非经典抗精神病药与恶性综合征

恶性综合征(Neuroleptie malignant syndrome,NMS)是一种罕见的、可致命的由抗精神病药物所致的严重的药物不良反应.NMS是1960年由法国学者Delay描述的,1968年命名,并在20世纪80年代后受到广泛重视.以往人们普遍认为高效价的经典抗精神病药物(如氟哌啶醇等)较易引起NMS的发生,但随着与非经典抗精神病药相关的NMS病例的不断报道,大家逐步认同所有抗精神病药物都能引起NMS[1].我们在本文中试图对于非经典与经典抗精神病药所致NMS的表现是否具有差异性进行探讨.     

精神药物致恶性综合征32例临床分析

目的:了解精神药物所致恶性综合征(NMS)的临床特征,并探讨NMS发生的影响因素. 方法:对32例精神药物所致NMS患者进行临床分析. 结果:精神药物致NMS男性多见于女性,青壮年居多,传统抗精神病药、多种抗精神病药联用、增加剂量过快是产生NMS危险因素. 结论:临床应尽量减少合并用药、加量过速,以免导致NMS.     

精神药物致恶性综合征32例I临床分析

目的：了解精神药物所致恶性综合征（NMS）的临床特征，并探讨NMS发生的影响因素。方法：对32例精神药物所致NMS患者进行临床分析。结果：精神药物致NMS男性多见于女性，青壮年居多，传统抗精神病药、多种抗精神病药联用、增加剂量过快是产生NMS危险因素。结论：临床应尽量减少合并用药、加量过速，以免导致NMS。     

氯氮平所致神经阻滞剂恶性综合征

氯氮平属二苯氧氮平类药物,是一种有相当疗效抗精神病药物,尤其是对其它抗精神病药物疗效不理想的某些精神分裂症患者,甚至会出现戏剧性效果。它具有较强的镇静作用,但几乎没有锥体外系副反应。一般认为它不会引起神经阻滞剂恶性综合症(NMS),因而对于既往有过NMS史的患者成为可选药物之一。然而近几年来,国内外有关氯氮平所致NMS已有多     

静脉滴注氯丙咪嗪致恶性症候群5例[日]

恶性症候群(NMS)是抗精神病药物所致的严重副作用，早已被人们现熟知与阻断DA受体有关，用DA受体激动剂治疗有效。但最近报导认为不但是DA受体阻断强的抗精神病药物即使对DA受体阻断弱的或几乎没有阻断DA受体作用的抗抑郁药也能发生NMS，     

抗精神病药物所致恶性症状群12例的临床资料分析

我们将抗精神病药物所致恶性症状群(NMS)12例的临床资料报道于后。     

恶性综合征继发横纹肌溶解1例报道

正恶性综合征(neuroleptic malignant syndrome,NMS)是抗精神病药物所致的严重不良反应,主要表现为高热、肌强直、意识障碍及肌酶升高,好发于突然停用或更换抗精神病药物时[1-3]。我科2018年5月收治1例继发横纹肌溶解的NMS患者,本文分析其临床资料并进行文献复习,探讨NMS严重并发症的处理方法,以提高对该病的认识。     

氯氮平引起恶性症状群

恶性症状群(NMS)一般由经典的抗精神病药物引起。氯氮平属非经典的抗精神病药物,也会引起NMS。本文报道一例因氯氮平引起的NMS。病人为30岁,因重性精神病用氯氮平治疗。在氯氮平治疗前一个月,已停用除氯羟安定以外的所有抗精神病药物,氯氮平从每天25mg,每日三次的剂量开始,第三次服药后3小时,病人出现了典型的NMS,突然高烧,多汗、严重的上肢齿轮样     

有NMS病史者再入院时如何治疗

近年来,临床医生面临着一个重要问题: 一个曾有恶性综合症(NMS)病史的病人,当其精神病复发时,怎样去治疗呢?有一系列证据表明:使用低效价的抗精神病药物可以减少 NMS 复发的危险。Shalev 和 Munitz(1986)报道:再次使用同剂量、同效价的药物治疗,6例病人中有5例又出现 NMS,其中2例生命垂危。而与其相对照,使用低效价抗精神病药物治疗,特别是甲硫达嗪,10例中有9例是安全的。同样,Carrof 和 Ma-nn(1988)发现使用高效价抗精神病药物48%(10/21)患者第二次发生 NMS,而用低效价者仅15%(4/26)再次出现 NMS。     

维思通导致恶性综合征1例

维思通(又名利培酮Resperidone)是一种新型抗精神病药物。具有低锥体外系反应,无抗胆碱能作用,不影响心血管系统,不损伤认知功能等特点。目前世界范围的使用已超过1200万人/月,有效性和安全性已得到验证。但国外有文献报导其能引起恶性综合征(NMS)。由于维思通在国内的应用尚未普及,目前未见有导致NMS的病例报告。现将我们发现的1例维思通所致NMS报告如下:     

The use of atypical antipsychotics in the treatment of catatonia.

