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Malignant catatonia is a life-threatening syndrome, associated mostly with psychiatric diseases but also with neurological and neurodegenerative syndromes. We report the case of a 72-year-old patient, hospitalized for a major depressive episode with delusional symptoms, who presented a malignant catatonia. The patient had been transferred to an intensive care unit and treated with electroconvulsive therapy (ECT) leading to a rapid disappearance of the catatonic syndrome associated with a remission of the depressive symptoms. Complementary investigations helped us to secondarily diagnose a Lewy Body Dementia, which probably caused, associated with a treatment by haloperidol, the onset of catatonia. This case illustrates the need of an early diagnosis of neurodegenerative diseases in psychiatric outpatients and the importance of a quick management of catatonia, including ECT., (Copyright © 2019 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Acute catatonia is a non-specific, relatively frequent syndrome, which manifests itself through characteristic motor signs that enables its diagnosis. It occurs in association with mood disorders, psychotic disorders and several somatic or toxic diseases. Its short-term prognosis is of paramount importance. Without effective treatment, it is associated with high mortality. Despite the vital risk inherent in this disorder, it is not recognized as an independent diagnostic category by international rankings, which makes its diagnostic detection difficult and consequently does not allow adequate therapeutic care. However, if benzodiazepines and electroconvulsive therapy have proved effective in the treatment of acute catatonia, the role of atypical antipsychotics remains controversial. In fact, despite the progress made by the DSM-IV-TR and CIM 10 by the recognition of the etiologic diversity of catatonia, we deplore the absence to date of a consensus on clinical management and therapy of catatonia, which constitutes a source of confusion for practitioners in their approach to catatonic patients. To illustrate the difficulty in supporting these patients, we report here a clinical vignette., Clinical Features: Mr. M. aged 21, without psychiatric history, has shown a functional acute psychotic episode involving a delirious and hallucinatory syndrome associated with a marked catatonic dimension. Olanzapine was initiated at a dose of 10mg/d on the nineth day of hospitalization; the clinical picture was complicated by a malignant catatonia justifying the halt of olanzapine and the institution, in intensive units, of 15mg per day of lorazepam. After 72hours, the patient has not responded to this treatment. ECT was expected, but the patient died on the 12th day., Discussion: This case raises a threefold question: the crucial issue of immediate vital prognosis, that of the truthfulness of the positive diagnosis of this psychotic table and finally the issue of therapeutic care, primarily the well-founded or otherwise use of an atypical antipsychotic for the treatment of this type of psychotic disorder. For Mr. M., the clinical diagnosis that he has shown, according to the DSM IV-TR, is brief psychotic disorder "temporary diagnosis". This diagnosis - brief psychotic disorder - does not actually allow for a specific clinical approach to this type of psychotic table. The immediate vital prognosis inherent in the catatonic dimension may not be properly evaluated and the therapeutic conduct may miss the application of the specific treatment of the catatonic syndrome. The proper diagnosis for this type of psychotic disorder would be "catatonia" as proposed by Taylor and Fink, instead of "brief psychotic disorder" if the international rankings have included this disorder as a separate and independent diagnosis. The identification by international rankings of the catatonic syndrome as an independent diagnostic category seems essential for clinicians to allow: its clinical detection, the establishment of a syndromic diagnosis of catatonic disorder, appropriate prognostic evaluation and finally, the application of a suitable therapeutic strategy. Conventional treatment, benzodiazepine- and/or ECT-based, can solve the catatonic episode in a few days, irrespective of its etiology and its severity. Moreover, while all authors agree that conventional antipsychotics may induce a catatonic state or worsen a preexisting catatonia into a malignant catatonia and should thus be avoided for catatonic patients or with prior catatonic episodes, recent data from the literature emphasize the frequent and successful use of atypical antipsychotics, including olanzapine, in various clinical forms of benign catatonia. However, our patient did not respond to treatment with olanzapine and got even more complicated. Was the malignant catatonia that this patient has shown induced by olanzapine ? The answer to this question seems difficult since some authors report the efficacy of olanzapine in malignant catatonia. We wonder if we should have kept olanzapine and strengthen its dosage like Cassidy et al. in 2001 and Suzuki et al. in 2010 for the treatment of the malignant form constituted in this patient rather than having stopped it and used lorazepam as indicated by Taylor and Fink in 2003., In Conclusion: The non-recognition of catatonia as an independent entity, the lack of a therapeutic consensus and the pending issue on the safety and efficacy of atypical antipsychotics in the treatment of catatonia are at the origin of the difficulties of therapeutic support of catatonic patients., (Copyright © 2012 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Catatonia and neuroleptic malignant syndrome are both conditions that