Rivera V M, Patten B M
J Clin Psychiatry. 1978 Jan;39(1):67-71.
A 31-year old male developed malignant hyperthermia (MH) during the initial minutes of Halothane induction. CPK rose to 6120 U/ml and decreased to normal levels as the patient became afebrile over a 10 day period of cooling measures and metabolic management. Muscle weakness, predominantly proximal and depressed deep tendon reflexes were found upon examination during convalescence. Muscle biopsy showed neurogenic changes characterized by fiber type grouping and targetoid fibers. CPK was elevated in one of the patient's children. This case supports the view of underlying hereditary neuromyopathy in MH.
一名31岁男性在氟烷诱导的最初几分钟内发生恶性高热（MH）。肌酸磷酸激酶（CPK）升至6120 U/ml，在采取10天的降温措施和代谢管理后，随着患者体温恢复正常，CPK降至正常水平。康复期检查发现肌肉无力，主要为近端肌肉无力，且深部腱反射减弱。肌肉活检显示神经源性改变，其特征为纤维类型分组和靶样纤维。该患者的一个孩子CPK升高。此病例支持恶性高热存在潜在遗传性神经肌肉病的观点。
