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PubMedDate not supplied

The switch mechanism in periodic catatonia and manic-depressive disorder.

Both in periodic catatonia and in manic-depressive disorders sudden switches occur in behavior, in the autonomic nervous system and in the catecholamine metabolism during the transition from interval or depression into catatonia or mania. Both the manic and the catatonic attacks seem to be superimposed on the basic depressive or schizophrenic illnesses. The attacks can be counteracted or suppressed by psychotropic drugs such as alpha-methyldopa, disulfiram, reserpine, haloperidol or chloropromazine which interfere with the catecholamine metabolism or their receptor sites. The involvement of the catecholamines may however be secondary to primary defects in the thyroid, the hypothalamus or the limbic system. The strict periodicity in periodic catatonia points to an accumulation of some active metabolite which may be produced centrally during the interval. At a certain level it may trigger the switch-mechanism and then be reduced during the catatonic phase. In periodic catatonia both the basic schizophrenic disease as well as the periodic manifestations are compensated by thyroxine-thyroid treatment.

Behavior↗

PubMed2006

[Benzodiazepines in the treatment of catatonia].

A patient who developed acute catatonia during benzodiazepine withdrawal is discussed. The case prompted us to review the literature on the role of benzodiazepines in the treatment of acute catatonia. Only retrospective and open studies were found which indicate that benzodiazepines do have a beneficial effect. Lorazepam is the most widely studied benzodiazepine and at present is the best treatment option. In the specific case of acute catatonia brought on by benzodiazepine withdrawal the recommended dosage is the same as for acute catatonia caused by something other than benzodiazepine withdrawal.

Anti-Anxiety Agents↗

PubMedDate not supplied

[Catatonia as an element of submissive behavior in mice during interspecies agonistic interactions].

A catatonia-like state was elicited in male mice with different experience of social interactions, by pinch of scruff of the neck in a suspended state. In submissive males with long experience of defeat the total time of catatonia reaction during test is considerably greater than in aggressive individuals with a long experience of victories. The change of the social status of the individuals resulting from agonistic interactions leads to a change of the catatonia reaction: manifestation of submissive behaviour is accompanied by an increase of total time of catatonia reaction in the test, the aggressive behaviour is accompanied by its decrease.

Aggression↗

PubMed1993

[Acute amphetamine intoxication with catatonia: a case report].

A marked increase of cases of amphetamine intoxication has been witnessed in Taiwan over the past two years, and poisoning accounts for the direct cause of death in some cases of them. We report a case of 30-year-old woman, who developed immobility, rigidity, mutism and staring after the intake of four grams of amphetamine powder. She initially had generalized twitching, but finally came to a state of total immobility. One hour after admission, apnea and cyanosis occurred suddenly and she died about half an hour later. Chronic amphetamine intoxication with catatonia has been reported in Japan, but acute amphetamine intoxication with catatonia has never been reported in the literature. In this report, we explore the possible mechanisms of catatonia in amphetamine intoxication and its clinical significance. Catatonia is supposed to be one of the poor prognostic signs of acute amphetamine intoxication that requires intensive care.

Acute Disease↗

PubMed1996

[Catatonia, malignant neuroleptic syndrome and myositis ossificans].

Lethal catatonia and the malignant neuroleptic syndrome represent two potentially fatal disorders that require different therapeutic regimens. Clinical differentiation is considered difficult because of a number of similarities with respect to mode of onset, signs and symptoms, and outcome. Recent observations emphasizing similarities between the two disorders, however, suggest that catatonia and the malignant neuroleptic syndrome may not represent separate diagnostic entities. Instead, the malignant neuroleptic syndrome has been hypothesized to be a neuroleptic-aggravated form of catatonia. In the present paper, we report the case of a 22-year-old male who developed different forms of malignant neuroleptic syndromes subsequent to a catatonic episode and overlapping it. In addition, the course was complicated by the occurrence of heterotopic calcification within skeletal muscles. The clinical value of diagnostic criteria that help distinguish catatonia from neuroleptic malignant syndrome and their therapeutic consequences are discussed.

