抗精神病药致恶性综合征16例分析

目的：探讨抗精神病药物致恶性综合征（NMS）的临床特点与治疗。方法：回顾性分析16例因长期服用抗精神病药致NMS的临床资料。结果：发病后4d内确诊9例,全部存活,几乎无明显后遗症;发病4～7d确诊6例均存活;第8天后确诊1例,死亡。结论：长期服用抗精神病药易致NMS,以肌强直、发热、CK值增高为主要特征。其预后重点在早期诊断,早期治疗,尽可能避免或减少并发症的发生。     

恶性综合征10例临床分析

目的：分析恶性综合征的临床特点,以提高对本病的认识,减少误诊率。方法回顾性分析确诊的10例恶性综合征患者的临床资料,并复习相关文献。结果10例患者中,8例有抗精神病药物服用史,2例不规律服用美多芭,临床表现为发热、肌强直、肌酶增高、意识障碍及自主神经功能障碍,影像学等检查排除其他疾病,综合治疗有效。结论恶性综合征临床少见,多有抗精神病药物服药史,主要与药物影响脑内递质有关,临床表现及肌酶增高为主要的诊断依据,及时治疗大多预后良好。     

神经阻滞剂恶性综合征的早期诊断和救治

神经阻滞剂恶性综合征(NMS)是一组因临床用药或某些手术而诱发的临床症候群,以发热、肌强直、意识障碍及自主神经紊乱为主要表现,病情危重,若处理不当,病死率高。为提高对本病的认识和警觉性,本文将结合一例典型病例就其早期诊断和治疗进行分析讨论。1临床资料患者女,75岁,以“     

抗精神病药物所致恶性综合征10例临床分析

目的：探讨抗精神病药物所致恶性综合征（NMS）的临床表现及诊治方法。方法：对我院2007年1月至2012年3月收治的10例抗精神病药物所致NMS病例进行临床分析。结果：NMS发病前表现精神运动性兴奋7例（70%）,进食差9例（90%）;60%的患者发病于夏季;合并用药8例（80％）,且多合并高效价药物,其中4例为长效药物;发生于用药后1周内4例（40%）,1月内9例（90%）。临床表现意识障碍、肌强直、发热、心动过速、呼吸急促、血压不稳、多汗等。实验室检查表现白细胞增高、肌酸磷酸激酶升高等。经停用致病药物、提供支持和对症治疗、应用多巴胺受体激动剂、苯二氮类药物等治疗,均获痊愈。结论：恶性综合征是与抗精神病药物治疗有关的严重并发症,应及时发现,合理治疗。     

多次利培酮治疗致抗精神病药恶性综合征

1例31岁女性患者因精神分裂症给予利培酮1 mg,2次/d口服,1周后剂量增至2 mg,2次/d。此前患者曾3次间断应用利培酮治疗。本次治疗规律服药49 d,患者精神症状缓解。第50～52天未遵医嘱规律服药。第54天患者出现大汗淋漓,体温达38.5℃。第55天出现意识障碍、心动过速、双上肢肌强直、肌张力增高。心电图示窦性心动过速。实验室检查示:白细胞计数12.3×109/L,胆碱酯酶13 268 U/L,肌酸激酶1447 U/L,利培酮血液浓度70.5μg/L。诊断为抗精神病药恶性综合征(NMS)。立即停用利培酮,进行物理降温、补液、抗心律失常、抗感染、纠正酸碱平衡、护肝等治疗。6 d后患者体温恢复正常,NMS症状消失。换用奥氮平治疗后,未再出现类似症状。     

口服抗精神病药物引起神经阻滞剂恶性综合征1例

神经阻滞剂恶性综合征(neuroleptic malignant syndrome, NMS)又名抗精神病药物恶性综合征是一由抗精神病药物治疗时所产生的危及生命的严重并发症，主要临床表现为高热、意识障碍、肌强直和自主神经功能紊乱以及肌酸磷酸激酶(CPK)升高［１］。作者曾遇到1例，介绍如下。     

恶性症状群23例临床分析

对23例恶性症状群(NMS)进行回顾性研究，证明NMS均在抗精神病治疗过程中发生，为使用抗精神病（神经阻滞剂）所致，多药联用及长效针剂易促发。临床表现为高烧、大汗、震颤、肌强直或意识障碍。实验室检查及辅助检查一般无特殊发现，及时对症处理可降低NMS死亡率。     

氯丙嗪致恶性综合征2例

笔者在临床实践中，发现2例因服用氯丙嗪治疗精神分裂症致恶性综合征（简称NMS），介绍如下。例1，女，60岁。因精神分裂症服用氯丙嗪500mp／d已1年，1周来出现流诞、低热、肌肉强直、震间等植物神经症状及锥体外系症状，入院前Zh开始高热伴意识不清，肌肉强直更明显。查体：T39．7C，P134次／min，R28次／min，BP18／llkPa，神志不清，气促，唇做错，双瞳孔等圆等大，对光反射灵敏，颈强直，四肢肌张力明显增强，伴震颤，巴氏征（－）。拟诊：恶性综合征，即停用抗精神病药，给氧，保持水电解质平衡，物理降温，预防感染等治疗，体温…     

