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PubMed1996

Baclofen-induced catatonia: modification by serotonergic agents.

Baclofen, a GABAB receptor agonist can induce catatonia in rats. This catatonia may serve as a tool for the study of GABAB receptor function. Reciprocal interactions between serotonin (5-HT) and GABAB receptors in the CNS are known to occur. In the present study we examined the effect of various agents that influence serotonergic neurotransmission on baclofen-induced catatonia in rats. The catatonia was rated by means of a scoring method, according to the severity of motor symptoms produced by baclofen (10-15 mg/kg, i.p.). All serotonergic drugs were injected intraperitoneally 30 min prior to baclofen, except the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA), which was injected 72 and 48 hr prior to baclofen. The 5-HT releaser fenfluramine (10 mg/kg) and the uptake inhibitor fluoxetine (10 mg/kg) reversed, whereas the 5-HT1A agonist buspirone (3 mg/kg) potentiated baclofen-induced catatonia. The 5-HT synthesis inhibitor PCPA (150 x 2 mg/kg), the non-specific 5-HT antagonist cyproheptadine (5 mg/kg), the 5-HT1A/1B antagonist pindolol (3 mg/kg) and the 5-HT2 antagonist sulpiride (20 mg/kg) enhanced baclofen-induced catatonia. It is concluded that the manipulations of central serotonergic mechanisms modulate baclofen-induced catatonia.

Animals↗
PubMed2006

A systematic examination of catatonia-like clinical pictures in autism spectrum disorders.

Three studies concerning catatonia-like clinical pictures in people with autism spectrum disorders (ASDs) referred to clinics are described. The first investigated the frequencies, in children and adults with autistic disorders, of 28 specific disorders of movement, speech, and behavior similar to those occurring in chronic catatonia spectrum conditions. The second compared the frequency of these items among groups of children with, ASDs, learning disabilities, specific language impairment, and a group with typical development, respectively. The third study examined the pattern of catatonia-like deterioration occurring in a minority of adolescents and adults with ASDs. The studies demonstrated the high frequency of catatonia-like features in people with autistic disorders. There was some tendency for improvement with increasing age, especially for those with IQ 70 or over. The items were also found in children with learning disabilities and specific language disorders but significantly less often. They occurred least often in the children with typical development. Severe catatonia-like deterioration occurred in 17% of those with autistic disorders, who were aged 15 years or over when assessed at a diagnostic center. A history of passivity in social interaction and impairment of expressive language were associated with the deterioration. No clear relationship was found between a history of catatonia-like features, singly or combined, and catatonia-like deterioration. The findings pose questions for future research.

Adolescent↗
PubMed2006

Is there a common neuronal basis for autism and catatonia?

Neuronal bases for autism and catatonia are unknown although integrative theories may soon become feasible as research in autism and catatonia advances. Catatonia and autism may both qualify as neurobiological syndromes in their own right. There is emerging evidence that catatonia may be a common syndrome in autism. Although the relation between autism and catatonia is unclear, coexpression of autism and catatonia may be due to abnormalities in common neuronal circuitries. This possibility constitutes another level of complexity to neurobiological inquiry, but also provides an opportunity to advance our understanding of both disorders. There is a great potential benefit in studying the relation between catatonia and autism in order to focus future research on subtype-specific causes and treatments. Future research avenues are outlined.

Autistic Disorder↗
PubMed2000

Catatonia in a psychiatric intensive care facility: incidence and response to benzodiazepines.

This study was performed to establish the incidence of catatonia in a psychiatric intensive care unit, to test the Bush-Francis Catatonia Screening Instrument (BFCSI) and to assess the response of catatonic signs to benzodiazepines. During a 12-month period all patients admitted to a psychiatric intensive care unit were screened for catatonic signs using the BFCSI. Patients with catatonia were further assessed with the Bush-Francis Catatonia Rating Scale (BFCRS), the Modified Rogers Scale (MRS), and scales for associated psychotic and parkinsonian symptoms. They were treated with oral lorazepam or parenteral clonazepam and their responses evaluated daily. Neuroleptics were stopped for at least 3 days. Twenty four patients met the DSM IV criteria for catatonia, giving an incidence of 15% with a significantly higher proportion of non-Europeans. The most common associated diagnosis was schizophrenia (54%). Twenty two patients completed the benzodiazepine trial. All showed significant responses after 3 days of treatment. Sixteen (16/22, 73%) had full remission within 6 days, most within 2 to 4 days. Partial responders (n = 6) all had schizophrenia and were more likely to have longer pre-trial catatonic episodes. We find the BFCSI a simple and reliable tool to screen for catatonia, and our data attest to the efficacy of benzodiazepines in the treatment of catatonia.