can compromise survival and whose successful treatment depends on early diagnosis., Objective: Distinguishing between these two conditions is difficult in a clinical setting and is further complicated by diagnostic criteria overlap. Are they both variations of a single disorder or two distinct conditions that happen to share certain characteristics? The goal of this paper is to review the available published data concerning the existence of a link between these two conditions and to specify the nature of the link between them., Method: We identified relevant articles from the PubMed registry by cross-referencing "catatonia" and "neuroleptic malignant syndrome". The articles returned were selected according to language (English and French) and publication date (before November 2007)., Results: Opinions are clearly divided concerning the existence of a link between these two conditions. The most commonly held opinion is that catatonia and neuroleptic malignant syndrome are two entities on the same spectrum. There are, however, no less than five different hypotheses concerning the nature of the link between them: first hypothesis: neuroleptic malignant syndrome is a drug-induced form of catatonia; second hypothesis: neuroleptic malignant syndrome is a drug-induced form of malignant catatonia; third hypothesis: neuroleptic malignant syndrome and malignant catatonia are one and the same; fourth hypothesis: catatonia is a risk factor for neuroleptic malignant syndrome; fifth hypothesis: neuroleptic malignant syndrome is a heterogeneous syndrome that includes both catatonic and non-catatonic responses to antipsychotic drugs. Other research maintains that catatonia and neuroleptic malignant syndrome are two distinct conditions. This point of view has fewer proponents, but benefits from historical, clinical and neurobiological studies that comfort this hypothesis. A careful clinical examination should in theory enable the distinction between these two entities and various neurobiological hypotheses are put forward to explain the differences between them. ANALYSIS AND DISCUSSION: The analysis of the data does not enable the elaboration of a single consensus on the existence of a link between catatonia and neuroleptic malignant syndrome. Additionally, the different hypotheses' level of scientific proof is insufficient to confirm or reject them. We only have at our disposal isolated case studies or studies with varying diagnostic criteria., Conclusion: A review of the literature does not enable us to confirm or invalidate a link between catatonia and neuroleptic malignant syndrome. However, answering this question would have direct consequences, since the suggestion of a link has led to the contraindication of neuroleptics for the treatment of catatonia, which contraindication has been extended on principle to the use of all newer antipsychotic medication. But since the link between catatonia and neuroleptic malignant syndrome has not been established according to scientific criteria, should the contraindication of atypical antipsychotic drugs be maintained in the treatment of catatonia?, (2009 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Introduction: Child and adolescent catatonia has been poorly investigated. Moreover, diagnosis criteria only exist for adult psychiatry, and there are no therapeutic guidelines. The aim of this paper is to describe the case of a 14-year-old girl presenting an overlap between psychogenic and neuroleptic induced catatonia, acute treatment and ten year's follow-up., Case Report: A 14-year-old Caucasian French girl, Elsa, was admitted in February 1998 to a University adolescent mental health center with an acute psychotic disorder. She showed agitation, impulsivity (sudden engagement in inappropriate behaviour), paranoid delusions, visual and auditory hallucinations, diurnal and nocturnal urinary incontinence, lack of self-care, inadequate food intake because of fear of poisoning, and vomiting after meals leading to rapid weight loss of 5 kg. Clinical examination, laboratory tests, EEG and RMI were normal. Toxicological tests were negative. Her IQ, assessed six months before admission, was in the dull average range (70-75). Elsa was treated with loxapine 150 mg per day for one week without improvement and this was then replaced by haloperidol 30 mg per day. One week after the start of haloperidol her agitation, impulsivity, and hallucinatory symptoms decreased. Twenty four days after loxapine introduction and 17 days after the haloperidol, her condition deteriorated rapidly over less than 48 hours. She exhibited immobility, minimal response to stimuli, staring and catalepsy with waxy flexibility. The diagnosis of catatonia was established. Examination revealed tremulous extremities, tachychardia (110 pm) and apyrexia. Creatine phosphokinase levels were 106 UI/l (normal range 0-250). Human immunodeficiency virus, hepatitis, listeria and Lyme serology were negative. Cerebrospinal fluid analysis was normal. Haloperidol was stopped and intravenous clonazepam 5mg/kg was begun. It was not possible to obtain signed consent from the two parents for Electroconvulsive therapy. The patient was transferred to a pediatric intensive care unit. The treatment was standard parenteral nutrition, nursing, intravenous clonazepam 0.05 mg/kg, with regular attendance by a child psychiatrist. Elsa stayed three weeks in this condition. She then began to notice the child psychiatrist, and a few days later she was able to carry out simple requests. Elsa was transferred to an adolescent psychiatric unit. As soon as she could eat by herself again, carbamazepine 400mg per day was begun. Her agitation reduced at a carbamazepine level of 7 mg/l. One month later her condition was