Case Of Neuroleptic Malignant Syndrome Research Articles

Neuroleptic Malignant Syndrome in Children and Adolescents on Atypical Antipsychotic Medication: A Review

Neuroleptic malignant syndrome (NMS) is a severe iatrogenic complication of treatment with antipsychotic medication. The purpose of this report is to examine the published cases of NMS in children and adolescents receiving atypical antipsychotic medication and review early warning symptoms, risk factors, and treatment in this population. An extensive review of the literature from 1990 to 2008 was conducted via computerized searches (PubMed and Ovid) to identify case reports. Descriptive statistics were employed to describe our findings. There were 23 episodes in 20 subjects, with ages ranging from 11 to 18 years. Increased creatine phosphokinase (CPK) was the most common finding (100%), followed by fever (78%), tachycardia (74%), rigidity (70%), and altered mental status (61%). The number of NMS symptoms ranged from 1 to 11 (mean 4.7 +/- 2.4) and positive laboratory findings ranged from 1 to 4 (2.2 +/- 1). The duration of NMS (mean 6.1 +/- 6.4 days) was one third of the duration associated with typical antipsychotics. Patients treated with bromocriptine had a shorter duration of illness, whereas the same was not true for those receiving dantrolene. In all cases, the NMS symptoms eventually resolved and there were no reported deaths or permanent sequelae. NMS is a serious condition. Symptom presentation related to atypical agents differs from that seen with older antipsychotic medications.

A Case of Neuroleptic Malignant Syndrome Induced by Risperidone in a Schizophrenic Woman

We report a case of neuroleptic malignant syndrome in a woman who assumed risperidone for schizoaffective disorders. A 45-year-old woman affected by schizoaffective disorders was admitted to Infectious Disease unit of Crotone Hospital because of a diagnosis of a fever of unknown origin. Clinical evaluation documented confusion and dysphoria, whereas chemical blood evaluation revealed acidosis and liver dysfunction. After few days she was transferred to the Operative Unit of Internal Medicine of San Giovanni in Fiore Hospital because of an increase in liver transaminases. Clinical evaluation showed the persistence of fever (38.8 degrees Celsius), with an increase in CPK, and liver enzymes. Pharmacological evaluation indicated a probable relationship between risperidone and NMS and led to a diagnosis of neuroleptic malignant syndrome associated with risperidone in a woman with schizophrenia. About seven days later, we recorded a complete resolution of her psychiatric symptoms. We postulate a possible interaction between risperidone and neuroleptic malignant syndrome and we suggest to use risperidone with caution in both young and middle aged people.

Neuroleptic Malignant Syndrome Associated with Atypical Antipsychotic Drugs

Neuroleptic malignant syndrome (NMS) is a rare but potentially severe idiosyncratic adverse reaction usually seen in the context of treatment with antipsychotic drugs. Although NMS is historically associated with the classic or 'typical' antipsychotic drugs, it is also a potential adverse effect of atypical antipsychotic drugs. The widespread use of atypical antipsychotic drugs highlights the need to examine the data relating to the symptomatology, diagnosis, classification and management of NMS with these newer agents. We used MEDLINE and EMBASE to identify NMS case reports and systematic reviews published to June 2008 related to the atypical antipsychotic drugs clozapine, olanzapine, risperidone, paliperidone, aripiprazole, ziprasidone, amisulpride and quetiapine. Case reports and reviews were systematically examined. Our review suggests that, in general, NMS associated with atypical antipsychotic drugs manifests in a typical manner. One notable exception is clozapine-induced NMS, which appears less likely to manifest with extrapyramidal features, including rigidity and tremor. The available literature highlights the divergence of opinion relating to the core diagnostic features of NMS and its conceptualization as a categorical versus dimensional disorder. Both these issues have relevance for the identification of atypical or milder forms of NMS, which are sometimes seen with atypical antipsychotic drugs.

