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PubMed2006

Blueprints for the assessment, treatment, and future study of catatonia in autism spectrum disorders.

The blueprints for the assessment, treatment, and future study of catatonia in autism spectrum disorders (ASDs), which are submitted in this chapter aim to increase early recognition and treatment of catatonia in ASDs, show the urgency of controlled treatment trials, and increase collaborative and interdisciplinary research into the co-occurrence of these two enigmatic disorders. Catatonia should be assessed in any patient with ASDs when there is an obvious and marked deterioration in movement, pattern of activities, self-care, and practical skills, compared with previous levels, through a comprehensive diagnostic evaluation of medical and psychiatric symptoms. A formal diagnosis should be ascertained using ASD specific criteria for catatonia that takes into account baseline symptoms like muteness, echophenomena, stereotypy, negativism, or other psychomotor abnormalities. Any underlying medical and neurological conditions should be treated, and culprit medications or other substances that may cause catatonia should be eliminated. Separate treatment blueprints are presented for mild, moderate, and severe catatonia, featuring combinations of a psychological approach developed by Shah and Wing and medical treatments that have shown efficacy in catatonia: lorazepam challenge, lorazepam trial, lorazepam continuation, and bilateral electroconvulsive therapy (ECT). These treatment modalities in themselves are well established. Side effects and complications are known and manageable. Legal, ethical, and practice guidelines governing all treatment aspects should be followed. The treatment blueprints should be viewed as best estimates pending future controlled studies. The blueprint for the future study of catatonia in ASDs describes promising clinical and preclinical research avenues. Longitudinal studies need to assess the possible effect of early recognition and adequate treatment of catatonia in ASDs in order to avoid the impairment associated with chronicity. Effects of current and new anticatatonic treatments should be examined in experimental models of autism and catatonia. Finally, the role of gamma-aminobutyric acid (GABA) dysfunction in autism, catatonia, and abnormal stress responses in these disorders should be further assessed.

Adult↗
PubMed2004

Autism as early expression of catatonia.

BACKGROUND: Reports indicate that catatonia often occurs in autism. The association lacks a conceptual basis. Modern classificatory schemes define autism and catatonia separately and are not conducive to study areas of overlap. The exploration of the relation between autism and catatonia may be important because autism is increasingly recognized but effective treatments are lacking. Catatonia, on the other hand, is thought to be treatable, but is poorly recognized. MATERIAL/METHODS: The literature on autism and catatonia are reviewed to identify areas of overlap. A hypothesis is formulated that, in some cases, autism may the early expression of catatonia. RESULTS: Several areas of overlap between autism and catatonia are found. Catatonic symptoms are common in autism. Effects of anti-catatonic treatments on autistic symptoms are unknown. Abnormal gamma-aminobutyric acid (GABA) function has been implicated in both disorders. Neuroimaging studies show small cerebellar structures in both disorders. There is genetic evidence that susceptibility genes for autism and catatonia are located on the long arm of chromosome 15. Differences between autism and catatonia of age-of-onset, symptoms, and illness course, do not exclude a common genetic etiology. CONCLUSIONS: Focused research is needed to further evaluate the phenomenological, biological, and genetic overlap between autism and catatonia and to test the hypothesis that a subgroup of autism is early-onset catatonia.

Adolescent↗
PubMed2025

Systematic Review of Symptoms of Catatonia in Autism Spectrum Disorder.