Adolescent↗
PubMed2006

Clozapine in schizophrenia patients with recurrent catatonia: report of two cases.

Prolonged catatonia can be a source of extremely serious morbidity and mortality. Lorazepam is effective in rapidly relieving most cases of catatonia. Reports have also shown that second-generation antipsychotic drugs are also efficacious in relieving catatonia. This report describes two schizophrenia patients who demonstrated recurrent catatonic features mutism and stupor. Both patients were treated with lorazepam, diazepam or electroconvulsive therapy (ECT). Patient 1 responded well and rapidly to lorazepam each time catatonia happened; but catatonia recurred once a year under treatment with many antipsychotic drugs. Patient 2 had catatonia features associated with discontinuing or decreasing clozapine. With each recurrent episode, the duration of catatonia increased, requiring an increased dosage of benzodiazepine. The patient's response to lorazepam and ECT gradually decreased, until the patient had almost no response to lorazepam, diazepam or ECT. Both patients had no recurrence during a period of 2-year follow up with continuous clozapine therapy.

Adult↗
PubMed2005

Drug-induced catatonia.

Catatonia is a heterogeneous syndrome that varies in etiology, presentation, course and sequelae. Initially conceptualized as a subtype of schizophrenia, catatonia is now recognized to occur not only with other psychiatric conditions but also with medical conditions and drug-induced and toxic states. While drug-induced catatonia is now a recognized entity, most studies club it with catatonia due to general medical conditions or organic catatonia, thus precluding any meaningful interpretation of such cases. The literature on drug-induced catatonia mostly draws from scattered case reports. This article attempts to review the available literature in this realm and integrate the information in an attempt to explore the epidemiology, etiology, mechanism and treatment of drug-induced catatonia.

Antidepressive Agents↗
PubMed2002

Role of adenosine in drug-induced catatonia in mice.

Parkinson's disease is one of the most common neurodegenerative disorders affecting large majority of population who are older than age of 65. Apart from dopamine, acetylcholine and glutamate, adenosinc has also been identified in the basal ganglia. Adenosine modulates the release of a variety of neurotransmitters including dopamine. In order to establish adenosine-dopamine interactions in drug-induced catatonia we studied the effect of adenosine in drug-induced catatonia in mice. In the present study adenosine dose dependently produced catatonia when assessed on rota-rod and bar tests in mice. Adenosine also potentiated the catatonic effect of perphenazine. L-dopa plus carbidopa or OR-486 (a potent centrally acting COMT inhibitor) completely reversed adenosine-induced catatonia. Since reversal by scopolamine of adenosine-induced catatonia was not to the same extent as with l-dopa and OR-486 it appears that catecholamines particularly dopamine rather than cholinergic modulation is more important in adenosine induced catatonia. The motor dysfunction (catatonia) could be easily assessed using rota-rod test apparatus in mice.

Adenosine↗
PubMed1998

Catatonia-like events after valproic acid with risperidone and sertraline.

A patient with schizoaffective disorder developed signs of catatonia while on a regimen of valproic acid, sertraline, and risperidone. The catatonic features evolved for the first time after a single dose of valproate and were alleviated by lorazepam. The same catatonic signs recurred after a second dose of valproate and again remitted after lorazepam. Catatonia did not recur subsequent to discontinuing valproate, and the patient had tolerated the combination of valproate and risperidone in the past without developing catatonia. Although the catatonia in this case initially appears to be paradoxical, the phenomenon is actually consistent with current models of catatonia. A unique drug interaction may account for this phenomenon. Possible pharmacokinetic and pharmacodynamic explanations are discussed, including the relation of catatonia to increased activity of the medial globus pallidus and current models of catatonia.