Neuroleptic Malignant Syndrome Secondary to Quetiapine

To report a case of neuroleptic malignant syndrome (NMS) secondary to quetiapine in which the patient developed extrapyramidal symptoms (EPS). A 34-year-old male with a history of severe brain damage, mental retardation, and seizures was admitted to the hospital with changes in mental status, development of tremors, and a temperature of 39.9 degrees C. Initial differential diagnoses included seizure, aspiration, stroke, and infection. Once these were excluded, NMS was considered. The patient exhibited other characteristics of NMS during hospitalization, including lead pipe rigidity, tachycardia, and high creatine kinase level (up to 12,654 IU/L). Drug therapy on presentation included quetiapine 200 mg 3 times per day, guanfacine 2 mg/day, carbamazepine 400 mg every 12 hours, valproic acid 500 mg twice daily, and lorazepam 2 mg (unknown schedule). He reportedly had received these medications for at least a month before admission. On hospital day 2, quetiapine was discontinued. The patient received traditional treatment for NMS, which included bromocriptine, dantrolene, intravenous fluids, and supportive care. The NMS resolved in 7 days. In cases of NMS, clinicians previously believed that the risk for developing severe adverse effects such as EPS was lower with atypical versus typical antipsychotics. We identified 13 cases of NMS secondary to quetiapine in the literature via a search of MEDLINE/PubMed (1950-2008), and Iowa Drug Information Service (1966-2008). Seventy-five percent of previous reports of NMS secondary to quetiapine had reactions that included EPS. Common patient characteristics in our report and others included male sex, history of mental retardation, and treatment modalities used in NMS. Unique characteristics in this case included length of therapy without dosage change or titration and no known history of drug-related EPS. The Naranjo probability scale indicated a probable relationship between the development of NMS and quetiapine. NMS with associated EPS has been previously associated with quetiapine. Clinicians should be aware that NMS with EPS can occur with quetiapine at steady state doses without recent dosage adjustments or titration.

Neuroleptic malignant syndrome developing after acute overdose with olanzapine and chlorpromazine

Neuroleptic malignant syndrome (NMS) is a relatively uncommon side effect that may develop after a recent increase in the therapeutic dose of an antipsychotic medication or the addition of a new agent in therapeutic doses. We report a case of NMS developing in a 36-year-old female patient 2 days following deliberate self-poisoning with 30 x 10-mg olanzapine tablets, 7 x 100-mg chlorpromazine tablets and an unknown amount of escitalopram. These were the patient's own medications. She had not been taking these for several weeks. The patient initially presented with sedation from her overdose which resolved over the next 24 hours. Following this, over the subsequent 24 hours, she became progressively confused, ataxic, hypertonic, ferbrile and tachycardic, with marked lead pipe rigidity of the limbs. Head CT, lumbar puncture and septic screen were all negative. She was treated with intravenous midazolam infusion, nasogastrically administered bromocriptine, external cooling and was mechanically ventilated. She gradually improved over a period of 10 days, with residual confusion lasting another week, and was discharged well with no deterioration from her premorbid neurologic state. To our knowledge, although there are numerous cases reported with therapeutic use, NMS has not been reported to develop following acute olanzapine overdose. Clinicians should be aware that this may be an uncommon side effect of antipsychotic medication.

A rare case of neuroleptic malignant syndrome presenting with serious hyperthermia treated with a non-invasive cooling device: a case report.