PURPOSE: Evidence indicates that classical antipsychotics may aggravate non-malignant and malignant catatonia (MC). Atypical antipsychotics are less likely to cause movement disorders than classical antipsychotics and they are being frequently prescribed in disorders that can be associated with catatonia. Therefore, the important question that arises is whether atypical antipsychotics have a role to play in the treatment of catatonia. MATERIALS AND METHODS: A Medline search was performed to locate papers on the use of atypical antipsychotics in catatonia published between 1970 and 31st December 2004. RESULTS: The literature on the use of atypical antipsychotics in catatonia consists of case reports and retrospective studies. In most cases of non-MC a reduction of the catatonic symptoms is reported upon treatment with atypical antipsychotics. Cases of MC relate mainly to the neuroleptic malignant syndrome (NMS), which is considered as an iatrogenic stuporous variant of MC caused by antipsychotics. CONCLUSION: There are indications that atypical antipsychotics may be useful in non-MC. As a consequence, one should not only focus on the possible extrapyramidal and autonomic side effects of these drugs, but also on the possible beneficial effects on certain brain functions and on the catatonic symptomatology. However, randomized controlled trials are needed to evaluate the effect of these drugs, and caution is advisable, since cases of NMS have been linked to treatment with atypical antipsychotics. There is no evidence to prescribe atypical antipsychotics in MC.     

Clinical Management of Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome (NMS) continues to be an unpredictable and rare, but potentially fatal complication of antipsychotic medications. Presumptively linked to dopamine blockade, it nonetheless occurs in patients receiving newer atypical antipsychotics. The features of NMS, its pathophysiology, differential diagnosis, clinical course, risk factors, and morbidity and motality are reviewed. Nonpharmacologic management centers on aggressive supportive care including vigilant nursing, physical therapy, cooling, rehydration, anticoagulation. Pharmacologic interventions include immediate discontinuation of antipsychotics, judicious use of anticholinergics, and adjunctive benzodiazepines. The utility of specific agents in actively treating NMS is reviewed. Bromocriptine and other dopaminergic drugs and dantrolene sodium have alternatively been considered without merit or efficacious. Guidelines for using these agents are presented. Electroconvulsive therapy, also somewhat controversial, is identified as a second line of treatment. Finally, management of the post-NMS patient is also reviewed.     

Two cases of neuroleptic malignant syndrome in elderly patients taking atypical antipsychotics

Summary： Neuroleptic malignant syndrome （NMS） is a rare, life-threatening adverse reaction to antipsychotic medication that typically includes high-fever, extra pyramidal symptoms, autonomic nervous system dysfunction and disturbances in consciousness. Though reported to be more common following use of the older, first generation antipsychotic medications, it can also occur in patients taking the newer, second generation antipsychotic medications. This report discusses the clinical presentation, possible etiology, pathogenesis and treatment of two cases of NMS that occurred in elderly patients after taking atypical antipsychotics. With the increasing use of atypical antipsychotic medication in elderly patients - who may be more susceptible to this adverse reaction - there is a need to increase clinical vigilance about this condition, particularly among internists and gerontologists who maybe unfamiliar with this rare complication to antipsychotic medication.     

A case of clozapine-induced neuroleptic malignant syndrome.

The treatment of psychotic symptoms in patients with a previous history of neuroleptic malignant syndrome (NMS) remains a dilemma. The authors describe a case in which clozapine caused NMS in a schizophrenic man who had previously experienced NMS during treatment with various antipsychotics. To their knowledge, this is the first report of "classical" NMS caused by clozapine alone.     

Neuroleptic malignant syndrome. Diagnostic and therapeutic dilemmas in a general hospital setting

Neuroleptic malignant syndrome (NMS) is a rare life-threatening condition, usually induced by typical and atypical antipsychotics. A middle-aged woman with bipolar disorder and acute back pain due to multiple falls was admitted to the trauma ward of a general hospital. After 3 days, she suddenly developed signs and symptoms of NMS possibly caused by PRN injectable haloperidol, although the additional role of olanzapine could not be ruled out. A 3-day delayed diagnosis of NMS led to serious complications, which could be prevented by its prompt management contingent on its early diagnosis, even in the absence of certain diagnostic criteria. Although she improved substantially with treatment interventions and continued to have dialysis, she died later due to renal complications. The PRN administration of antipsychotic medications needs to be avoided among such psychiatric patients admitted to general hospitals.     

Neuroleptic malignant syndrome induced by atypical neuroleptics and responsive to lorazepam

Objective

The authors report three cases of neuroleptic malignant syndrome (NMS) induced by atypical antipsychotics (olanzapine and clozapine) which showed classic features of NMS including muscular rigidity and prominent fever.

Method

Case reports.