Adult↗

PubMed1997

ECT treatment and cerebral perfusion in Catatonia.

A 40-yr-old woman with a diagnosis of schizoaffective disorder developed catatonia in the context of a depressive episode. A dramatic decrease in perfusion of the inferior frontal, posterior temporal and parietal lobes bilaterally and in posterior frontal lobes corresponding to the motor cortices was noted on the 99mTc-HMPAO SPECT scan obtained in the acute phase. The most dramatic decreases compared to normal control subjects were observed in the left parietal and left motor cortices. The patient was treated with a five-treatment course of electroconvulsive therapy (ECT), which resulted in a complete resolution of catatonia and some resolution of her symptoms of depression. The repeat HMPAO-SPECT scan showed improved perfusion in all areas. The most dramatic increases occurred in the left parietal and left motor cortices. Decreased perfusion in motor and parietal cortices could be state-specific to catatonia. Thus, SPECT imaging may be a useful method for monitoring catatonia treatment response.

Adult↗

PubMed1994

Triplet repeats in clinical subtypes of schizophrenia: variation at the DRPLA (B 37 CAG repeat) locus is not associated with periodic catatonia.

Clinical evidence for a dominant mode of inheritance and anticipation in periodic catatonia, a distinct subtype of schizophrenia, indicates that genes with triplet repeat expansions or other unstable repetitive elements affecting gene expression may be involved in the etiology of this disorder. Because patients affected with dentatorubral-pallidoluysian atrophy (DRPLA) may present with "schizophrenic" symptoms, we have investigated the DRPLA (B 37 CAG repeat) locus on chromosome 12 in 41 patients with periodic catatonia. The B 37 CAG repeat locus was highly polymorphic but all alleles in both the patient and control group had repeat sizes within the normal range. We conclude that variation at the DRPLA locus is unlikely to be associated with periodic catatonia. The evidence for dominant inheritance and anticipation as well as the high prevalence of human brain genes containing trinucleotide repeats justifies further screening for triplet repeat expansions in periodic catatonia.

Adult↗

PubMed2001

The pharmacological treatment of catatonia: an overview.

Over the past two decades, catatonia, particularly its acutely emerging akinetic-hypokinetic (stuporous) variant, has gradually regained its importance in descriptive psychopathology. Electroconvulsive therapy and lately benzodiazepines are not only effective treatment options in this form of catatonia, but also helped generate neurobiological hypotheses concerning its pathophysiology. Within this broad framework, this paper summarizes the results of recent benzodiazepine treatment response studies in catatonic movement disorders with particular reference to the authors' own studies in Chinese patients with catatonia.

Benzodiazepines↗

PubMed2000

hKCNN3 which maps to chromosome 1q21 is not the causative gene in periodic catatonia, a familial subtype of schizophrenia.

The human calcium-activated potassium channel gene (hKCNN3, hSKCa3) contains two tandemly arranged, multiallelic CAG repeats located in exon 1 which result in short to moderate polyglutamine stretches of unknown functional significance. Case-control and family-based association studies suggested an association of hKCNN3 repeats with susceptibility for schizophrenia. Twelve multiplex pedigrees with periodic catatonia, a schizophrenia subtype with major gene effect and patterns of anticipation, were genotyped using the multiallelic hKCNN3 repeat polymorphism. Using a dominant model of inheritance with sex- and age-dependent penetrance classes, cumulative results showed exclusion of linkage of hKCNN3 to periodic catatonia under the assumption of genetic homogeneity with lod score of -48.01 at zero recombination fraction. Our results provide evidence that hKCNN3 is not the causative gene in the familial schizophrenia subtype of periodic catatonia. By fluorescent in situ hybridization we confirmed the assignment of hKCNN3 to chromosome 1q21 near the heterochromatin region. Linkage mapping showed segregation with marker D1S498 (theta = 0.05) and placed hKCNN3 in the genetic linkage map in a cluster of genes near the centromeric region of chromosome 1.

Adult↗

PubMed1986

'Catatonia' produced by alfentanil is reversed by methylnaloxonium microinjections into the brain.

