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.     

A case of recurrent neuroleptic malignant syndrome

Summary:Neuroleptic malignant syndrome (NMS) is a life-threatening neurologic complication associated with the use of neuroleptic agents and characterized by a distinctive clinical syndrome of fever, r...     

Case study. Risperidone-Induced neuroleptic malignant syndrome in an adolescent

Neuroleptic malignant syndrome (NMS) is a potentially fatal complication of neuroleptic therapy, characterized by fever, rigidity, mental status changes, and autonomic instability. Although NMS was previously associated with the use of high-potency neuroleptics, cases have begun to emerge with atypical neuroleptics. This article presents a risperidone-induced case in the youngest patient to date, raising issues concerning our perceptions, the safety of newer neuroleptics, and treatment of NMS.     

Neuroleptic malignant syndrome during olanzapine and levomepromazine treatment

OBJECTIVE: To date only five reports of neuroleptic malignant syndrome (NMS) related to olanzapine exist. The first case report was published in November 1998. METHOD: We report the case of a 78-year-old woman suffering from chronic schizophrenia who developed a NMS while being treated with olanzapine and levomepromazine. Before this her medication had been unchanged for more than 2 years. RESULTS: When treated with olanzapine and levomepromazine, the patient had a fulminant NMS which was complicated with pneumonia. When the neuroleptic drug treatment was discontinued, the patient recovered. However, when this combination was restarted later due to severe agitation and hallucinations, the symptoms of NMS reappeared. CONCLUSION: This case report shows that the neuroleptic malignant syndrome can occur during olanzapine treatment as well as during treatment with conventional neuroleptics. This syndrome may develop even after a long and stable neuroleptic treatment.     

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.     

Electroconvulsive Therapy of the Lethal Catatonia Syndrome

Lethal catatonia (LC) is a life-threatening syndrome associated with diverse neuropsychiatric or systemic disorders. Neuroleptic agents appear inadequate in treating LC. We report a case of LC successfully treated by electroconvulsive therapy (ECT) that adds to the experience of ECT as a safe and effective treatment for LC occurring in the context of the major psychoses. Anecdotal evidence suggests that ECT is dramatically effective in LC regardless of etiology. The use of ECT in the treatment of neuroleptic malignant syndrome (NMS), viewed here as a subtype of LC, is considered and compared with that of specific drug therapies for NMS.     

Neuroleptic malignant syndrome associated with clozapine use

Clozapine, an atypical antipsychotic drug, is indicated for severely ill schizophrenic patients refractory to treatment with conventional neuroleptics. One advertised advantage of clozapine is the absence of associated neuroleptic malignant syndrome (NMS). On the basis of a clinical case, the authors question this claim. They are concerned that this potentially fatal condition may be misdiagnosed if physicians are not aware of possible NMS associated with the use of clozapine.     

Rechallenging Clozapine After Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome (NMS) is a potentially fatal manifestation of antipsychotic use associated with symptoms that include mental status changes, muscle rigidity, fever and autonomic dysfunction. An occurrence of NMS with clozapine has been reported in the past but there are very few reports of successfully rechallenging the drug in individuals who have developed the syndrome. This case report discusses one of the few instances in literature where clozapine has been re-administered successfully to a patient without a reoccurrence of NMS. In conclusion, a rechallenge of clozapine after neuroleptic malignant syndrome can be done if care is taken to avoid concurrent use of lithium and other psychotropics, monitoring for NMS symptoms and titrating the dose upward slowly after a reasonable period of time.     

Electroconvulsive Therapy in the Neuroleptic Malignant Syndrome

A case of neuroleptic malignant syndrome (NMS) successfully treated with electroconvulsive therapy (ECT) is presented and the literature on this subject is summarized. The possibility of an etiologic link between catatonia related to a psychiatric disorder and NMS is explored. Possible relationships between NMS and lethal catatonia are explored. ECT may be a useful treatment in selected cases of NMS, especially those with evidence of a preexisting ECT responsive disorder.     

Toxic interaction between risperidone and clozapine: a case report

Although atypical antipsychotics have generally a decreased risk of neurotoxicity, there are reports regarding various neurotoxic or idiosyncratic reactions including neuroleptic malignant syndrome (NMS). The authors present here the toxic interaction between risperidone (RIS) and clozapine (CLZ) in a first-episode schizophrenic patient. A 20-year-old man suffering from first-episode schizophrenia--catatonic subtype, developed a neurotoxic syndrome, which has been characterized as a mild form of NMS, after CLZ (100 mg/day) was added to a regimen of RIS (16 mg/day). The NMS symptomatology subsided only by drug discontinuation and supportive care. Later, CLZ monotherapy restarted without further complications. This case report shows that neurotoxic syndromes, even NMS, may occur during combination therapy with RIS and CLZ.     

Reinstitution of neuroleptic treatment with molindone in a patient with a history of neuroleptic malignant syndrome

The decision to reinstitute neuroleptic treatment in patients with a history of neuroleptic treatment is fraught with hazards. A case is reported in which neuroleptic treatment was successfully reintroduced with molindone after previous bouts of neuroleptic malignant syndrome (NMS) with trifluoperazine and thioridazine. Molindone may represent an alternative neuroleptic to consider in patients with a history of NMS, although all neuroleptics including clozapine and molindone may potentially precipitate this syndrome.     