stable. However, language difficulties persisted for a further six months. One year after the episode she scored 66 on a repeat IQ test and her RMI was normal. She exhibited no significant residual symptoms except some cognitive impairment. She integrated into a special education facility. These attempts to stop the carbamazepine were followed by depressed mood, aggressiveness and impulsivity; carbamazepine was finally stopped successfully after seven years. Ten years later, Elsa is the mother of two young children and is able to take care of them. She has never had a relapse of her psychotic disorder or catatonic state., Discussion: The etiopathogenic diagnosis is problematic. Some indices in the familial history may suggest a traumatic event. But one to the total residual amnesia it was never confirmed, and traumatic catatonia are extremely rare. Normal CPK levels, with autonomic disturbance limited to tachycardia and the lack of resolution after discontinuance of medication, argues against a diagnosis of neuroleptic malignant syndrome (NMS). But CPK levels are non specific, and NMS without pyrexia has been described. The occurrence of the catatonic syndrome 21 days after the first dose of a neuroleptic could be diagnostic. This case involved a non organic catatonic psychosis followed by neuroleptic induced catatonia. Catatonia is described as a risk factor for the development of NMS and some consider NMS to be a variant of malignant catatonia. The interest of this report is (1) it reinforces the need to be cautious before prescribing neuroleptics in adolescents presenting with symptoms of catatonia; (2) the complete recovery from catatonia after treatment with intensive care and more than three weeks of intravenous clonazepam without the use of ECT and (3) the effectiveness of carbamazepine over a long period of follow-up. Although trials on carbamazepine in catatonia are published, there are no data available for the control of residual symptoms or the long term prognosis, especially in child and adolescent psychiatry., (Copyright (c) 2009 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Neuroleptics are the main biological treatment for psychotic patients. The brutal withdrawal of a neuroleptic treatment may induce an important aggravation of the psychotic symptoms. A few of those relapses may occur very early after the interruption of treatment; they are often associated with a modification of the symptoms and an unfavorable evolution in the course of the illness. Using those clinical observations a few authors have developed the concept of supersensitivity psychosis to explain those kinds of relapses and to formulate hypothesis about tolerance and resistance to neuroleptics. They focus on the possible correlation between supersensitivity psychosis and tardive dyskinesia. We report three cases of a dramatic aggravation of the psychotic symptomatology following the withdrawal of clozapine in three schizophrenic patients resistant to classical neuroleptic treatment. According to the clinical data and to the physiopathological hypothesis, the concept of supersensitivity psychosis can have implications in the therapeutic management of resistant schizophrenic patients.

Similar clinical and biological features in lethal catatonia (LC) and neuroleptic malignant syndrome (NMS) suggest a relationship between both affections and common physiopathologic mechanisms. Pharmacological effects of several drugs--dopaminergic agonists, benzodiazepines, carbamazepine--suggest an impairment of several systems of neurotransmitters. We report the case of a young woman with infantile psychosis who developed catatonic syndrome worsened by neuroleptic treatment, arising the problem of the chronology of both affections. The evolution with treatment may partially explain the physiopathology. A 18-year old woman with an history of infantile psychosis, experienced insomnia, anorexia, paradoxical agitation developed after affective traumatism (mother's hospitalization). Chlorazepate (150 mg) remained inefficient and hospitalization was necessary. The patient was dumb, prostate in bed. She presented negativism, rigidity of the four limbs, catalepsia and hyperpyrexia (38.5 degrees C). Hepatic transaminases were increased (SGOT: 71 UI/l; N < 30). After cumulated dose of levomepromazine (100 mg) profuse sudation, thermic and cardiovascular instability, alteration of consciousness, major rigidity of limbs appeared. (Blood) hepatic transaminases and muscular enzymes increased. Bacteriological samples, cerebrospinal fluid analysis, CT-scan and EEG were normal. Within 48 hours after rehydratation and bromocriptine (30 mg per day) alteration of consciousness and autonomic disorders decreased but hyperpyrexia (38 degrees C) persisted. Biological parameters were normalized 10 days later. Negativism and psychomotor inertia remained. Lorazepam (3 mg per day) failed to be clinically beneficial. On carbamazepine (600 mg per day) she started speaking and moving spontaneously. Catalepsia disappeared but rigidity and anorexia persisted. Electroconvulsivotherapy (ECT) was necessary. After 2 shocks she started standing up, walking, taking food and speaking fluently.(ABSTRACT TRUNCATED AT 250 WORDS)

After a review of the literature centered on the possible relationship of acute psychiatric symptomatology and death, more specifically in relation with acute catatonia, the writers examine all cases of schizophrenic patients admitted to the Psychiatric University Hospital of Lausanne (Hôpital de Cery) during the period from 1961 to 1981. The importance of acute catatonia is discussed and compared to other similar syndromes (the porcine stress syndrome, malignant hyperthermia, the neuroleptic "malignant" syndrome).