression, and (c) its possible relationship to extrapyramidal reactions. Of 127 episodes of acute catatonia prospectively identified, 18 were diagnosed with NIC. All catatonia episodes received benzodiazepines. The NIC episodes were analyzed noting their clinical presentations, laboratory findings, and responses to treatments. Their responses to benzodiazepines were compared, with retrospective rating on a 7-point scale, to that for catatonia episodes associated with mania and schizophrenia. The progression of symptoms in each NIC episode was reviewed. The NIC episodes presented predominantly in the stuporous form associated with parkinsonism. Delirium, autonomic abnormality, and elevated serum creatine phosphokinase were all common. Neuroleptic malignant syndrome was diagnosed in 3 episodes (17%). The 3 catatonia groups did not differ significantly in their benzodiazepines responses: 78% (14/18) of NIC, 75% (12/16) of manic catatonia, and 67% (34/51) of schizophrenic catatonia episodes showed full responses. A spectrum of presentation across episodes was noted with simple NIC without delirium, autonomic disturbances, or fever at one end and NMS or malignant NIC at the other end. Symptoms in individual episodes showed a similar continuum progression. No extrapyramidal reactions immediately preceded the NIC episodes. Findings of this study support the hypothesis that NIC and NMS are disorders on the same spectrum and reveal no indication that extrapyramidal reactions progress to NIC.
神经阻滞剂所致紧张症（NIC）表现为锥体外系紧张症，在文献中偶有报道。目前对其与神经阻滞剂恶性综合征（NMS）和神经阻滞剂引起的锥体外系反应的关系仍存在争议。本研究旨在：（a）检查其临床表现和苯二氮䓬类药物的反应；（b）假设 NIC 和 NMS 是同一谱系的疾病，存在症状进展的连续谱；（c）研究其与锥体外系反应的可能关系。在前瞻性确定的 127 例急性紧张症发作中，有 18 例被诊断为 NIC。所有紧张症发作均接受苯二氮䓬类药物治疗。分析 NIC 发作的临床表现、实验室发现和治疗反应。采用 7 分制进行回顾性评分，比较其对苯二氮䓬类药物的反应与躁狂症和精神分裂症相关的紧张症发作的反应。回顾每个 NIC 发作的症状进展情况。NIC 发作主要表现为伴有帕金森病的昏迷形式。谵妄、自主神经异常和血清肌酸磷酸激酶升高均很常见。3 例（17%）被诊断为神经阻滞剂恶性综合征。3 组紧张症（NIC、躁狂症和精神分裂症）的苯二氮䓬类药物反应无显著差异：NIC 组 78%（14/18）、躁狂症组 75%（12/16）和精神分裂症组 67%（34/51）的患者反应完全。在各发作中注意到存在从单纯 NIC 到 NMS 或恶性 NIC 的表现谱，表现为单纯 NIC 时不伴有谵妄、自主神经紊乱或发热，而在 NMS 或恶性 NIC 时则存在这些症状。各发作中的症状表现出类似的连续谱进展。在 NIC 发作之前没有出现明显的锥体外系反应。本研究结果支持 NIC 和 NMS 是同一谱系疾病的假设，没有证据表明锥体外系反应进展为 NIC。
