Revuelta E, Bordet R, Piquet T, Ghawche F, Destee A, Goudemand M
Service de Psychiatrie Adulte, CHRU Unités de Soins Normalisées, Lille.
Encephale. 1994 May-Jun;20(3):351-4.
Similar clinical and biological features in lethal catatonia (LC) and neuroleptic malignant syndrome (NMS) suggest a relationship between both affections and common physiopathologic mechanisms. Pharmacological effects of several drugs--dopaminergic agonists, benzodiazepines, carbamazepine--suggest an impairment of several systems of neurotransmitters. We report the case of a young woman with infantile psychosis who developed catatonic syndrome worsened by neuroleptic treatment, arising the problem of the chronology of both affections. The evolution with treatment may partially explain the physiopathology. A 18-year old woman with an history of infantile psychosis, experienced insomnia, anorexia, paradoxical agitation developed after affective traumatism (mother's hospitalization). Chlorazepate (150 mg) remained inefficient and hospitalization was necessary. The patient was dumb, prostate in bed. She presented negativism, rigidity of the four limbs, catalepsia and hyperpyrexia (38.5 degrees C). Hepatic transaminases were increased (SGOT: 71 UI/l; N < 30). After cumulated dose of levomepromazine (100 mg) profuse sudation, thermic and cardiovascular instability, alteration of consciousness, major rigidity of limbs appeared. (Blood) hepatic transaminases and muscular enzymes increased. Bacteriological samples, cerebrospinal fluid analysis, CT-scan and EEG were normal. Within 48 hours after rehydratation and bromocriptine (30 mg per day) alteration of consciousness and autonomic disorders decreased but hyperpyrexia (38 degrees C) persisted. Biological parameters were normalized 10 days later. Negativism and psychomotor inertia remained. Lorazepam (3 mg per day) failed to be clinically beneficial. On carbamazepine (600 mg per day) she started speaking and moving spontaneously. Catalepsia disappeared but rigidity and anorexia persisted. Electroconvulsivotherapy (ECT) was necessary. After 2 shocks she started standing up, walking, taking food and speaking fluently.(ABSTRACT TRUNCATED AT 250 WORDS)
致死性紧张症（LC）和抗精神病药物恶性综合征（NMS）相似的临床及生物学特征提示这两种病症之间存在关联以及共同的生理病理机制。几种药物——多巴胺能激动剂、苯二氮䓬类药物、卡马西平——的药理作用提示多个神经递质系统受损。我们报告了一例患有婴儿期精神病的年轻女性病例，其在接受抗精神病药物治疗后出现紧张症综合征且病情加重，引发了两种病症时间顺序的问题。治疗过程中的病情演变可能部分解释其生理病理机制。一名有婴儿期精神病病史的18岁女性，在情感创伤（母亲住院）后出现失眠、厌食、矛盾性激越。氯氮䓬（150毫克）治疗无效，需要住院治疗。患者沉默不语，卧床不起。她表现出违拗症、四肢僵硬、蜡样屈曲和高热（38.5摄氏度）。肝转氨酶升高（谷草转氨酶：71国际单位/升；正常范围<30）。在累积服用左美丙嗪（100毫克）后，出现大量出汗、体温和心血管不稳定、意识改变、四肢严重僵硬。（血液）肝转氨酶和肌肉酶升高。细菌学样本、脑脊液分析、CT扫描和脑电图均正常。补液和服用溴隐亭（每天30毫克）48小时内，意识改变和自主神经功能障碍减轻，但高热（38摄氏度）持续。10天后生物学参数恢复正常。违拗症和精神运动迟缓仍存在。劳拉西泮（每天3毫克）临床治疗无效。服用卡马西平（每天600毫克）后，她开始自发说话和活动。蜡样屈曲消失，但僵硬和厌食仍存在。需要进行电休克治疗（ECT）。经过2次电击后，她开始站起来、行走、进食并流利地说话。（摘要截断于250字）