皮质基底节综合征2例临床分析及文献复习

目的皮质基底节综合征(CBS)是一种缓慢进展的神经退行性疾病,临床上以锥体外系症状如肌强直、肌张力障碍、震颤和皮质功能障碍如失用、异己肢现象、皮质感觉缺失、肌阵挛、失语为特征。此病较少见,不易被神经内科医生所认识。现将我院收治的2例进行报道,探讨皮质基底节变性综合征的临床表现、神经心理学、影像学和病理特征。方法对2例临床诊断为CBS患者的资料进行回顾分析,并进行文献检索以总结提高临床医师对该疾病的识别及诊治。结果 2例患者均为男性,右利手,起病隐匿,均有肢体不对称性肌张力增高、肢体失用、记忆力和视空间损害。病例1合并有进行性少词性失语,病例2伴有意向性震颤。神心理量表提示2例患者均有视空间和记忆力下降。头颅磁共振均有明显的不对称性脑皮质萎缩,以额、顶、枕叶显著。2例患者脑脊液总tau蛋白增高,β-淀粉样蛋白42降低,符合阿尔茨海默病病理改变。结论不对称性肌张力增高、肢体失用以及视空间障碍是CBS较为常见的临床表现,详细的神经心理学量表、影像学及脑脊液病理检测可提高疾病的诊断以及指导治疗。     

抗精神病药物致恶性综合征22例临床分析

目的 总结抗精神病药物致恶性综合征(恶性综合征)的临床特点.方法 采用Levenson的恶性综合征诊断标准,对22例患者的临床特点进行回顾性分析.结果 22例患者中,以使用高效价抗精神病药物较多(90.91%),临床表现以发热、肌张力增高、意识障碍、血清肌酸磷酸激酶升高以及植物神经功能紊乱等较明显,及时停药、对症处理可降低死亡率.结论 早期发现恶性综合征并及时处理.可收到较好治疗效果.     

Neuroleptic rechallenge after neuroleptic malignant syndrome: case report and literature review

Neuroleptic malignant syndrome (NMS) is associated with essentially all of the currently available antipsychotic agents. The signs and symptoms associated with the syndrome are hyperpyrexia, defined by body temperature greater than 38 degrees C; extreme muscle rigidity, with or without elevated creatine phosphokinase or hyperreflexia; and other symptoms such as altered level of consciousness and/or autonomic dysfunction as manifested by labile blood pressure, tachycardia, tachypnea, urinary or fecal incontinence, pallor, or diaphoresis. This potentially fatal syndrome complicates the treatment of patients with recurrent psychotic symptoms because of the possibility for recurrence of the NMS. A case of recurrent NMS is presented in which the patient was rechallenged with an antipsychotic agent. In addition, 41 reported cases of antipsychotic rechallenge after NMS are reviewed. The results of the review suggest that neuroleptic rechallenge following NMS is associated with an acceptable risk of recurrence in most patients. However, close monitoring for NMS and careful selection of patients for antipsychotic rechallenge is mandatory. A minimal time period of five days before rechallenge may also reduce the risk of recurrent NMS. Recurrence was not associated with patient age or gender, nor the antipsychotic agent used.     

Neuroleptic malignant syndrome: a review of the literature

The neuroleptic malignant syndrome (NMS) involves fever, extrapyramidal rigidity, and disturbances of autonomic function and consciousness. It occurs more often with high potency and depot forms, frequently 3 to 9 days after initiation and sometimes years later, and is not related to dose or previous exposure. About 40% of cases had evidence of an affective disorder. NMS apparently results from deficient compensatory mechanisms following blockade of dopaminergic regulation of muscle tone and autonomic function. Possible indicators of vulnerability and various treatments are discussed. Neuroleptic challenge resulted in recurrence of symptoms in about one third of cases. Symptoms sometimes subsided despite continued treatment. Early diagnosis and effective treatment have reduced the risk of such challenge.     

High serum creatinine kinase level: possible risk factor for neuroleptic malignant syndrome

