Delirious mania is an uncommon condition that is challenging to diagnose and treat. More often seen in patients with a history of bipolar disorder, it frequently presents with prominent catatonic features and overlaps with other diseases in the catatonic spectrum, such as neuroleptic malignant syndrome, serotonin syndrome and malignant catatonia. We present a case of delirious mania refractory to high doses of lorazepam, several antipsychotics and valproic acid, which responded dramatically to therapy with lithium after 26 days of minimal improvement with the other medications. The pathophysiology of delirious mania is reviewed, and the unique actions of lithium are discussed, highlighting possible reasons as to why lithium might offer advantages in the treatment of this disease.

In forensic settings, the most common indication for clozapine is treatment-resistant schizophrenia (TRS). Clozapine has also been shown to be effective in reducing hostility, aggression and violence in patients with schizophrenia and is of benefit in comorbid substance use disorders. The decision to initiate or to discontinue recently initiated clozapine can have a profound beneficial or detrimental influence on the lives and safety of patients and the staff caring for them. We present a case in which treatment with clozapine proved effective in spite of earlier repeated discontinuation of clozapine out of fear of neuroleptic malignant syndrome (NMS). Elevation of creatine kinase was deemed to be indicative of NMS in the absence of clinical signs of NMS. In somatic medicine, it is well known that creatine kinase elevation has many causes, most of them non-harmful. Collaboration with clinical chemistry was shown to be very useful, if not essential; research in the 1980s found replicated evidence for both sex and race differences in creatine kinase levels. In addition, substantial intra-individual variation has been found over time in healthy individuals. The creatine kinase levels of this patient of African descent were within normal limits for the African population. Baseline creatine kinase assessment and repetition of this assessment after 2 weeks with careful interpretation are recommended in all clozapine-treated patients. The authors advocate the introduction of evidence-based creatine kinase cut-off points that reflect the biological differences between the sexes and among races. More intensive contact between psychiatrists and clinical chemist can facilitate faster diagnosis and better treatment.

Neuroleptic malignant syndrome (NMS) is a rare and potentially fatal adverse reaction to drugs. In psychiatric practice, it is mainly associated with antipsychotics. The classic presentation is that of hyperpyrexia, muscle rigidity, mental state changes and autonomic instability. Subtle forms are difficult to recognise owing to symptom overlap with other conditions. This article discusses the clinical presentation of the syndrome, its differential diagnosis and use of supportive care, medication and electroconvulsive therapy in its treatment. It also explores prevention of NMS and reinstatement of treatment after an episode. It is stressed that all but the mildest forms of NMS should be considered a medical emergency that is properly managed in an acute hospital.

A ten-year prospective survey of neuroleptic malignant syndrome (NMS) was performed in a major psychiatric hospital (1,510 beds) in Moscow. All inpatients who developed a persistent and severe extrapyramidal rigidity accompanied by fever after exposure to neuroleptic medication were screened for NMS. The diagnosis of NMS was established according to Levenson’s criteria and at a later stage all NMS cases were reevaluated using the DSM-IV research criteria. Data on age, gender and psychiatric diagnoses were analyzed. Of the 78,708 inpatients treated with neuroleptic agents, 19 separate patients had an episode of NMS, for a frequency of 0.02%. Mortality rate was 10.5% (2/19 patients). Of the three potential risk factors studied, only young age (≤ 25 years) was significantly associated with an increased frequency of NMS (P < 0.01). The low rate of NMS found here compared to studies in other countries may be due to the stringent demands for NMS diagnosis. More large-scale prospective studies including detailed clinical and laboratory data are needed to clarify these differences and their impact on the prevalence and risk factors of NMS.

Neuroleptic malignant syndrome (NMS) is associated with the administration of antipsychotic agents and other drugs such as l-dopa, antidepressants, and antihistaminic agents. Unexpected changes in mental status, new-onset catatonia, episodic tachycardia, tachypnea, hypertension, dysarthria, dysphagia, diaphoresis, sialorrhea, incontinence, low-grade temperature elevations, and rigidity should arouse suspicion. Several lines of evidence provide support for the involvement of dopamine. Most of the drugs implicated in NMS are D2 dopamine receptor antagonists. Central noradrenergic activity is also possibly related to the disorder, as sympathetic hyperactivity is associated with the active phase of NMS. Currently, the definitive role of GABA deficiency in NMS is yet to be established. Differential diagnosis should include malignant hyperthermia, lethal catatonia, lithium toxicity, serotonin syndrome, and heat stroke. A high degree of suspicion and the discontinuation of antipsychotic agents even if the diagnosis is not established are essential for the safety of the patient. Treatment of NMS should be individualized and be based empirically on the character, duration, and severity of the clinical signs and symptoms noted. The initial step in the treatment of NMS is the removal of the offending agent. Full-blown NMS is a serious condition and requires immediate supportive, nutritive, and electrolyte therapies. The administration of drugs that can improve NMS, such as IV dantrolene and/or oral bromocriptine, may also be taken into consideration, based on the severity and nature of the NMS.

