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This case report highlights the risk of development of Neuroleptic Malignant-Like Syndrome secondary to withdrawal of procyclidine with brief withdrawal of L-dopa and long-term typical antipsychotic depot. The patient responded to reintroduction of procyclidine, sedation and supportive treatment. The mechanism and management of NMS and NMLS is also reviewed. This case emphasises that any changes in antipsychotic and antiparkinsonian medications should be undertaken with extreme caution and patient should be closely monitored for development of NMLS after alteration in these medications.

Ropivacaine is commonly used for post-operative pain management. We describe a case of neuroleptic malignant-like syndrome in a woman administered ropivacaine delivered using a drug infusion balloon. The presenting symptoms were confusion, agitation and fever. Blood analysis showed elevated C-reactive protein, leucocytosis and increased creatine phosphokinase. As intoxication was suspected, ropivacaine was suspended and the patient gradually improved. Possible leakage of ropivacaine into the intrathecal space may have resulted in central nervous system toxicity. LEARNING POINTS It is important to be aware of the secondary effects of common drugs. The differential diagnosis should always include side effects and drug interactions. Intoxication can lead to poor outcomes, so early recognition is key.

The neuroleptic malignant syndrome is a rare, life-threatening idiosyncratic reaction to neuroleptic medication. The use of newer antipsychotics combined with its rare incidence has made NMS seem as a complication of the past. Here we report a patient in his early 20s suffering from a psychotic disorder developing a life-threatening neuroleptic malignant syndrome on an inpatient psychiatric ward in Canada without the characteristic overt change in autonomic stability. We review the clinical characteristics to facilitate the early recognition of neuroleptic malignant syndromes and discuss why this condition still is highly relevant for practising physicians. doi: https://doi.org/10.12669/pjms.36.6.2963 How to cite this:Dolp R, Ansari MA, Chan M, Hassan T. A ‘benign’ extrapyramidal side effect masking a life-threatening neuroleptic malignant syndrome. Pak J Med Sci. 2020;36(6):1429-1432. doi: https://doi.org/10.12669/pjms.36.6.2963 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Dementia with Lewy bodies (DLB) is characterised by neuroleptic hypersensitivity. It is unclear, however, whether the neuroleptic hypersensitivity implies an increased incidence of neuroleptic malignant syndrome (NMS) or of akinetic crisis (AC), which are expressions of the same possibly lethal clinical event, and whether AC in DLB can appear independently of neuroleptic treatment. In our prospective study, we assessed the incidence of AC in a cohort of DLB as compared with that in patients with Parkinson disease (PD).In total, 614 patients with PD and 236 DLB were recruited and followed during 2005-2013. AC was diagnosed as sudden akinetic state unresponsive to dopaminergic rescue drugs, dysphagia and serological alterations without recovery for 48 h or more requiring hospital admission. Exposure to neuroleptics was specifically evaluated, because of the high implicit risk in DLB.24 patients with PD (3.9%) and 16 patients with DLB (6.8%) developed AC. 77 (32.6%) DLB and 32 (5.2%) PD were exposed to typical neuroleptics, but only 8 DLB and 3 PD presented with AC. Disease duration before AC was lower in DLB than in PD group (p0.01). Outcome was fatal in 8 patients with (50%) DLB and 3 (12.5%) PD (p=0.05). When age and use of neuroleptics were adjusted for into a Cox proportional hazards model predicting time to AC, the HR of patients with DLB was 13.0 (95% CI 4.23 to 39.9; p0.001).AC in DLB can appear independently of neuroleptic treatment, occurs earlier and is more frequently fatal than in PD.

Objective: To describe a case of quetipiane- and escitalopram-associated rhabdomyolysis and secondary acute renal failure in a young adult suffering from recurrent depression. Methods: detailed clinical description of the subject’s case and relevant literature was reviewed. Results: A 35-year old male suffering from recurrent mayor depression treated with quetiapine and escitalopram, developed rhabdomyolysis and acute renal failure after ingesting an overdose of quetiapine (900 mg). Quetiapine and other antipsychotics have been related with rhabdomyolysis with or without renal failure in association or not with neuroleptic malignant syndromes.

The Neuroleptic Malignant Syndrome and the Serotonin Syndrome are two rare but potentially fatal complications of psychopharmacology. This review focuses on the clinical aspects of these conditions, exploring the diagnosis, differential diagnosis, treatment and prognosis.

We want to underline the importance of the pathophysiological mechanism that implies the reduction of availability of dopamine for the D-2 receptors, that can follow the interruption of dopaminergic medication in patients suffering of Parkinson’s disease. Early recognition and quick decision making can increase the outcomes of a condition that still has a fatal potential. We believe that this can be a useful tool for consultation/liaison psychiatrists in the general hospital.