Results

A 66-year-old man with dementia and alcohol abuse developed NMS while on olanzapine for agitation and combativeness. A 62-year-old man with schizophrenia developed NMS 6 days after starting clozapine. A 43-year-old man with bipolar disorder developed NMS 14 days after starting clozapine. All three cases showed classic features of NMS including muscular rigidity and fever. Resolution of fever and muscular rigidity occurred within 72 hours with discontinuation of neuroleptics, supportive care, and lorazepam. The NMS rating scale reflected daily clinical improvement.

Conclusion

Classic NMS characterized by muscular rigidity and prominent fever may occur with atypical neuroleptics. Our cases suggest recovery from NMS associated with atypical neuroleptics may be hastened by lorazepam, as was previously reported for NMS from typical neuroleptics. Also, the NMS rating scale was sensitive to clinical improvement.     

Olanzapine-induced neuroleptic malignant syndrome in a patient with paranoid schizophrenia

A case of a male patient with schizophrenic illness who developed neuroleptic malignant syndrome (NMS) following treatment with olanzapine is reported. Although typical neuroleptics are more frequently associated with NMS, atypical antipsychotics may also cause NMS. Case reports have been published concerning NMS and clozapine, ¹ risperidone ² and olanzapine. ^3–6 This case report emphasizes the importance of being cautious when rapidly increasing doses of olanzapine are used in patients with psychiatric illnesses.     

Atypical neuroleptic malignant syndrome caused by olanzapine

OBJECTIVE: Neuroleptic malignant syndrome (NMS) is a rare syndrome with four main symptoms: rigidity, hyperthermia, altered mental status and autonomic instability. We report a patient with an atypical manifestation of NMS. METHOD: A single case was reported. RESULTS: A patient with pneumonia developed delirium and was treated with olanzapine and developed a NMS with fluctuating hyperthermia and autonomic instability during a month. Only slight rigidity was present. Creatine kinase was not elevated. The patient was severely agitated and manic. After discontinuation of olanzapine the patient showed no psychopathology or hyperthermia. CONCLUSION: NMS should be considered when patients treated with antipsychotics develop one or more symptoms of NMS.     

Antipsychotic treatment and extrapyramidal symptoms amongst schizophrenic inpatients

Extrapyramidal symptoms (EPS) are seen in 50-75% of patients treated with typical antipsychotics and are a cause of treatment failure in at least 30% of the patients. Using atypical antipsychotics, the EPS incidence is lower, but a low-dosage strategy using typical antipsychotics is also known to cause fewer EPS. What conclusions can be drawn for the daily clinical practice? A naturalistic study including all schizophrenic inpatients in a psychiatric ward (n=123) analysed the effects of treatment concerning positive/negative symptoms, EPS, number of days to re-hospitalization and inpatient-days in the year after baseline admittance, using atypical and typical antipsychotics as recommended by the Danish Society of Psychiatry. The incidence of EPS was significantly higher in patients who were treated with typical antipsychotics in relation to atypical antipsychotics (46% vs. 12%, P<0.001). Patients with EPS had significantly more negative symptoms and a poorer level of function at discharge. Nevertheless, no difference regarding re-hospitalization and inpatient-days was found, whether the patient was treated with typical or atypical antipsychotics. However, it is important to underline that patients treated with atypical oral antipsychotic do as well as patients on typical depot antipsychotics.     

Catatonic variants, hyperthermic extrapyramidal reactions, and subtypes of neuroleptic malignant syndrome.

BACKGROUND: This case series study examines the hypothesis that neuroleptic malignant syndrome (NMS) is a heterogeneous condition including catatonic variants and non-catatonic pathological reactions to antipsychotics. METHODS: Fourteen episodes of NMS were prospectively identified. Patients were examined for catatonia during the course of NMS. Close monitoring of catatonia episodes and suspected cases of evolving NMS for possible NMS development provided data on the pre-NMS clinical course. All NMS episodes received benzodiazepines. Episodes with catatonia diagnosed were compared with those without catatonia, noting their presentation, clinical course and responses to treatment. RESULTS: Concurrent catatonia was diagnosed in 9 episodes. In 6 of them antecedent catatonia progressed to NMS following antipsychotic exposure (NMS of antipsychotic-converted catatonia). In 3 episodes, a parkinsonian-catatonic syndrome with fever and autonomic abnormality developed in reaction to antipsychotics (NMS of antipsychotic-induced catatonia). Catatonia was not diagnosed in 5 during the longitudinal course of NMS. A severe extrapyramidal reaction to antipsychotics with associated delirium preceded all 5 episodes. Seven of the 9 NMS episodes with catatonia and none of the 5 without catatonia showed significant responses to benzodiazepines. CONCLUSIONS: The preliminary findings support the hypothesis that NMS is a heterogeneous condition including catatonic variants and non-catatonic hyperthermic extrapyramidal reactions to antipsychotics, differing in presentation, clinical course, and treatment responses.