IntroductionA rare side effect of antipsychotic medication is neuroleptic malignant syndrome, mainly characterized by hyperthermia, altered mental state, haemodynamic dysregulation, elevated serum creatine kinase and rigor. There may be multi-organ dysfunction including renal and hepatic failure as well as serious rhabdomyolysis, acute respiratory distress syndrome and disseminated intravascular coagulation. The prevalence of neuroleptic malignant syndrome is between 0.02% and 2.44% for patients taking neuroleptics and it is not necessary to fulfil all cardinal features characterizing the syndrome to be diagnosed with neuroleptic malignant syndrome. Because of other different life-threatening diseases matching the various clinical findings, the correct diagnosis can sometimes be hard to make. A special problem of intensive care treatment is the management of severe hyperthermia. Lowering of body temperature, however, may be a major clinical problem because hyperthermia in neuroleptic malignant syndrome is typically unresponsive to antipyretic agents while manual cooling proves difficult due to peripheral vasoconstriction.Case presentationA 22-year-old Caucasian man was admitted unconscious with a body temperature of 42°C, elevated serum creatine phosphokinase, tachycardia and hypotonic blood pressure. In addition to intensive care standard therapy for coma and shock, a non-invasive cooling device (Arctic Sun 2000®, Medivance Inc., USA), originally designed to induce mild therapeutic hypothermia in patients after cardiopulmonary resuscitation, was used to lower body temperature. After successful treatment it became possible to obtain information from the patient about his recent ambulant treatment with Olanzapin (Zyprexa®) for schizophrenia.ConclusionNumerous case reports have been published about patients who developed neuroleptic malignant syndrome due to Olanzapin (Zyprexa®) medication. Frequently hyperthermia has been observed in these cases with varying outcomes. In our case the only residual impairment for the patient is dysarthria with corresponding symmetric cerebellar pyramidal cell destruction demonstrated by increased signal intensity in T2-weighted magnetic resonance imaging, most likely caused by the excessive hyperthermia.

A rare case of neuroleptic malignant syndrome presenting with serious hyperthermia treated with a non-invasive cooling device: a case report

A rare case of neuroleptic malignant syndrome presenting with serious hyperthermia treated with a non-invasive cooling device: a case report

Association Between Selective Serotonin-Reuptake Inhibitors, Second-Generation Antipsychotics, and Neuroleptic Malignant Syndrome

To review the published reports of neuroleptic malignant syndrome (NMS) associated with the use of selective serotonin-reuptake inhibitors (SSRIs) and second-generation antipsychotics. Information was selected from a MEDLINE search of English-language literature (1950-May 2008). Manual search of all published cases indexed in MEDLINE (English language only) of NMS associated with second-generation antipsychotics was also performed. Pertinent information from all reports obtained was included, with specific emphasis on patient age, sex, second-generation antipsychotic involved, SSRI or other antidepressant involved, time of onset of NMS symptoms in relation to medication changes, treatment administered, and outcome of the reaction. NMS has been reported with every second-generation antipsychotic agent. It is unclear whether concomitant therapy with other agents may increase the risk of NMS development via pharmacodynamic or pharmacokinetic mechanisms or both. The suggested pharmacodynamic mechanism for increased risk of NMS with concomitant use of SSRIs is the effect of serotonin on dopamine release. Serotonin further inhibits dopamine release and thereby may worsen a hypodopaminergic state induced by antipsychotics. Pharmacokinetic factors may also play a role in some NMS cases involving an SSRI by increasing antipsychotic concentrations. An examination of case reports seems to indicate that at least in some cases, a temporal relationship exists with the addition of an SSRI to existing antipsychotic therapy. The use of SSRIs may be associated with an increased risk of NMS development in those receiving second-generation antipsychotics. Clinicians should closely monitor patients for the potential development of NMS.

Neuroleptic Malignant Syndrome Associated With Atypical Antipsychotics in Pediatric Patients

To retrospectively examine published cases of neuroleptic malignant syndrome (NMS) in patients aged 18 and below who had been treated with atypical antipsychotics (clozapine, risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole). Information was collected via MEDLINE searches in February 2006 and May 2007. The term neuroleptic malignant syndrome was used and cross-referenced with individual atypical antipsychotics. The authors also contacted (by telephone and in writing) pharmaceutical companies that produce and market atypical antipsychotics for any data on NMS. Twenty case reports (written in English only and published from 1991-2007) were identified and reviewed. These publications all described symptoms of NMS in patients aged 18 or younger who had been treated with atypical antipsychotics. Data were reviewed and compared with 3 diagnostic criteria (DSM-IV-TR, Levenson's, and Caroff and Mann's) for NMS. Interventions and outcomes were also reviewed. Twenty case reports were identified and presented with a descriptive approach. Sixteen cases met criteria for NMS, with at least 1 of the diagnostic sets utilized. The majority of cases involved male subjects. All patients recovered. Young patients can develop NMS during treatment with atypical antipsychotics. Symptoms of this disorder are consistent with those described in adults. Although NMS is rare in this population, clinicians should maintain a high index of suspicion. Appropriate caution in treating children and adolescents with any antipsychotic is warranted.

