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PubMed2007

MLC1 polymorphisms are specifically associated with periodic catatonia, a subgroup of chronic schizophrenia.

BACKGROUND: The MLC1, located on chromosome 22q13.33, has been suggested as a risk gene for schizophrenia, especially the periodic catatonia subtype. An initially identified missense mutation was found to be extremely rare in other patient cohorts; however, a recent report again argued for an association of two intronic MLC1 single nucleotide polymorphisms (SNPs) with schizophrenia and bipolar disorder. METHODS: A case-control study of these polymorphisms as well as SNPs in the transcriptional control region of MLC1 was conducted in 212 chronic schizophrenic patients, 56 of which suffered from periodic catatonia, 106 bipolar patients, and 284 controls. RESULTS: Both intronic and promoter polymorphisms were specifically and significantly associated with periodic catatonia but not schizophrenia or bipolar disorder in general. A haplotype constructed from all polymorphisms was also associated with periodic catatonia. CONCLUSIONS: The MLC1 variation is associated with periodic catatonia; whether it constitutes a susceptibility or a modifier gene has to be determined.

Bipolar Disorder↗
PubMed2001

Towards the genetic basis of periodic catatonia: pedigree sample for genome scan I and II.

In a genome-wide linkage study, we mapped two major susceptibility loci for periodic catatonia, a phenotype with qualitative disturbances of the psychomotor sphere and a morbidity risk of 26.9% in first-degree relatives of index cases, to chromosome 15q15, and to chromosome 22q13 using nonparametric as well as parametric (autosomal dominant model) analyses. The study included 12 multiplex pedigrees with 135 individuals, among them 57 affected persons. A second genome scan is in progress investigating four families with 21 affected individuals, aiming to confirm linkage results. Age at onset patterns as well as the clinical outcome were similar among affected individuals in both sets of families. Within the pedigrees we observed no physical diseases segregating with periodic catatonia. Under the assumption of genetic homogeneity, the statistical power to detect LOD scores > or = 2.0 was 98.5% in the first set of families, and 57.9% in the second set. Thus, the panel of multiplex pedigrees segregating periodic catatonia seems to represent a homogenous clinical sample, and possesses sufficient statistical power to delineate and confirm linkage to major genetic loci for periodic catatonia.

Adult↗
PubMed2001

The many varieties of catatonia.

About 10% of patients with severe acute psychiatric illness exhibit a cluster of motor signs (mutism, negativism, rigidity, posturing, stereotypy, staring, etc.) that are identified as the syndrome of catatonia. Catatonia responds to sedative anticonvulsant treatment (barbiturates, benzodiazepines) and to electroconvulsive therapy. These treatments raise seizure thresholds. The commonality in response indicates that catatonia, malignant catatonia, neuroleptic malignant syndrome, toxic serotonin syndrome, delirious mania, catatonic excitement, benign stupor, and oneirophrenia are best evaluated as diverse manifestations of one syndrome for clinical and neuroscience research purposes.

Acute Disease↗
PubMed2001

Catatonia: syndrome or schizophrenia subtype? Recognition and treatment.

Two views of catatonia influence clinical practice. In the classical European view, adopted by DSM classifications, the signs of catatonia indicate a form of schizophrenia. In the syndromal view, the signs of catatonia are motor signs that are readily identified in many psychiatric disorders. Catatonia is a parallel behavior phenomenon to delusions (in thought) and delirium (in cognition). The syndromic view includes the neuroleptic malignant syndrome. It encourages a different treatment algorithm, the use of benzodiazepines and electroconvulsive therapy, to replace the customary use of antipsychotic drugs alone. The benefits of such treatment warrant the recommended change in concept and classification.

Catatonia↗
PubMed1987

Baclofen induces catatonia in rats.

Baclofen (10 and 20 mg/kg, i.p.) induced catatonia in rats within 10 min of its administration and the effect lasted for 3 hr. Muscimol (100 ng i.c.v. or 1 mg/kg, i.p.) as well as GABA (5 micrograms i.c.v.) potentiated the effect without producing any effect per se. Bicuculline, bromocriptine and scopolamine failed to modify the catatonia induced by baclofen, thereby ruling out the involvement of GABAA receptors, dopaminergic and cholinergic mechanisms. However, GABAB receptor antagonists, such as homotaurine and delta-amino-n-valeric acid, reversed the catatonia induced by baclofen in rats. Since baclofen is known to bind to a subpopulation of GABA receptors (bicuculline-insensitive) and baclofen-induced catatonia was susceptible to reversal by homotaurine and delta-amino-n-valeric acid, it is suggested that this effect could be mediated through GABAB receptors.