Adult↗
PubMed2006

Shared susceptibility region on chromosome 15 between autism and catatonia.

We have compiled significant linkage results from 20 genome scans for the autism syndrome disorder (ASD) and 2 for catatonia in schizophrenia (SZ). Localization of the markers has been updated across the studies using the same cytological (Genetic Location Database), physical (National Center for Biological Information), and genetic (Marshfield) maps. Eight autosomal chromosomes (1, 2, 3, 7, 9, 13, 15, and 17) showed significant linkages with ASD, and one with catatonia (15). Chromosome 15 was further characterized for SZ genome scans (N = 4) since catatonia was observed in SZ patients, for candidate genes for ASD and catatonia, and for the numerous chromosomal rearrangement and abnormalities associated to ASD. From these results, we observed that four potential susceptibility regions for ASD could be observed on chromosome 15 at 15q11-q13, 15q14-q21, 15q22-q23, and 15q26, respectively. All the four regions were shared between ASD and SZ, with 15q15-q21 being also shared with catatonia. Strong candidate genes, such as gamma-aminobutyric acid receptor B3, A5, and G3, have shown associations with ASD at 15q11-q13 susceptibility region where the majority of the chromosomal rearrangements are also found. On the other hand, negative association results were observed at 15q14-q21 susceptibility region for catatonia with the genes encoding the zinc transporter SLC30A4, the cholinergic receptor nicotinic alpha polypeptide 7, and the delta-like 4 Drosophila. Further, fine mapping and candidate gene analyses are needed to highlight potential common genes between ASD and catatonia for this chromosome.

Autistic Disorder↗
PubMed1999

Catatonia as a psychomotor syndrome: a rating scale and extrapyramidal motor symptoms.

BACKGROUND: Catatonia was first described by Kahlbaum as a psychomotor disease with motor, behavioral, and affective symptoms. In keeping with this concept, we developed a rating scale for catatonia (Northoff Catatonia Scale [NCS]) with three different categories of symptoms (i.e., motor, behavioral, affective). Furthermore, the question of the relationship among catatonic symptoms, extrapyramidal motor symptoms, and neuroleptics was addressed in the present study. METHOD: 34 acute catatonic patients and 68 age-, sex-, diagnosis-, and medication-matched psychiatric control subjects were investigated on days 0, 1, 3, 7, and 21 with the NCS, with other already validated catatonia rating scales by Rosebush, Bush (BFCRS), and Rogers (MRS), as well as with scales for hypokinetic (SEPS) and dyskinetic (AIMS) extrapyramidal motor features. Validity and reliability of the new scale, factor analysis, correlational analysis, and differences between catatonic patients and psychiatric control subjects were statistically calculated. RESULTS: NCS showed high validity (i.e., significant positive correlations [p <0.0001] with the other scales, significant differences between catatonic and control subjects), high intra-and interrater reliabilities (r = 0.80-0.96), and high affective subscores. Factor analysis revealed four factors best characterized as affective, hypoactive, hyperactive, and behavioral. Catatonic scores in NCS correlated significantly with AIMS on day 0 and SEPS on days 7 and 21. There were no significant differences in catatonic (i.e., NCS, MRS, BFCRS) and extrapyramidal (i.e., AIMS, SEPS) scores between neuroleptically treated and untreated catatonic subjects. CONCLUSIONS: The following conclusions were drawn: (1) the NCS has to be considered as a valid and reliable rating instrument for catatonia; (2) catatonia can be characterized by psychomotor symptoms encompassing motor, affective, and behavioral alterations; and (3) extrapyramidal hyperkinesias like dyskinesias are apparently closely related to catatonic symptoms which, in general, seem to be relatively independent of previous neuroleptic medication.

Acute Disease↗
PubMed2006

Catatonia in autistic spectrum disorders: a medical treatment algorithm.

Autism is a developmental syndrome with an unknown biology and inadequate therapeutics. Assessing the elements of the syndrome for the presence of depression, psychosis, mania, or catatonia, offers opportunities for systematic intervention. Since almost all descriptions of autism highlight the presence of motor symptoms that characterize catatonia, an assessment for this eminently treatable syndrome is recommended for all patients considered to be autistic. A minimum examination includes a catatonia rating scale and for those patients with defined catatonia, a lorazepam test. For those whose catatonia responds to lorazepam, high dose lorazepam therapy is recommended. If this fails, electroconvulsive therapy is recommended. The assessment and treatment of catatonia offers positive medical therapy for the victims of autism and their families.