Biological Perspectives

He's gone country Everybody's gone country Yeah we've gone country The whole world's gone country --Alan Jackson Psychotropic drugs are in. Even psychiatric nurses who once considered psychotropic drugs a necessary evil or a treatment of last resort, now embrace the inevitability of the times--the fusion of public expectations, third-party considerations, and time constraints. As a result, psychotropic medications have become firstline options in treatment. However, several serious and potentially fatal side effects are related to these agents--for example, neuroleptic malignant syndrome, serotonin syndrome, and agranulocytosis. All these adverse responses were discovered the fact: that is, these effects were not anticipated but were described after patients had developed symptoms or had died. With careful assessments demanded by unacceptable levels of morbidity and mortality, both incidence and death rates have dropped significantly in recent years. Rather than risk allowing these catastrophic consequences to drift to the periphery of practice, we attempt in the following pages to bring the discussions up to date. Neuroleptic Malignant Syndrome Neuroleptic malignant syndrome (NMS) is a potentially fatal reaction to dopamine blockade caused by antipsychotic and other medications. The majority of these medications are prescribed in the treatment of schizophrenia and work by antagonizing dopamine D2 receptors (Keltner & McIntyre, 1985). Although uncommon, NMS may be fatal if left untreated. Estimates of the incidence of NMS range from 0.5% to 2.4%, and the mortality rate may be as high as 20% in those who are not treated (Reeves, Mack, & Torres, 2001). Persing (1994) identified four cardinal symptoms of NMS: hyperthermia, muscle rigidity, mental status changes, and autonomic instability. NMS most often occurs with high potency antipsychotics, and was first described during clinical trials with haloperidol in 1960 (Reeves, Torres, Liberto, & Hart, 2002). Although haloperidol has been most often implicated, cases also are reported with atypical antipsychotic and other dopamine receptor-blocking medications (Beauchemin, Millaud, & Nguyen, 2002; Harradine, Williams, & Doherty, 2001; Philibert, Adam, Frank, & Carney-Doebbeling, 2001; Solomons, 2002). Ninety-six percent of NMS cases occur within the first 30 days of treatment (Persing), with a duration of 5 to 10 days after antipsychotic medications are discontinued (Lappa et al., 2002). Dopamine and NMS. Dopamine is a catecholamine. It has as its immediate precursor levodopa and is itself a precursor to norepinephrine. Dopamine is synthesized from the amino acid tyrosine, which crosses the blood brain barrier and is converted to levodopa in dopaminergic and noradrenergic neurons. Dopamine's metabolic pathway, then, may be summarized as: tyrosine [right arrow] levodopa [right arrow] dopamine [right arrow] norepinephrine (Keltner, Hogan, & Guy, 2001). Pathophysiology of NMS. Central nervous system dopamine is localized in four specific pathways. Altered functioning in two of these pathways is thought to induce the positive and negative symptoms of schizophrenia. Treatment strategies aimed at manipulating dopamine affect all four tracts. Chemical manipulation of three of these pathways may contribute to NMS (Table 1). Some of these symptoms of NMS are interrelated. For example, high temperatures may develop and can be exacerbated by massive muscle contraction and hypermetabolism (Lappa et al., 2002). Rigidity also may cause rhabdomyolysis, which can lead to acute renal failure when kidneys are flooded with myoglobin. Severity is assessed by measurement of creatine phosphokinase (CPK). Renal failure is the most common cause of death in NMS (Persing, 1994). Mental status changes can be an early sign of NMS and may progress to coma. Changes in mental status may be characterized by delirium, catatonia, and agitation. …

CORRESPONDENCE

The recent article in your journal by Khan and Tham (vol 69(3), 2008, p. 171) usefully highlights a case of neuroleptic malignant syndrome associated with the atypical antipsychotic drug quetiapine.