High creatinine kinase (CK) levels and leukocytosis are known to be associated with neuroleptic malignant syndrome (NMS). The authors sought to determine if their presence during non-NMS psychotic episodes is predictive of the later development of NMS. Sixteen psychotic inpatients who met the criteria for NMS were included. For statistical comparison, two control groups were formed by matching each study patient with two non-NMS patients for age, gender, ethnicity, and year and ward of hospitalization (n = 32). The maximal individual serum levels of CK, lactate dehydrogenase (LDH), serum glutamic oxaloacetic transaminase (SGOT), and white blood cell count (WBC) during all non-NMS psychotic episodes (Brief Psychiatric Rating Scale 40) were averaged. To normalize the distribution, the individual averages were transformed to natural logarithms (Ln). Mean Ln (average [CK]) in the patients with NMS was found to be 6.46 +/- 0.91 IU/L, and in the non-NMS patients, 5.24 +/- 0.90 IU/L (actual serum CK levels, 911 +/- 747 IU/L and 343 +/- 620 IU/L, respectively). This difference was statistically significant (F [2,15] = 10.5, p < 0.0001). In addition, CK levels above the upper limit of normal were noted in 76% of psychotic episodes in the patients with NMS and in only 30% of psychotic episodes in the non-NMS patients (p < 0.0001). There was no significant difference between the NMS and non-NMS groups in Ln(LDH), Ln(SGOT), or Ln(WBC) (F [2,15] = 1.4, 2.1, and 0.9, respectively). The authors concluded that high serum CK level during non-NMS psychotic episodes seems to be a risk factor for future NMS. Therefore, CK measurement may be justified on admission of acutely psychotic patients who have other risk factors and a history of psychosis-associated CKemia.     

Zotepine-induced catatonia as a precursor in the progression to neuroleptic malignant syndrome

A 39-year-old man with schizophrenia developed severe catatonia, hyperthermia, muscle rigidity, tachycardia, leukocytosis, and elevated muscle enzyme levels while receiving zotepine therapy. Neuroleptic malignant syndrome (NMS) was diagnosed. After withdrawal of zotepine therapy, transfer to a neurologic intensive care unit, provision of supportive care, and administration of adjunctive bromocriptine therapy, the patient's fever and catatonia subsided. Biochemical irregularities spontaneously returned to normal with no complications. Antipsychotic therapy was restarted with risperidone 12 days after the patient's NMS resolved. After more than 1 year of follow-up, he experienced no adverse events. A recent decrease in mortality from NMS is related to increased awareness of this disorder, but not to treatment with specific agents. Clinicians need to recognize NMS early; although rare, it is a potentially fatal complication of antipsychotic treatment.     

抗精神病药物致恶性综合征3例诊治体会

目的为了解抗精神病药物致恶性综合征临床表现的特点.方法对3例恶性综合征临床资料进行分析.结果恶性综合征的临床表现以肌强直、发热、意识障碍及植物神经功能紊乱等为主.结论恶性综合征可由高效价抗精神病药物,多种药物联合使用或新型抗精神病药物等引起.可能与患者抗精神病药物慢代谢型有关、超慢代谢型及不代谢型有关.     

Olanzapine induced neuroleptic malignant syndrome

An 18 year old male diagnosed as a case of bipolar affective disorder (BPAD), developed neuroleptic malignant syndrome (NMS) following treatment with olanzapine (20 mg per day), an atypical antipsychotic drug. NMS is usually seen with typical antipsychotic drugs. The patient was diagnosed as a case of NMS, offending agent was immediately withdrawn and prompt treatment with bromocriptine and levodopa produced a good recovery. The various features of the case are discussed in view of the potential mortality of the syndrome.KEY WORDS: Bipolar affective disorder, Neuroleptic malignant syndrome, olanzapine     

外源补充辅酶Q10治疗他汀相关性肌损害的回顾性病例研究

目的探究外源补充辅酶Q10对他汀相关性肌损害的影响。方法将某院近3年发生他汀相关性肌损害且符合入、排标准的患者44例分为2组,每组22例。常规治疗组(常规组):患者发生他汀相关性肌损害时,停用或减量应用他汀类药物,未给予其他特殊处置,仅根据病情适当给予补液、碱化尿液和利尿治疗;辅酶Q10治疗组(辅酶Q10组):其他处置与常规组相同,但出现他汀相关性肌损害后加用辅酶Q10片10 mg,3次/d治疗。比较两组患者治疗5~7 d后肌酶较峰值时的回落情况、急性肾损伤发生比例以及肌酶从峰值回落至正常水平的时间。结果辅酶Q10组CK、CK-MB、LDH、cTn的回落幅度略大于常规组,但两组比较差异无统计学意义(P>0.05);辅酶Q10组Myo回落幅度显著大于常规组,差异有统计学意义(P<0.05)。在CK峰值时和干预5~7 d后,两组急性肾损伤发生率比较,差异均无统计学意义(P>0.05)。辅酶Q10组患者CK从峰值回落至正常范围的时间明显短于常规组,差异有统计学意义(P<0.05)。结论辅酶Q10不能明显降低CK、CK-MB、LDH的水平,但能明显降低Myo的水平,并缩短患者CK恢复时间。     

Neuroleptic malignant syndrome due to three atypical antipsychotics in a child

Neuroleptic Malignant Syndrome (NMS) is a rare, potentially fatal and idiosyncratic drug reaction. It is characterized by a sudden loss of body temperature control, renal and respiratory failure, muscle rigidity, loss of consciousness and impairment of autonomic nervous system. Although NMS was previously associated with the use of classical high-potency neuroleptics, cases have started to emerge with atypical neuroleptics. This article discusses the first case of NMS in a child, induced by the use of risperidone, olanzapine and quetiapine.