Adolescent↗
PubMed2001

L-NAME precipitates catatonia during ethanol withdrawal in rats.

The effect of N(G)-nitro-L-arginine methyl ester (L-NAME), a non-specific inhibitor of nitric oxide (NO) synthase, on catatonia in ethanol dependent rats was investigated. Ethanol was given to rats by a modified liquid diet. An isocaloric liquid diet without ethanol was also given to control rats. L-NAME (50, 100 and 200 mg/kg) and saline were injected intraperitoneally to ethanol-dependent rats 30 min before ethanol withdrawal. Then, catatonia was evaluated by vertical wire test at the 30th min, 2nd, 4th and 6th h of ethanol withdrawal. The injections were repeated 30 min before the observation of 6 h. Locomotor activity was also recorded for 5 min in the same observation intervals. L-NAME (200 mg/kg) or saline were also injected to ethanol non-dependent control rats. L-NAME (50 and 100 mg/kg) inhibited both incidence and intensity of the audiogenic seizures which appeared at 6 h of ethanol withdrawal. L-NAME (200 mg/kg) produced a significant augmentation in both incidence and intensity of the catatonia in ethanol dependent rats. This dose of L-NAME also reduced the locomotor activity of both ethanol dependent and non-dependent rats. The locomotor inhibitory effect was more prominent in ethanol-dependent group. The catatonia precipitating effect of L-NAME was not prevented by L-arginine (1 g/kg, i.p.), a NO precursor, pretreatment. In the naive rats, L-NAME also did not produce catatonia. These results indicate that L-NAME has a catatonia precipitating effect during ethanol withdrawal in rats and this effect seems to be independent from NO mediated mechanisms.

Acoustic Stimulation↗
PubMed2006

Benzodiazepines in catatonia associated with systemic lupus erythematosus.

Neuropsychiatric disturbances are found in 50-70% of systemic lupus erythematosus (SLE) patients. However, there are rare cases of catatonia being described in SLE. Some studies have shown the effectiveness of high-dose steroid, plasma exchange and electroconvulsive therapy (ECT) in lupus catatonia. Herein are described two SLE patients with catatonia who had good response to i.v. diazepam (i.e. relief of catatonia symptoms). Patient 1, with mild cortical atrophy, had great improvement in catatonia symptoms on i.v. diazepam 150 mg during a period of 5 days. Patient 2, without cortical atrophy, had quick response to i.v. diazepam 10-20 mg. Both patients had no recurrence during 6-month follow up. In conclusion, benzodiazepines may play an important role in the treatment of catatonia associated with SLE if patients refuse ECT treatment.

Adult↗
PubMed1993

Idiopathic catatonia: validity of the concept.

Although catatonic features can be seen in various psychiatric and organic disorders, some patients with catatonia cannot be fitted into existing classification systems. In the current study various sociodemographic and clinical variables were compared between patients who presented with catatonia only (idiopathic catatonia), or with catatonia as a symptom of an identifiable underlying functional disorder. Patients seen over one year (1988) were classified into idiopathic catatonia (n = 30) and according to diagnosis (n = 35; schizophrenia n = 19, depression n = 16). There was an excess of females in the idiopathic group and the illness was of a shorter duration. There were no other differences between the groups. All subjects showed good response to ECTs and required almost the same mean number of ECTs. No clusters were observed using the average method. The current study suggests that catatonic symptoms can occur in the absence of any other identifiable psychiatric syndrome, although they cannot be otherwise differentiated from other psychiatric syndromes in which catatonia can present.

Adult↗
PubMed1995

Periodic catatonia: a schizophrenic subtype with major gene effect and anticipation.