Animals↗
PubMed2006

The importance of catatonia and stereotypies in autistic spectrum disorders.

Motor disturbances are often observed in individuals with autistic spectrum disorders (ASDs) and recognized as diagnostic features of these disorders. The movement disorders characteristically associated with autism include stereotypies and self-injurious behavior. Yet, individuals with ASD may also be at the risk for catatonia. Although not as frequent as stereotypies, up to 17% of older adolescents and adults with autistic disorder may have severe catatonic-like symptoms. Catatonia may be a comorbid risk factor of autism that warrants further empirical and clinical evaluations. Clinicians may need to be attentive to more subtle signs of catatonic-like symptoms in individuals diagnosed with ASDs, especially as they enter adolescence and young adulthood. Stress has been implicated as a possible precursor for symptoms; however, its role has not been empirically proven as a potential risk factor. Clinicians might also need to assess for signs of significant declines in motor movements, as this appears to be a useful diagnostic indicator of catatonic-like symptoms. The literature on stereotypies and autism is more extensive than for catatonia and ASDs, probably because of the higher rate of stereotypies with autism. Explanations for the occurrence of stereotypies range from genetic to behavioral contingencies, with evidence for a multifactor explanation. Assessment measures often include items that assess for stereotypies to aid with diagnosing these symptoms in individuals with autism. Treatment for stereotypies is largely behavioral at the present time and requires consistent reinforcement of treatment gains to manage the symptoms successfully. An important area of future research in autism is the relation among different types of motor abnormalities, including stereotypies and catatonia.

Adolescent↗
PubMed2000

Right lower prefronto-parietal cortical dysfunction in akinetic catatonia: a combined study of neuropsychology and regional cerebral blood flow.

BACKGROUND: Catatonia is a psychomotor syndrome that can be characterized by behavioural, affective and motor abnormalities. In order to reveal further underlying pathophysiological mechanisms of psychomotor disturbances in catatonia we investigated neuropsychological function and regional cerebral perfusion (r-CBF) in a combined study. METHODS: Ten catatonic patients were investigated with Tc-99mECD brain SPECT and compared with 10 psychiatric (similar age, sex, medication and underlying psychiatric diagnosis but without catatonic syndrome) and 20 healthy controls. Neuropsychological measures included tests for general intelligence, attention, executive functions and right parietal visual-spatial abilities. Correlational analyses were performed between neuropsychological measures, catatonic symptoms and r-CBF. RESULTS: Catatonic patients showed a significant decrease of r-CBF in right lower and middle prefrontal and parietal cortex compared with psychiatric and healthy controls as well as significantly poorer performance in visual-spatial abilities associated with right parietal function. Correlational analysis revealed significant correlations between visual-spatial abilities and right parietal r-CBF only in psychiatric and healthy controls but not in catatonic patients. In contrast, attentional measures correlated significantly with motor symptoms, visual-spatial abilities and right parietal r-CBF in catatonia only but not in psychiatric or in healthy controls. CONCLUSION: Findings are preliminary but suggest right lower prefronto-parietal cortical dysfunction in catatonia, which may be closely related to psychomotor disturbances.

Adult↗
PubMed2001

Catatonia: an open prospective series with carbamazepine.

In view of reports in the literature that catatonia responds well to benzodiazepines, and the possible association between catatonia and seizure disorders, an open prospective study was conducted to explore the possibility that catatonia may be successfully treated with carbamazepine. Patients meeting DSM-IV criteria for catatonia were challenged with lorazepam IMI and their response assessed. Non-responders, partial responders and patients who had a recurrence of symptoms were put on a trial of carbamazepine and their response assessed. Nine patients were assessed at our unit. Six of the 9 had a complete, but transient response to lorazepam. All of the patients were given a trial of carbamazepine: 4 had a complete resolution of catatonic symptoms, 1 had a partial resolution and 4 patients did not show a significant improvement. Carbamazepine seems to be an effective treatment, both in the acute phase, and as maintenance in a subgroup of retarded catatonic patients.

Acute Disease↗
PubMed1997

Catatonia in an adolescent with Prader-Willi Syndrome.