Antipsychotiques atypiques et syndrome malin des neuroleptiques : brève revue de la littérature

Neuroleptic malignant syndrome (NMS) is an uncommon, but potentially life threatening complication of neuroleptic drugs. In 1960, Delay et al. [Ann Med Psychol 118 (1960) 145-152] described the "syndrome akinétique hypertonique"(hypertonic akinetic syndrome) and its cardinal symptoms: hyperthermia, extrapyramidal symptoms, altered mental status and autonomic dysfunctions. The syndrome often develops after a sudden increase in dose of neuroleptic medication or in states of dehydration. The frequency of NMS with conventional neuroleptic drugs ranges from 0.02 to 3.3%. The pathophysiology of NMS is not clearly understood. It has been suggested that the potential to induce NMS of neuroleptics is parallel to the potency of dopamine blockade in the nigrostriatal tract, mesocortical pathway and hypothalamic nuclei. It is, however, intriguing that NMS may appear with atypical antipsychotics (AA) and especially clozapine (CLZ), which is mainly characterized by its low affinity to D1 and D2 receptors. The purpose of this study was to review cases of NMS induced by AA agents reported in the literature and to discuss the pathophysiology of this complication. Cases of NMS related to AA were collected by means of a MEDLINE literature search between January 1986 and June 2005. As key words we used: (NMS and AA), amisulpride (AMS), clozapine (CLZ), olanzapine (OLZ), risperidone (RIS), quetiapine (QTP), ziprazidone (ZPS) and side effects. For the purpose of our review, all cases were critically examined against standard NMS diagnostic criteria according to DSM-IV. Cases involving a coprescription of classical neuroleptics were excluded. Our search yielded 47 cases (eight women, 39 men) of NMS associated with AA meeting DSM-IV criteria. Patients' mean age was 37 years, primary patient diagnoses were schizophrenia (n=26), schizoaffective disorder (n=9), bipolar disorder (n=3), mental retardation (n=4) and other diagnoses (n=5). Drugs involved were: CLZ (n=12), OLZ (n=18), OLZ and CLZ (n=1), OLZ and RIS (n=1), RIS (n=11), RIS and CLZ (n=2), QTP (n=3) and ZPS (n=1). No cases were reported with AMS. Twenty-nine of these 47 patients treated with AA received no other concomitant psychotropic medications; the remaining 18 patients received respectively, benzodiazepines (n=5), Valproate (n=5), lithium (n=4) and antidepressants (n=4). A lethal evolution occurred in two patients receiving in one case olanzapine, risperidone in the second, at a normal dose range. Our review indicates that atypical antipsychotics can cause NMS even when prescribed in monotherapy. The occurrence of NMS when prescribing AA and especially CLZ is, however, intriguing, given its low potency to block D2 receptors. This indicates that a low extrapyramidal syndrome-inducing potential does not prevent NMS and suggests the possible role of serotoninergic and noradrénergic receptors in the pathophysiology of NMS.