We describe two cases of confirmed anti-NMDA receptor encephalitis; one patient initially presented with a clinical picture that resembled delirium and later appeared to present with a conversion reaction and the second patient presented with a first psychotic break followed by the clinical picture of neuroleptic malignant syndrome with catatonia. Neither patient had a previous history of psychiatric illness or recreational drug use. These cases illustrate the diagnostic and treatment challenges associated with this neuropsychiatric condition and underscore the role of psychosomatic medicine psychiatrists in diagnosing anti-NMDA receptor encephalitis.

In this case report, we describe the clinical course of a 16 yr old asylum seeker from Afghanistan who developed paranoid schizophrenia complicated by catatonia and was successfully treated with diazepam and clozapine. To our knowledge, this is the first case report of its kind in this age group.

Our patient became psychotic and presented to A&E after cutting off the tip of his nose in response to command hallucinations telling him to kill himself, his mother and his siblings. His catatonic features, which emerged after hospitalization, were those of mutism, akinesia, posturing including the psychological pillow. He did not respond to risperidone or haloperidol; showed a partial response to lorazepam and diazepam. His catatonic features and psychosis only resolved upon the introduction of clozapine.

We go on to review the literature about catatonia in children and adolescents. We discuss the nosological dilemma with classification, the evolution of treatments and the role of anti-psychotic medication in the treatment of catatonia. Specifically, we advocate the usefulness of clozapine as an adjunct and as monotherapy.

Neuroleptic malignant syndrome (NMS) is a severe and potentially lethal complication of antipsychotic medication. Differential diagnosis is extremely important because severe catatonia, which has some simi??larities to NMS, may also be lethal but requires antipsychotic treatment. We present a case report of a 62-year-old woman who was admitted to hospital for differential diagnosis of NMS and suffered from severe haloperidol intoxication, which complicated the diagnostic evaluation. Further differential diagnostic aspects are summarised and their therapeutic implications are outlined.

Objective: Neuroleptic malignant syndrome (NMS) is a life-threatening reaction to neuroleptics. Several prospective studies have reported NMS occurrence rates ranging from 0.07% to 2.2% of patients receiving neuroleptics. However, few occurrences of NMS have been reported in cancer patients despite frequent complications of cancer and its treatment by mental disorders managed with neuroleptic drugs. Exhaustion, dehydration, and malnutrition are considered risk factors for NMS, and cancer patients represent a high risk group for NMS.

Methods: We describe a patient with metastatic chondrosarcoma who had received frequent neuroleptic injections prior to brain surgery and developed NMS in the intensive care unit immediately after surgery. The patient showed delirium, hyperpyrexia, tachycardia, diaphoresis, and extrapyramidal symptoms. After a diagnosis of NMS was made, supportive care and careful monitoring were carried out, and the patient recovered over an interval of 11 days.

Results and significance of the research: Clinical NMS studies have been conducted mainly in psychiatric units, but NMS can occur wherever psychotropic drugs are administered. NMS can be difficult to diagnose due to multiple complicating factors in cancer treatment, but the diagnosis is highly important given the risk of death. Recognition of prodromal NMS symptoms can facilitate actions to decrease morbidity and mortality. It is suggested that special attention to cancer patients undergoing psychopharmacologic treatment is required in clinical oncologic practice.

Neuroleptic malignant syndrome (NMS) is a potentially life-threatening condition that has been associated with antipsychotic use. Most diagnostic criteria include fever and muscle rigidity, although NMS may present without either. Diagnostic uncertainty in such cases may result in delays in diagnosis and management, leading to adverse consequences for these patients. The differential diagnosis of NMS is broad and includes a number of neurological, medical and psychiatric conditions as well as substance and medication-induced disorders. A case is described that illustrates an atypical presentation of NMS and demonstrates some of the challenges in its diagnosis. Limitations of current NMS criteria are also examined, and suggestions for future criteria are presented.

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.

Malignant hyperthermia is an autosomal-dominant inherited disorder of the skeletal muscle cell characterized by a hypermetabolic response to all commonly used inhalational anaesthetics and depolarizing muscle relaxants. The clinical syndrome includes muscle rigidity, hypercapnia, tachycardia and myoglobinuria as result of increased carbon dioxide production, oxygen consumption and muscle membrane breakdown. In human beings and animals susceptible to malignant hyperthermia, it is generally accepted that an increase in the level of myoplasmic free calcium is the cause of the syndrome. Various hypotheses have been proposed to account for the increase of intracellular calcium levels, e.g. a defect in the calcium release channel of the sarcoplasmic reticulum (ryanodine receptor), an abnormality of the excitation-contraction coupling mechanisms, or alterations in second messenger systems of skeletal muscles. This review gives an overview of the main features of this disease and recent advances in research including pathophysiology, treatment, diagnosis and genetics as well as association with other disorders.

We report a case of neuroleptic malignant syndrome (NMS) secondary to clozapine treatment in which re-introduction of two different antipsychotics led to elevation of creatinine kinase (CK) levels without associated symptoms of NMS. The significance of CK levels as a marker for NM S is discussed in the light of previous findings in this area. We suggest clinical guidelines for antipsychotic rechallenge after the occurrence of NMS.