Catatonia in children and adolescents has received little research attention. Treatment and course of catatonia in an adolescent patient with Prader-Willi Syndrome are presented. Clinical features of a small series of published case reports of catatonia in children and adolescents are reported. The association between catatonia, Prader-Willi Syndrome, and other neurodevelopmental disorders is discussed.

Adolescent↗
PubMed1999

A case of agitated catatonia.

Agitation is one of the diagnostic features of catatonia in the DSM IV classification, but permanent forms of agitated catatonia have occasionally been described. We report the case of a 43-year-old man who had already suffered from undifferentiated schizophrenia for 7 years, and in whom we diagnosed agitated catatonia. While our patient was being treated with a neuroleptic during a second episode of paranoia, a state of agitation was observed which persisted for a further 8 months. During this period, he was treated with several different neuroleptics and benzodiazepines, either alone or in association, without any improvement. No organic cause was found. He was then transferred to our electroconvulsive therapy (ECT) unit, with a diagnosis of schizophrenic agitation resistant to drug therapy. ECT was begun, and he was only given droperidol in case of agitation and alimemazine for insomnia, neither of which had any effect. In view of his persistent agitation without any purpose, echolalia and echopraxia, stereotyped movements with mannerisms and marked mimicking and grimacing, we diagnosed him as having agitated catatonia. After the fourth session of ECT, we decided to stop all treatment and gave him lorazepam at a dose of 12.5 mg daily. Twenty-four hours later, all symptoms of agitation had disappeared. In our opinion, permanent catatonic agitation is not rare. In our case, the neuroleptic treatment maintained and may even have worsened the symptomatology. Lorazepam can be used as a therapeutic test for this type of agitation, especially if it does not respond to neuroleptics. This also allows the patient to be sedated rapidly and effectively, thus preventing him from injuring himself further.

Adult↗
PubMed1996

Catatonia after benzodiazepine withdrawal.

The use of benzodiazepine medication is associated with a variety of acute and well-recognized withdrawal syndromes including anxiety, agitation, insomnia, and confusion. Catatonia has not previously been described. We report five patients who became catatonic after withdrawal of benzodiazepines. All five were older individuals (53-88 years) who had acutely become immobile, mute, and rigid with refusal or inability to eat or drink. Each of the five showed pronounced and rapid improvement after administration of low-dose lorazepam, which has previously been reported to be effective in the treatment of catatonia. Careful review of the records showed that each of the patients had been taking benzodiazepine medication for anywhere from 6 months to 15 years and that it had been rapidly tapered or abruptly discontinued 2 to 7 days before the onset of catatonia. These cases illustrate that severe and potentially life-threatening catatonia can develop in the wake of benzodiazepine withdrawal. Older individuals may be particularly vulnerable to this side effect.

Aged↗
PubMed2005

Catatonia in autism: a distinct subtype?

Catatonia is a life-threatening disorder characterized by motor abnormalities, mutism, and disturbances of behaviour, which is increasingly being diagnosed in persons with autism. In this report, we describe the presentation and course of catatonia in an adolescent with autism who responded to electroconvulsive therapy (ECT). The illness started with depressive symptoms, but the predominant feature was one of extreme obsessive slowing and immobility. We propose that catatonia should be ruled out as a cause of regression sometimes seen in adolescents with autism, and that catatonia of autism may index a distinct subtype with a particularly poor outcome.

Adolescent↗
PubMed2005

Catatonia: disappeared or under-diagnosed?

BACKGROUND: Over the last century, especially during the latter half, the prevalence of the diagnosis of catatonic schizophrenia decreased considerably. Several explanations for this phenomenon have been put forward. SAMPLING AND METHODS: The present study investigated the frequency of the diagnosis of catatonic schizophrenia in a large sample of admitted psychiatric patients (n = 19,309). In addition, the presence of catatonic symptoms was studied in a sample of patients with schizophrenia (n = 701) and in a group of consecutively admitted psychotic patients (n = 139). In these two groups the effect of the diagnostic procedures on the recognition of catatonia was examined. RESULTS: The diagnosis of catatonic schizophrenia dropped from 7.8% in 1980-1989 to 1.3% in 1990-2001 (p < 0.001). In addition, a possible under-diagnosis of catatonic schizophrenia was found in an independent sample of patients with schizophrenia. Application of a systematic catatonia rating scale in patients admitted with acute psychosis identified a bimodally distributed catatonic dimension. At least 18% of these patients fulfilled the criteria for catatonia. Interestingly, the catatonic subgroup used atypical antipsychotic compounds more frequently (p < 0.05). CONCLUSIONS: The results suggest that changes in diagnostic criteria and the diagnostic procedure itself are responsible for the under-recognition of catatonia.