A Case Report With Ziprasidone-Induced Catatonic Symptoms

Back to table of contents Previous article Next article LETTERFull AccessA Case Report With Ziprasidone-Induced Catatonic SymptomsCourtney Markham-Abedi M.D.,Connie McNeely A.R.N.P.,Jose de Leon M.D.,Courtney Markham-Abedi M.D.Search for more papers by this author,Connie McNeely A.R.N.P.Search for more papers by this author,Jose de Leon M.D.Search for more papers by this author,Published Online:1 Oct 2007AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail IntroductionSIR: Double-blind placebo-controlled studies in schizophrenic patients without major comorbidities and not taking other antipsychotics suggest that some atypical antipsychotics such as ziprasidone may have extrapyramidal symptom profiles not different than placebo and definitively better that typical antipsychotics. 1 The use of atypicals in the general population of psychiatric patients with multiple comorbidities and polypharmacy has provided a less optimistic picture 1 and the different types of extrapyramidal symptoms have started to be described for the atypical antipsychotics. Few cases of neuroleptic malignant syndrome (NMS) in patients taking atypical antipsychotics 2 have been described but there are almost no cases of uncomplicated catatonic syndromes associated with atypical antipsychotics. No prior cases have been published of ziprasidone-induced uncomplicated catatonia but we have found three cases of NMS associated with ziprasidone treatment. 3 – 5 This case appears to be the first case of ziprasidone-induced uncomplicated catatonic picture. Case ReportThe 21-year-old Caucasian man had a 3-year history of DSM-IV schizophrenia and no prior catatonic episodes on risperidone (up to 10 mg/day), olanzapine (up to 30 mg/day), quetiapine (up to 400 mg/day), clozapine, (up to 500 mg/day), aripiprazole (up to 30 mg/day), and haloperidol decanoate (50 mg/3 weeks).In April 2003, the patient was taking 30 mg of aripiprazole and agreed to be switched to ziprasidone. A dose of 80 mg of ziprasidone was added on the first day, and the next day he received 160 mg of ziprasidone divided in two doses (added to the 30 mg/day of aripiprazole). The staff noted that the patient was mute, staring into space and exhibiting bizarre behavior. On day 3 after the fourth 80 mg ziprasidone dose (and no aripiprazole), the patient was examined by a psychiatrist who using the Bush-Francis Catatonia scale found the patient had posturing, mutism, bilateral arm cogwheeling and a parkisonian generalized resting tremor. He did not have other catatonic symptoms such as autonomic instability. Ziprasidone was discontinued and the patient was treated with a stat 1 mg dose of oral lorazepam. Approximately 2 hours later he became more cooperative but continued to have bilateral cogwheeling in three arm joints as well as the generalized tremor. The patient was restarted on 30 mg/day of aripiprazole on day 4. Gradually his catatonic symptoms improved and he returned to baseline by day 7.The patient had never had catatonic symptoms on prior antipsychotics, or on aripiprazole before adding ziprasidone. He did not develop them on aripiprazole after discontinuing ziprasidone. Thus, it appears reasonable to hypothesize that ziprasidone caused the catatonic symptoms.This case points out that atypical antipsychotics may cause catatonic symptoms as typical antipsychotics do and they need to be added to the differential diagnoses of catatonic symptoms.University of Kentucky, Mental Health Research Center at Eastern State Hospital, Lexington, KY, U.S.Eastern State Hospital, Lexington, KYUniversity of Kentucky, Mental Health Research Center at Eastern State Hospital, Lexington, KYReferences1 . Pierre JM: Extrapyramidal symptoms in atypical antipsychotics: incidence, prevention and management. Drug Safety 2005; 28:191–208Google Scholar2 . Caroff SN, Mann SC, Campbell EC, et al: Movement disorders associated with atypical antipsychotic drugs. J Clin Psychiatry 2002; 63(suppl 4):12–19Google Scholar3 . Leibold J, Patel V, Hasan RA: Neuroleptic malignant syndrome associated with ziprasidone in an adolescent. Clin Ther 2004; 26:1105–1108Google Scholar4 . Gray NS: Ziprasidone-related neuroleptic malignant syndrome in a patient with Parkinson’s disease: a diagnostic challenge. Hum Psychopharmacol 2004; 19:205–207Google Scholar5 . Murty RG, Mistry SG, Chacko RC: Neuroleptic malignant syndrome with ziprasidone. J Clin Psychopharmacol 2002; 22:624–626Google Scholar FiguresReferencesCited byDetailsCited ByWestphal Variant Huntington Disease and Refractory CatatoniaCognitive and Behavioral Neurology, Vol. 24, No. 4Memantine and CatatoniaJournal of Psychiatric Practice, Vol. 17, No. 4Catatonia: Clinical Aspects and Neurobiological CorrelatesJessica Daniels, M.D.1 October 2009 | The Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 21, No. 4Research in Developmental Disabilities, Vol. 30, No. 4 Volume 19Issue 4 Fall, 2007Pages 476-477 Metrics PDF download History Published online 1 October 2007 Published in print 1 October 2007

