Koch Alexander, Reich Karin, Wielopolski Jan, Clepce Marion, Fischer Marie, Kornhuber Johannes, Thuerauf Norbert
Department of Psychiatry and Psychotherapy, Friedrich-Alexander-University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
Case Rep Psychiatry. 2013;2013:542303. doi: 10.1155/2013/542303. Epub 2013 Dec 12.
Case. We report a case of catatonia with elevated CK, elevated temperature, and hypoferritinemia after abrupt discontinuation of clozapine in a patient with known proneness to catatonic symptoms. Reinstatement of clozapine therapy was contraindicated due to leukopenia. Neuroleptic malign syndrome could not be ruled out by the administration of quetiapine; this prevented the quick use of other potent D2 antagonists. Some improvement was achieved through supportive therapy, high dose of lorazepam, and a series of 10 ECT sessions. Returning to baseline condition was achieved by a very careful increase of olanzapine. Discussion. Catatonic symptoms in schizophrenia as well as in NMS might be caused by a lack of striatal dopamine (CS) or dopamine D2 antagonism (NMS). CS might be a "special" kind of schizophrenia featuring both hypo- and hyperactivity of dopaminergic transmission. ECT has been described as a "psychic rectifier" or a "reset for the system." The desirable effect of ECT in cases of CS might be dopaminergic stimulation in the striatum and decrease of both the dopaminergic activity in the limbic system and the serotonergic activity on 5-HT2 receptors. The desirable effect of ECT in NMS would be explained by activation of dopaminergic transmission and/or liberation of dopaminergic receptors from the causative neuroleptics.
病例。我们报告了一例已知有发生紧张症倾向的患者在突然停用氯氮平后出现紧张症、肌酸激酶升高、体温升高和低铁蛋白血症的病例。由于白细胞减少,恢复氯氮平治疗是禁忌的。使用喹硫平不能排除神经阻滞剂恶性综合征;这妨碍了迅速使用其他强效D2拮抗剂。通过支持性治疗、高剂量劳拉西泮和一系列10次电休克治疗取得了一些改善。通过非常谨慎地增加奥氮平使患者恢复到基线状态。讨论。精神分裂症以及神经阻滞剂恶性综合征中的紧张症症状可能是由于纹状体多巴胺缺乏(紧张症)或多巴胺D2拮抗作用(神经阻滞剂恶性综合征)所致。紧张症可能是一种“特殊”类型的精神分裂症,其特征是多巴胺能传递既有功能减退又有功能亢进。电休克治疗被描述为一种“精神矫正器”或“系统重置”。电休克治疗在紧张症病例中的理想效果可能是纹状体中的多巴胺能刺激以及边缘系统中多巴胺能活性和5 - HT2受体上5 - 羟色胺能活性的降低。电休克治疗在神经阻滞剂恶性综合征中的理想效果可以通过多巴胺能传递的激活和/或致病神经阻滞剂使多巴胺能受体释放来解释。