Alfentanil, a short-acting and powerful analgesic, when injected peripherally to rats (0.5 mg/kg) produced a catatonic state characterized by a rigid akinesia. The present study was designed to explore the neuroanatomical location of the opiate receptors mediating the alfentanil induced catatonia. The catatonic effect of alfentanil was measured using a bar test and depression of locomotor activity in rats tested in photocell cages during an active nocturnal phase of their cycle. Methylnaloxonium HCl (MN), a quaternary derivative of naloxone which does not readily cross the blood-brain barrier, injected into the lateral ventricle significantly reduced the catatonia at doses of 0.125-2.0 micrograms as measured in both the locomotor and bar test. MN perfusion of similar doses directly into the nucleus raphe pontis, but not in the caudate nucleus significantly antagonized the catatonia. These data complement results on alfentanil-induced muscular rigidity (Blasco et al., see companion paper) where EMG indices of rigidity in rats were reversed by microinjections of low doses of MN (0.125 and 0.5 microgram) in the nucleus raphe pontis, but not the caudate nucleus even at a high dose (4.0 micrograms). Together these results suggest that the region of the nucleus raphe pontis is an important neural substrate for opiate-induced muscular rigidity, and that the catatonic state produced by opiates depends on more diffuse opiate receptor activation of which one important component may be the nucleus raphe pontis.

Alfentanil↗

PubMed2005

Electroconvulsive therapy for malignant catatonia in childhood.

A 13-year-old female is described with presumed viral encephalitis, who developed progressive catatonia, agitation, and autonomic dysfunction. The diagnosis of malignant catatonia was made, and the patient improved with electroconvulsive treatment. This article discusses features, causes, differential diagnosis, and treatment of malignant catatonia. In children with this syndrome, electroconvulsive treatment should be considered.

Adolescent↗

PubMed2005

Catatonia induced by levetiracetam.

Levetiracetam (Keppra) is a novel antiepileptic drug approved as adjunctive treatment for adults with partial onset seizures. Although the drug is generally well tolerated, behavioral side effects have been reported in variable frequency. Most behavioral problems are mild in nature (agitation, hostility, anxiety, emotional lability, apathy, depression) and quickly resolve with discontinuation of medication. However, serious psychiatric adverse events may also occur with rare cases of psychosis and suicidal behavior. We report here the case of a 43-year-old woman who developed symptoms compatible with catatonia after being exposed to levetiracetam for the treatment of epilepsy. To our knowledge, it is the first reported case of catatonia induced by levetiracetam. We review the difficulties that may be encountered in the differential diagnosis of medical catatonia.

Adult↗

PubMed1997

Synergism of lorazepam and electroconvulsive therapy in the treatment of catatonia.

Electroconvulsive therapy (ECT) and lorazepam are effective treatments for catatonia. ECT combined with benzodiazepines has been associated with reduced efficacy and efficiency and therefore is not recommended in the routine practice of ECT. We report 5 prospectively identified cases of catatonia treated either sequentially or concurrently with lorazepam and ECT. In each case, the combination of lorazepam with ECT was superior to monotherapy. This apparent synergism, its possible mechanisms, and its implications for treating catatonia are discussed.

Adolescent↗

PubMedDate not supplied

The catatonia rating scale I--development, reliability, and use.

The study objective is to present reliability data on the Catatonia Rating Scale (CRS). The CRS is a 21-item clinician-administered rating scale. Items are individually defined and are scored from 0 (absent) to 4 (severe). A definition for each degree of severity is provided for each item. The diagnostic threshold for catatonia is 4 symptoms rated at least 2 (moderate). The CRS requires, at most, 45 minutes to administer. Reliability data were evaluated in a sample of 120 inpatients, 71 of whom were catatonic. Ratings were performed by 4 pairs of raters. Interrater reliability was high (Pearson correlation coefficient = .91 to .99, intraclass correlation coefficient = .94 to .99). Internal consistency was very good (Cronbach's alpha = .8890). Analysis of individual items showed that all were frequently endorsed and occurred across a wide range of severity. The CRS is a reliable rating scale for the diagnosis of catatonia. Advantages of the scale, areas of use, and clinical implications are discussed.

