Kawajiri Masakazu, Ohyagi Yasumasa, Furuya Hirokazu, Araki Takehisa, Inoue Naohide, Esaki Shigemitsu, Yamada Takeshi, Kira Junichi
Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University.
Rinsho Shinkeigaku. 2002 Feb;42(2):136-9.
A 59-year-old man, who was diagnosed as having Parkinson's disease and depression seven years ago and was on oral antiparkinsonian agents, antianxiety agents, and antidepressants, developed a high fever, disturbed consciousness, and marked muscle rigidity after discontinuation of etizolam and amitriptyline. He was admitted to a nearby hospital. Hypothyroidism had been noted two months before admission. Marked muscle rigidity and increased serum CK were observed. Since discontinuation of benzodiazepine has been known to rarely trigger a neuroleptic malignant syndrome (NMS), he was diagnosed as having NMS. After receiving dantrolene and bromocriptine, these symptoms temporarily improved but he again developed consciousness disturbance, and convulsive seizures associated with an elevated serum CK. He was transferred to our hospital. On admission, the CK level was normal at 168 IU/l, while free T4 was 0.6 ng/dl (normal range, 0.9-2.3) and TSH was 108.7 mU/ml (normal range, 0.2-4.2) in serum, indicating the presence of primary hypothyroidism. As an increase in thyroid hormone dosage improved the thyroid function to normal level, his disturbed consciousness and muscle rigidity gradually improved. Convulsive seizure and recurrence of NMS in a short interval are unusual in neuroleptic malignant syndrome. In this patient, hypothyroidism may have contributed to the development of malignant syndrome through metabolic changes of the central dopaminergic system, and discontinuation of etizolam, a kind of benzodiazepine, may have triggered NMS, since there has not been reported that discontinuation of antidepressants including amitriptyline triggers NMS.
一名59岁男性，7年前被诊断为帕金森病和抑郁症，一直在服用口服抗帕金森病药物、抗焦虑药物和抗抑郁药物。在停用依替唑仑和阿米替林后，他出现了高热、意识障碍和明显的肌肉僵硬。他被送往附近医院。入院前两个月发现甲状腺功能减退。观察到明显的肌肉僵硬和血清肌酸激酶（CK）升高。由于已知停用苯二氮䓬类药物很少引发神经阻滞剂恶性综合征（NMS），他被诊断为患有NMS。在接受丹曲林和溴隐亭治疗后，这些症状暂时有所改善，但他再次出现意识障碍以及与血清CK升高相关的惊厥发作。他被转至我院。入院时，CK水平正常，为168 IU/l，而血清游离甲状腺素（T4）为0.6 ng/dl（正常范围0.9 - 2.3），促甲状腺激素（TSH）为108.7 mU/ml（正常范围0.2 - 4.2），表明存在原发性甲状腺功能减退。随着甲状腺激素剂量增加使甲状腺功能恢复至正常水平，他的意识障碍和肌肉僵硬逐渐改善。在神经阻滞剂恶性综合征中，短时间内惊厥发作和NMS复发并不常见。在该患者中，甲状腺功能减退可能通过中枢多巴胺能系统的代谢变化促成了恶性综合征的发生，而停用一种苯二氮䓬类药物依替唑仑可能引发了NMS，因为尚未有报道称停用包括阿米替林在内的抗抑郁药物会引发NMS。