Objectives: No information has been published on the incidence of neuroleptic malignant syndrome in learning disability. However, some studies of individuals who have developed neuroleptic malignant syndrome have suggested that individuals with learning disabilities may be over represented. This study aims to identify the association between learning disability and neuroleptic malignant syndrome.Method: A retrospective case-note analysis was performed with psychiatric case notes for clients with learning disability, in two geographical catchment areas. It was recorded whether clients had been exposed to neuroleptics, and whether any neurological symptoms had subsequently developed which could have been suggestive of neuroleptic malignant syndrome.Results: It was found that 301 individuals had been exposed to neuroleptics, out of 570 case notes examined. Only one case of neuroleptic malignant syndrome was identified, giving a lifetime prevalence rate of 0.3%.Conclusion: This study failed to demonstrate a higher than expected prevalence of neuroleptic malignant syndrome in clients with learning disability exposed to neuroleptics.

We present the case of a 36-year-old man who presented with a clinically neuroleptic malignant-like syndrome involving disorientation, signs of autonomic dysfunction, rigidity and raised total creatine kinase level, but in the absence of any neuroleptic medication. He had, however, abruptly stopped taking his longterm baclofen in the days prior to presentation. He improved markedly after the reintroduction of baclofen, and we postulate that his clinical syndrome resulted from the sudden withdrawal of this drug. We concur with the concept that neuroleptic malignant syndrome represents a spectrum of disorders, and add it to the list of possible sequelae after abrupt withdrawal of baclofen.

Section 1: General Considerations.Chapter 1: Movement Disorders: Approach, Definitions and differential Diagnosis.Martin Cloutier, Anthony E. Lang.Chapter 2: Rating Scales for Movement Disorders.Wonodi I, Hong EH, Avila MT, Gunvant Thaker.Chapter 3: Spontaneous movement disorders in psychiatric patients.Irene Richard, Christopher O'Brien, Roger Kurlan.Section 2: Antipsychotics.Chapter 4: Pharmacology of typical and atypical agents.Gary Remington, Shitij Kapur.Chapter 5: Acute Drug-induced Dystonia.Michael F. Mazurek, Patricia I. Rosebush.Chapter 6: Drug-Induced Parkinsonism.Joseph H. Friedman, Martha E. Trieschmann, Hubert H. Fernandez.Chapter 7: Acute Akathisia.Author: Lenard A. Adler, John Rotrosen, Burt Angrist.Chapter 8: Neuroleptic Malignant Syndrome.Stewart A. Factor.Chapter 9: Classical Tardive Dyskinesia.Thomas M. Hyde, MD, Jose A. Apud, Whitney C. Fisher, Michael F. Egan.Chapter 10: Tardive dyskinesia Variants.Skidmore F, Weiner W, Burke R.Chapter 11: Movement Disorders caused by atypical antipsychotics.Karen E. Anderson.Chapter 12: Commentary: Is Tardive dyskinesia disappearing?James Lohr, MD...Section 3: Dopaminomimetic Drugs.Chapter 13: Dyskinesia induced by levodopa and dopamine agonists in Parkinson's disease.John G. Nutt, Matthew Brodsky.Chapter 14: Stimulant Drugs.Anthony E. Munson, Juan Sanchez-Ramos, William J Weiner.Section 5: Other Drugs.Chapter 15: Antidepressants.Marie L. Moro-de-Casillas, David E. Riley.Chapter 16: Anticonvulsants.John C. Morgan, Madeline Harrison.Chapter 17: Miscellaneous Drugs.Daniel Tarsy

Neuroleptic malignant-like syndrome (NMLS) occurred after rapid switch from bromocriptine to pergolide in a Parkinsonian patient. Although the underlying mechanisms are as yet obscure, we hypothesize that differences in dopamine receptor affinities between bromocriptine and pergolide may be involved. Long-term treatment with bromocriptine may thus have induced plastic changes in intracellular signal processing in the nigrostriatal system, which resulted in reduced dopaminergic efficacy of pergolide. We recommend vigilant outpatient supervision during performance of rapid switchover from one dopamine agonist to another in advanced Parkinson's disease or in subjects with predisposing factors for onset of a neuroleptic malignant syndrome.