Adult↗
PubMed1989

Benzodiazepines and catatonia: a case report.

The case history of a patient with presumed psychogenic catatonia who responded dramatically to two mg of IM lorazepam is presented. This patient, who had been largely mute and immobile for over a week despite neuroleptic therapy, became freely conversant and mobile within 30 minutes of the administration of lorazepam. This response was repeated the next day after the patient had again become mute and immobile. Catatonia and its diverse etiologies are discussed, with an emphasis on its syndromic nature. The literature on the response of catatonia to the benzodiazepines is reviewed and it is suggested that a trial of benzodiazepines may be helpful in both the evaluation and long term management of patients with catatonia.

Aged↗
PubMed1995

Karl Ludwig Kahlbaum's concept of catatonia.

Catatonia is a neuropsychiatric syndrome described by Karl Ludwig Kahlbaum in 1874. Based on Kahlbaum's own description and Carl Wernicke's hypothesis about the mechanism of catatonia, we describe two types of catatonic domain: the akinetic motality psychosis, which is characterized by rigid immobility, fixed gaze, lack of blink, and cogwheel rigidity, and catatonia sensu strictu, which is characterized by spasms, iterations and verbigerations. The loss of motility allows the 'hypobulic levels' described by Kretschmer in 1920, which consist of aggressive acts, furious shouting, hyperactivity and orality, to break through. These behaviours are present in the hyperkinetic variant of catatonia and may result from a reduction of dopaminergic innervation and the release of limbic and neocortical mechanisms containing behavioural programmes.

Catatonia↗
PubMed1999

Multiple sclerosis presenting as catatonia.

OBJECTIVE: Catatonic disorder due to general medical condition must be excluded in psychiatric patients presenting with this movement disorder. This report emphasizes the association of catatonia with multiple sclerosis. METHOD: A patient with catatonia, psychotic depression, and the subsequent diagnosis of multiple sclerosis is described and the literature reviewed. RESULTS: Mutism, immobility, cataplexy, waxy flexibility, and other aspects of catatonia occur in multiple sclerosis, usually as a consequence of a severe mood disorder and extensive cerebral demyelination. These symptoms may be the presenting manifestations of multiple sclerosis. CONCLUSIONS: A high index of suspicion for neurological disease is indicated in patients with new-onset catatonia. Neuroimaging and other studies may reveal underlying demyelination requiring specific therapy.

Adult↗
PubMed1995

Psychopathology of catatonic speech disorders and the dilemma of catatonia: a selective review.

OBJECTIVE: Over the past decade there has been an upsurge of interest in the prevalence, nosological position, treatment response and pathophysiology of catatonia. However, the psychopathology of catatonia has received only scant attention. Once the hallmark of catatonia, speech disorders--particularly logorrhoea, verbigeration and echolalia--seem to have been neglected in modern literature. The aims of the present paper are to outline the conceptual history of catatonic speech disorders and to follow their development in contemporary clinical research. METHOD: The English-language psychiatric literature for the last 60 years on logorrhoea, verbigeration and echolalia was searched through Medline and cross-referencing. Kahlbaum, Wernicke, Jaspers, Kraepelin, Bleuler, Kleist and Leonhard's oft cited classical texts supplemented the search. RESULTS: In contrast to classical psychopathological sources, very few recent papers were found on catatonic speech disorders. Current clinical research failed to incorporate the observations of traditional descriptive psychopathology. CONCLUSIONS: Modern catatonia research operates with simplified versions of psychopathological terms devised and refined by generations of classical writers.

Catatonia↗
PubMedDate not supplied

[Lethal catatonia: clinical aspects and therapeutic intervention. A review of the literature].

Lethal catatonia continues to occur and represents a nonspecific syndrome associated with diverse organic as well as functional conditions. From this perspective, neuroleptic malignant syndrome may be conceptualized as a neuroleptic-induced toxic or iatrogenic form of organic lethal catatonia. Neuroleptics appear ineffective in the treatment of lethal catatonia and should be stopped whenever this disorder is suspected. Existing data suggest that ECT is a safe and effective treatment for lethal catatonia. ECT also appears effective in the treatment of neuroleptic malignant syndrome.

Antipsychotic Agents↗