Adult↗

PubMedDate not supplied

Factor analysis of the catatonia rating scale and catatonic symptom distribution across four diagnostic groups.

Catatonia is a frequent psychomotor syndrome, which has received increasing recognition over the last decade. The assessment of the catatonic syndrome requires systematic rating scales that cover the complex spectrum of catatonic motor signs and behaviors. The Catatonia Rating Scale (CRS) is such an instrument, which has been validated and which has undergone extensive reliability testing. In the present study, to further validate the CRS, the items composing this scale were submitted to principal components factor extraction followed by a varimax rotation. An analysis of variance (ANOVA) was performed to assess group differences on the extracted factors in patients with schizophrenia, pure mania, mixed mania, and major depression (N=165). Four factors were extracted, which accounted for 71.5% of the variance. The factors corresponded to the clinical syndromes of (1) catatonic excitement, (2) abnormal involuntary movements/mannerisms, (3) disturbance of volition/catalepsy, and (4) catatonic inhibition. The ANOVA revealed that each of the groups showed a distinctive catatonic symptom pattern and that the overlap between diagnostic groups was minimal. We conclude that this four-factor symptom structure of catatonia challenges the current conceptualization, which proposes only two symptom subtypes.

Analysis of Variance↗

PubMed2006

Classification matters for catatonia and autism in children.

Despite its chequered history, Kahlbaum's 1874 description of catatonia (tension insanity) and its categorization as a clinical illness is in outline still valid. Kahlbaum also acknowledged the existence of catatonia in children. Corresponding case studies have also been analyzed. The originators and disciples of the Wernicke-Kleist-Leonhard school proved catatonia in early childhood as a discrete entity with specific psychopathology. This does not mean that catatonic symptoms do not occur in other illnesses and in particular in organic psychoses. These are, however, of a totally different nature. Autism, as first described in connection with schizophrenic negativism by Bleuler in 1910, is one of the key symptoms of schizophrenia. As identified by Kanner in 1943, abnormal social interaction and communication, together with retarded development, are the main characteristics of autism in early childhood. Asperger's concept of autistic disorder (1944), although based on psychopathological theory, did not include retardation in development as an aspect. Consequently, autistic behavior can occur in a variety of mental disorders. Research into possible etiological and pathogenetic factors has been undertaken, but no clear link found as yet.

Adolescent↗

PubMed1999

Impairment in visual-spatial function in catatonia: a neuropsychological investigation.

Catatonia is a psychomotor syndrome with motor and behavioral abnormalities which may be due to alterations in fronto-parietal cortical function. We therefore investigated neuropsychological tasks (attention, executive, visual-spatial, working memory) associated with frontal and parietal cortical function. Thirteen catatonic patients, diagnosed as catatonic according to criteria by Rosebush and Bush, were compared with 13 psychiatric non-catatonic controls (matched with regard to underlying psychiatric diagnosis, age, sex, and medication), and 13 age- and sex-matched healthy controls. Catatonics showed significantly poorer performances and different neuropsychological intercorrelation patterns in visual spatial object perception (VOSPobject) than psychiatric and healthy controls. In addition, we found significant correlations between catatonic symptoms, visual-spatial abilities, and attentional measures (i.e., d2, CWI). Catatonia was characterized by specific visual-spatial deficits which are related to attentional abilities and right parietal cortical function. The data suggest attentional-motor and fronto-parietal dysfunction in catatonia, a conclusion which should be considered as preliminary, however, due to the small sample size.

Adult↗

PubMed1995

Catatonia LSD induced?

The case of a patient who developed catatonia one week following Lysergic Acid Diethylamide (LSD) ingestion is presented. The psychosis developed two days after the intake. The catatonic syndrome resolved dramatically following one treatment of electroconvulsive therapy (ECT). This is perhaps the first case report of catatonia following the use of LSD. The need for a diagnostic category of organic catatonia is highlighted.

Adult↗