Neuroleptic malignant-like syndrome (NMLS) is well described in the treatment of Parkinson's disease. The syndrome is characterized by fever, rigidity, autonomic instability, elevated creatine phosphokinase levels, and altered level of consciousness, which is usually precipitated by levodopa withdrawal. In recent years, patients have used fava beans to treat Parkinson's symptoms, because the beans contain appreciable amounts of levodopa and have been thought to be a safe adjunctive therapy. We describe a case of NMLS, which was precipitated by the abrupt cessation of fava bean ingestion.

Neuroleptic malignant syndrome is a potentiallyfa tal complication ifneuroleptic treatment. It is characterized fry a variery ifsigns and symptoms associated with autonomic instability, and hypothalamic and extrapyramidal dysfunction. Since othermedical disordersmay mimic its clinical presentation, the accurate recognition if this syndrome in the medical setting is often a diagnostic dilemma. Three medically ill patients with a clinical presentation suggestive if neuroleptic malignant syndromearepresentedhere. The authors discuss the complexity ifmaking the diagnosis, and qjfer a briefreview ifthe literature. Since it was firs t descr ibed in 1960, a pproximat ely 1000 cases of neurolep tic mali gn ant syndrome (NMS) have been reported in the lit e ra ture (1-2). Althou gh the precise pathophysiology is not well understood , NMS is widely recognized as a pot ent ially fa tal com plica t ion of treatmen t wit h neu rol eptic agents. Studies su ggest that it is related to decreased ce n t ra l dop a minergic act ivity , most com monly precipita te d by dop amine D2 receptor blockade in the stria tal and hypotha la mic systems (3) . Exp erts have not been able to ident ify accurate ly a subpopulat ion at incre ased risk for developingthe syndrome . However, a ge ne t ic component ofNMS vulne rability has been hypothesized , and a rece nt familial case report proposes th at NMS suscept ibility may be, in part , a heritabl e cha racterist ic (4) . Case reviews su gg est that r isk fact ors for developing NMS includ e: I) previou s hist ory ofNMS, 2) intramuscul ar delivery and / or abrup t increase in rate or tot al dosage of neuroleptic agent, 3) a n tecede n t dop amine agonist or an t icholine rg ic medi ca tion wit hd rawal, 4) concurre n t use of other psychotropi c drugs, 5) e tha nol abuse or dep endence, 6) pr e-existing br ain pathology, 7) concomitan t medical or neu rological illn ess, 8) dehydration, and 9) psychomot or ag itat ion (5-7). Gender ra t io of NMS is approximately 2: 1 mal e: Mahmou d A. Parsa, M.D. , Fellow, Depart men t of Psychi a try, U niversi ty Hospit als of C leveland, Case West ern Reserve U nivers ity , C levela nd , O hio. And rew] . Picken , Se nior Med ical Studen t, Case West ern Reserve Universi ty, C leve land, O hio. Robert Keating, M.D., Resid ent , Dep art ment of Fa mily Medi cine, Fairview Hospit al , Cleveland, Ohio.

The original letter to which this reply refers was published in Movement Disorders Mov Disord (2005)DOI 10.1002/mds.20689.

Editor—Haddow et al describe a severe adverse drug reaction but create an oxymoron in describing clomipramine induced “neuroleptic malignant syndrome.”1

The authors describe a case of combined lithium and haloperidol toxicity characterized by hyperpyrexia, severe rigidity, mutism, and development of irreversible tardive dyskinesia. This case is similar to four other cases described in the literature and to the neuroleptic malignant syndrome. The authors postulate that two types of combined lithium-neuroleptic toxicity occur: a neuroleptic malignant extrapyramidal syndrome and a lithium toxicity that occurs in combination with phenothiazines, primarily thioridazine. Possible mechanisms and preventive measures are discussed.

After a review of the normal physiology of temperature regulation, one of the three hyperthermic syndromes— heat stroke—is discussed in detail with respect to its pathogenesis, pathophysiology, diagnosis, differential diagnosis, and treatment. The other syndromes— malignant hyperthermia and neuroleptic malignant syndrome—are discussed in Part II. Heat stroke is a syndrome of acute thermoregulatory failure in warm environments; malignant hyperthermia is a drug or stress-induced hypermetabolic syndrome characterized by vigorous muscular contractions; and the neuroleptic malignant syndrome results primarily from an imbalance of central neurotransmitters, usually due to neuroleptic drug use and characterized by muscular rigidity. Knowledge of the normal physiology of temperature regulation and the causes and pathophysiology of heat stroke are keys to understanding the other two syndromes.

Of 1,470 patients treated with neuroleptics during 1 year at a private psychiatric hospital, only one patient developed neuroleptic malignant syndrome--an annual frequency of 0.07%. Use of low doses of neuroleptics may account for this frequency, which is below recent estimates.