A Case Report With Ziprasidone-Induced Catatonic Symptoms

Back to table of contents Previous article Next article LETTERFull AccessA Case Report With Ziprasidone-Induced Catatonic SymptomsCourtney Markham-Abedi M.D.,Connie McNeely A.R.N.P.,Jose de Leon M.D.,Courtney Markham-Abedi M.D.Search for more papers by this author,Connie McNeely A.R.N.P.Search for more papers by this author,Jose de Leon M.D.Search for more papers by this author,Published Online:1 Oct 2007AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail IntroductionSIR: Double-blind placebo-controlled studies in schizophrenic patients without major comorbidities and not taking other antipsychotics suggest that some atypical antipsychotics such as ziprasidone may have extrapyramidal symptom profiles not different than placebo and definitively better that typical antipsychotics. 1 The use of atypicals in the general population of psychiatric patients with multiple comorbidities and polypharmacy has provided a less optimistic picture 1 and the different types of extrapyramidal symptoms have started to be described for the atypical antipsychotics. Few cases of neuroleptic malignant syndrome (NMS) in patients taking atypical antipsychotics 2 have been described but there are almost no cases of uncomplicated catatonic syndromes associated with atypical antipsychotics. No prior cases have been published of ziprasidone-induced uncomplicated catatonia but we have found three cases of NMS associated with ziprasidone treatment. 3 – 5 This case appears to be the first case of ziprasidone-induced uncomplicated catatonic picture. Case ReportThe 21-year-old Caucasian man had a 3-year history of DSM-IV schizophrenia and no prior catatonic episodes on risperidone (up to 10 mg/day), olanzapine (up to 30 mg/day), quetiapine (up to 400 mg/day), clozapine, (up to 500 mg/day), aripiprazole (up to 30 mg/day), and haloperidol decanoate (50 mg/3 weeks).In April 2003, the patient was taking 30 mg of aripiprazole and agreed to be switched to ziprasidone. A dose of 80 mg of ziprasidone was added on the first day, and the next day he received 160 mg of ziprasidone divided in two doses (added to the 30 mg/day of aripiprazole). The staff noted that the patient was mute, staring into space and exhibiting bizarre behavior. On day 3 after the fourth 80 mg ziprasidone dose (and no aripiprazole), the patient was examined by a psychiatrist who using the Bush-Francis Catatonia scale found the patient had posturing, mutism, bilateral arm cogwheeling and a parkisonian generalized resting tremor. He did not have other catatonic symptoms such as autonomic instability. Ziprasidone was discontinued and the patient was treated with a stat 1 mg dose of oral lorazepam. Approximately 2 hours later he became more cooperative but continued to have bilateral cogwheeling in three arm joints as well as the generalized tremor. The patient was restarted on 30 mg/day of aripiprazole on day 4. Gradually his catatonic symptoms improved and he returned to baseline by day 7.The patient had never had catatonic symptoms on prior antipsychotics, or on aripiprazole before adding ziprasidone. He did not develop them on aripiprazole after discontinuing ziprasidone. Thus, it appears reasonable to hypothesize that ziprasidone caused the catatonic symptoms.This case points out that atypical antipsychotics may cause catatonic symptoms as typical antipsychotics do and they need to be added to the differential diagnoses of catatonic symptoms.University of Kentucky, Mental Health Research Center at Eastern State Hospital, Lexington, KY, U.S.Eastern State Hospital, Lexington, KYUniversity of Kentucky, Mental Health Research Center at Eastern State Hospital, Lexington, KYReferences1 . Pierre JM: Extrapyramidal symptoms in atypical antipsychotics: incidence, prevention and management. Drug Safety 2005; 28:191–208Google Scholar2 . Caroff SN, Mann SC, Campbell EC, et al: Movement disorders associated with atypical antipsychotic drugs. J Clin Psychiatry 2002; 63(suppl 4):12–19Google Scholar3 . Leibold J, Patel V, Hasan RA: Neuroleptic malignant syndrome associated with ziprasidone in an adolescent. Clin Ther 2004; 26:1105–1108Google Scholar4 . Gray NS: Ziprasidone-related neuroleptic malignant syndrome in a patient with Parkinson’s disease: a diagnostic challenge. Hum Psychopharmacol 2004; 19:205–207Google Scholar5 . Murty RG, Mistry SG, Chacko RC: Neuroleptic malignant syndrome with ziprasidone. J Clin Psychopharmacol 2002; 22:624–626Google Scholar FiguresReferencesCited byDetailsCited ByWestphal Variant Huntington Disease and Refractory CatatoniaCognitive and Behavioral Neurology, Vol. 24, No. 4Memantine and CatatoniaJournal of Psychiatric Practice, Vol. 17, No. 4Catatonia: Clinical Aspects and Neurobiological CorrelatesJessica Daniels, M.D.1 October 2009 | The Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 21, No. 4Research in Developmental Disabilities, Vol. 30, No. 4 Volume 19Issue 4 Fall, 2007Pages 476-477 Metrics PDF download History Published online 1 October 2007 Published in print 1 October 2007