In a family study involving 139 probands with DSM-III-R catatonic schizophrenia and 543 first-degree relatives, we investigated age-specific morbidity risk according to Leonhard's clinical distinction between systematic and periodic catatonia. This dichotomy is based on different types of symptomatology, course, and outcome. In systematic catatonia the age-corrected morbidity risk was 4.6%. In periodic catatonia, however, there was an age-corrected morbidity risk with homogenous psychoses of 26.9%, and more parents than siblings were affected. This points strongly to a major gene effect in periodic catatonia. Furthermore, a pairwise comparison of patients and their parents revealed patterns of anticipation, i.e., the probands' age at the onset of disease was significantly earlier than that of their parents (P < 0.001). Similarly, anticipation was apparent in pedigrees with three successive generations affected. This inheritance pattern with homogenous psychoses and anticipation indicates that genes with trinucleotid repeat expansion or other repetitive elements affecting gene expression may be involved in the etiology of periodic catatonia. Thus, periodic catatonia as a specific clinical subtype of schizophrenia is a promising candidate for molecular genetic evaluation.

Adult↗
PubMed2001

Classification issues in catatonia.

Kahlbaum described catatonia as a disorder in which mood syndromes were the primary features and the characteristic symptoms were the motor signs. In the present study, we examined the relationship between motor features and other syndromes of psychosis, the clinical validity of Kahlbaum's concept of catatonia, its relationship to schizophrenia and mood disorder, and its nosological position in relation to DSM-III-R, DSM-IV and Leonhard's classification of endogenous psychoses. Patients with Kahlbaum's catatonia differed from patients with schizophrenia or mood disorder in various demographic and clinical variables. Positive and negative motor syndromes, although interrelated, showed a different correlational pattern with other psychotic syndromes. Catatonia did not appear to fit into any particular nosological category, although this issue largely depends on whether schizophrenia and mood disorders are broadly or restrictively defined. When definitions are more restrictive as in Leonhard's system, catatonia seems to be better accommodated as a "third psychosis", i.e. described by the concept of cycloid psychosis.

Affective Disorders, Psychotic↗
PubMed2001

The different conceptions of catatonia: historical overview and critical discussion.

The present article outlines the different conception of catatonia from its initial description by Kahlbaum to current viewpoints. Originally considered to be an independent disease entity characterized by mental and motor abnormalities, catatonia was later viewed as a subtype of schizophrenia as it is the case in current classifications like ICD-10 and DSM-IV. Since catatonic symptoms were observable not only in schizophrenic psychoses, but also in affective, somatic or even psychogenic disorders, many researchers today consider catatonia as a nosologically unspecific syndrome. In the end, the traditional conceptions did not succeed in defining catatonia as a clinically homogeneous and valid diagnosis. An independent conception was elaborated by the Wernicke-Kleist-Leonhard school of psychiatry. Based on a precise differentiation of psychomotor disturbances, two essentially different forms of catatonic psychoses have been separated, systematic and periodic catatonias which differ in symptomatology, prognosis and treatment.

Catatonia↗
PubMed2005

The use of atypical antipsychotics in the treatment of catatonia.

PURPOSE: Evidence indicates that classical antipsychotics may aggravate non-malignant and malignant catatonia (MC). Atypical antipsychotics are less likely to cause movement disorders than classical antipsychotics and they are being frequently prescribed in disorders that can be associated with catatonia. Therefore, the important question that arises is whether atypical antipsychotics have a role to play in the treatment of catatonia. MATERIALS AND METHODS: A Medline search was performed to locate papers on the use of atypical antipsychotics in catatonia published between 1970 and 31st December 2004. RESULTS: The literature on the use of atypical antipsychotics in catatonia consists of case reports and retrospective studies. In most cases of non-MC a reduction of the catatonic symptoms is reported upon treatment with atypical antipsychotics. Cases of MC relate mainly to the neuroleptic malignant syndrome (NMS), which is considered as an iatrogenic stuporous variant of MC caused by antipsychotics. CONCLUSION: There are indications that atypical antipsychotics may be useful in non-MC. As a consequence, one should not only focus on the possible extrapyramidal and autonomic side effects of these drugs, but also on the possible beneficial effects on certain brain functions and on the catatonic symptomatology. However, randomized controlled trials are needed to evaluate the effect of these drugs, and caution is advisable, since cases of NMS have been linked to treatment with atypical antipsychotics. There is no evidence to prescribe atypical antipsychotics in MC.

Antipsychotic Agents↗