Neuroleptic malignant syndrome: observations on altered consciousness

A young man with a previously untreated schizophrenia developed a neuroleptic malignant syndrome (NMS) on the second day of neuroleptic treatment. The dominant symptom was deep coma. The NMS occurred on the second day of neuroleptic therapy with rapidly progressing mental deterioration, temperature elevation, and extrapyramidal signs. After anticholinergics were injected the patient regained consciousness. This suggests that a cholinergic hyperactivity in the central nervous system (rather than hyperthermia) is responsible for the disturbance of consciousness in NMS. The experimental evidence that central cholinergic systems are stimulated by neuroleptics is discussed. It is concluded that anticholinergics might be helpful in treating coma during NMS.     

Neuroleptic-induced catatonia or a mild form of neuroleptic malignant syndrome?

Neuroleptic-induced catatonia (NIC) and milder neuroleptic malignant syndrome (NMS) share parkinsonian features, catatonic symptoms, mild fever, and have been described in patients receiving antipsychotic agents. We report the case of a patient with a schizophreniform disorder and a mild mental retardation who developed a condition which can be diagnosed either as NIC or as a mild form of NMS and has been treated successfully with a combination of amantadine (600 mg/day) and diazepam (30 mg/day). The overlapping between NIC and mild NMS cases might lead to an overestimation of the incidence of current NMS and reinforces the view of the existence of a 'neuroleptic toxicity spectrum'.     

Catatonic syndrome and neuroleptic malignant syndrome

Several clinical reports suggest that neuroleptic malignant syndrome (NMS) is not a distinct clinical entity but an acute form of catatonic syndrome (CS). They both share many clinical features and it is impossible to differentiate them on the basis of biochemical findings. Both respond similarly to treatment. The article describes some case reports from the literature and our own case report of NMS as a form of CS.     

Resolution of neuroleptic malignant syndrome with dantrolene sodium: case report

A case of neuroleptic malignant syndrome (NMS) with an abrupt onset was terminated quickly with i.v. dantrolene sodium. The prompt and satisfactory outcome after early diagnosis indicates that dantrolene should be considered a useful treatment in NMS.     

无抽搐电痉挛治疗恶性综合征1例

随着新型抗精神病药物的广泛应用,药物所致恶性综合征发生率似已降低,但仍难以完全避免。电痉挛治疗作为恶性综合征的一种特殊治疗手段,国外文献报道较多,而国内报道极少。本文报道1例应用无抽搐电痉挛治疗恶性综合征的经验,并结合文献进行讨论。     

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.     

Cerebellar degeneration in neuroleptic malignant syndrome: neuropathologic findings and review of the literature concerning heat-related nervous system injury.

A selective subtotal cerebellar neuronal degeneration was found in a patient who died 4 1/2 months after suffering neuroleptic malignant syndrome (NMS), a rare, potentially fatal disorder associated with neuroleptic medications. It is suggested that the cerebellar neuronal degeneration in this case was due to hyperpyrexia, a cardinal clinical feature of NMS. Similar pathologic findings appear not to have been previously reported in NMS but have been described in heat-induced central nervous system (CNS) injury. The findings imply that a cerebellar syndrome might be encountered in patients who survive NMS complicated by a particularly high febrile course.     

Massive creatine kinase elevations with quetiapine: report of two cases

Massive elevations of serum creatine kinase (CK) can occur in a significant number of patients treated with neuroleptics in the absence of neuroleptic malignant syndrome (NMS). We report two cases of CK-elevations associated with quetiapine treatment, which disappeared after drug discontinuation. To our knowledge, case number one is the first case of quetiapine-induced CK elevation in a neuroleptic-na?ve patient. We thus suggest CK assessment when myalgia occurs with neuroleptic treatment.     

Neuroleptic malignant syndrome and serotonin syndrome in the critical care setting: case analysis.

BACKGROUND: Serotonin syndrome (SS) and neuroleptic malignant syndrome (NMS) are medical emergencies associated with psychotropic administration. Differentiation and treatment can be complex, especially when features of both syndromes are present and the patient has taken both serotonergic and neuroleptic agents. METHOD: Case analysis of a poly-drug overdose (venlafaxine, topiramate, divalproex sodium, risperidone, and carbamazepine) presenting with mixed SS/NMS features and whose clinical management suggests a practical algorithm for treatment of undifferentiated SS/NMS in critical care settings. RESULTS: The suggested algorithm includes: 1) Supportive care and withdrawal of all potentially offending agents; 2) Laboratory evaluation with prompt initiation of treatment for both disorders--cyproheptadine for SS and dantrolene for NMS; 3) Do not use bromocriptine (contraindicated in SS) or chlorpromazine (contraindicated in NMS) initially; 4) Add bromocriptine when clinical presentation becomes consistent with NMS (SS can be prolonged if serotonergic agent has long half-life). CONCLUSIONS: Prompt and appropriate identification and intervention are essential for successful management of SS and NMS. The suggested treatment algorithm allows for specific treatment of both disorders and avoids potentially exacerbating either one. The algorithm derived from this case could serve as both a practical guideline and impetus for further investigation in light of increasing psychotropic co-administration.