Risperidone-Induced Neuroleptic Malignant Syndrome in Neurodegenerative Disease

Risperidone-Induced Neuroleptic Malignant Syndrome in Neurodegenerative Disease

Neuroleptic Malignant Syndrome

Neuroleptic Malignant Syndrome

Aripiprazole as the Causative Agent of Neuroleptic Malignant Syndrome

Aripiprazole as the Causative Agent of Neuroleptic Malignant Syndrome

Meta-analytic evidence of systematic bias in estimates of neuroleptic malignant syndrome incidence

Objective The aim of this study was to examine published reports for sources of excessive variance in neuroleptic malignant syndrome (NMS) incidence estimates. Data Sources An unrestricted computerized MEDLINE search was conducted with a comprehensive search logic and supplemented by secondary references and a manual search of an extensive personal library. Study Selection Studies were analyzed if they presented original data and provided at least 2 of the following: number of NMS cases, number of patients at risk, or ratio of cases to patients at risk. Twenty-six of the 28 candidate studies met these minimal criteria. Data Extraction Variables included incidence, year of study publication, mean year of NMS occurrence, patient population at risk, study design, diagnostic criteria, and country of origin. Data Synthesis Standard error, which reflects study size, accounted for 90.8% of the variance ( β = .953, P < .001) in this international series of 26 NMS incidence estimates. Incidence was significantly lower in 7 studies the time end points of which were set in advance of case identification ( χ 2 = 71.08, P ≪ .001). No other variable was significantly related to incidence. Conclusions Neuroleptic malignant syndrome incidence estimates to date are non–trivially biased such that larger study size (patients at risk) is strongly related to lower observed incidence. Future studies can minimize the contribution of this and other sources of experimental error by incorporating several very feasible recommendations.

A case of neuroleptic malignant syndrome induced by olanzapine in postpartum period

Neuroleptic malignant syndrome (NMS) is a life-threatening medical complication that occurs as a result of dopaminergic receptor blockage in nigrostriatal pathways. This syndrome is mainly accepted to be an idiosyncratic reaction for antipsychotic medications. Incidence of NMS induced by olanzapine - an atypical antipsychotic - is extremely rare. However, there has been contradiction on postpartum period as a risk factor for NMS. This case is of interest due to the fact that it happens on postpartum period and is induced by olanzapine. We aimed in this study to evaluate the successfully cured case of neuroleptic malignant syndrome induced by olanzapine in postpartum period with the literature view.

Atypicality in presentation of neuroleptic malignant syndrome caused by olanzapine

Neuroleptic malignant syndrome (NMS) is the most serious of acute neurological side effects produced by antipsychotic medication, characterized by hyperthermia, rigidity, altered consciousness and autonomic dysfunction, the prevalence of which varies from 0.4-1.4%. NMS is usually seen in treatment with high potency typical antipsychotics and very rarely with atypical antipsychotics. However, NMS cases have been reported with risperidone, clozapine, olanzapine and quetiapine. The presentations of NMS have often varied and we report another atypicality in presentation of NMS due to olanzapine use.