Catatonia is a complex neuropsychiatric syndrome characterized by disturbances in mood, motor function, behavior and speech. It is increasingly recognized in individuals with autism spectrum disorder (ASD), although its identification remains challenging due to the overlapping clinical features of the two conditions. Shared characteristics, such as echophenomena, mannerisms, social indifference and repetitive behaviors can obscure accurate diagnosis. Although reports suggest a significant prevalence of catatonia among individuals with ASD, the condition remains poorly understood and frequently under recognized, leading to substantial diagnostic and treatment challenges. A systematic review was conducted to characterize the symptoms of catatonia in individuals with ASD. The literature search included peer-reviewed journal articles published in English from 1980 onward, focusing on studies examining co-occurring catatonia and ASD. A qualitative framework analysis was implemented to evaluate 45 peer-reviewed studies, with findings interpreted in relation to, and extending beyond, the diagnostic criteria for catatonia outlined in the International Classification of Diseases, 11th revision (ICD-11). The objective was to identify symptom patterns extending beyond current diagnostic frameworks and to support improved clinical recognition and diagnostic precision in ASD populations. The review identified six primary symptom clusters associated with catatonia in individuals with ASD: (1) psychomotor activity, (2) speech disturbances, (3) changes in behavior/skills/functions, (4) mental health symptoms, (5) physiological symptoms, and (6) symptoms related to arousal and awareness. Notably, several symptoms observed within these clusters are not currently included in the ICD-11 diagnostic criteria for catatonia. These additional symptoms include tics, motor compliance, incoherent speech, self-injury, impaired cognition, and appetite changes, suggesting a broader clinical presentation of catatonia in ASD populations than is presently captured in existing diagnostic frameworks. The findings of this review highlight the significance of enhancing clinicians' awareness and understanding of how catatonia manifests in individuals with ASD. Most notably, six symptom clusters, psychomotor changes, speech disturbances, behavioral and functional regression, affective and psychiatric symptoms, physiological symptoms, and arousal/awareness disturbances, were observed. Several symptoms identified in this review are not included in the current diagnostic criteria, and their recognition may facilitate in earlier identification and timely intervention, potentially preventing the severe consequences of untreated catatonia in this population.

Humans↗
PubMed1998

Serum iron in catatonia and neuroleptic malignant syndrome.

BACKGROUND: Preliminary data suggest that decreased serum iron levels predict the progression of catatonia to neuroleptic malignant syndrome (NMS). This study examines the predictive value of low serum iron in this NMS conversion and explores other potential significance of serum iron in catatonia. METHODS: Fifty patients with catatonia were prospectively identified at two psychiatric intensive care units during a 3-year period [incidence of 5% (39/716) and 13% (11/86) respectively]. Serum iron was measured in 39 episodes. Seventeen episodes (44%) showed low serum iron levels. A retrospective chart review of patients identified was conducted, comparing those with low and normal serum iron levels. RESULTS: Low serum iron levels were associated with malignant catatonia, excited catatonia, and poor responses to benzodiazepines. There were 7 episodes of malignant catatonia. All had low serum iron. Neuroleptic were used in 5 of them, and all 5 evolved into NMS. No such NMS conversion was noted in those with normal serum iron or in nonmalignant catatonia with low serum iron. Seven episodes (with low serum iron) failing benzodiazepine therapy responded subsequently to lithium-neuroleptic combination therapy. CONCLUSIONS: Malignant catatonia, associated with low serum iron, is at high risk of evolving into NMS. Low serum iron in nonmalignant catatonia does not predict this NMS conversion. Excited catatonia as a catatonic subtype (associated with low serum iron and unfavorable benzodiazepine responses) deserves more research attention. There appears to be a possible connection between treatment resistance to benzodiazepines, favorable responses to lithium-neuroleptic combination, and low serum iron.

Adolescent↗
PubMed2005

Presentation and frequency of catatonia in new admissions to two acute psychiatric admission units in India and Wales.

BACKGROUND: There are no modern cross-cultural comparative studies of the frequency and clinical presentation of catatonia in a Western country and India using standardized rating instruments and diagnostic criteria. METHOD: A total of 104 consecutively admitted patients in Wales and in India were screened for catatonic features using the same standardized rating instrument by the same psychiatrist to generate DSM-IV and other diagnostic criteria for catatonia, and a profile of signs in catatonia. Inter-rater reliability for the ratings made by the research psychiatrist was established with local psychiatrists at each unit. RESULTS: The frequency of DSM-IV criteria catatonia was 13.5% in India versus 9.6% in Wales ( N . S .). The severity of catatonia did not differ between the two units. However, retarded catatonia was more common in India (12.5%) versus Wales ( p <0.05) whereas the frequency of excited catatonia was equally common in both units. Catatonia was found in many different mental disorders not just schizophrenia and affective disorder. CONCLUSIONS: Catatonia is commonly found among psychiatric in-patients with a similar frequency and severity but differing clinical presentations in Wales and India. Some classic signs of catatonia like posturing, catalepsy, staring and stupor were more frequent among psychiatric admissions in India than Wales. The differing clinical presentations may be due to differences in demographic features rather than cultural or aetiological factors.

Catatonia↗
PubMed2003

Catatonia in childhood and adolescence.

Child and adolescent catatonia has been poorly investigated. A literature review was undertaken to clarify phenomenology, diagnosis, etiology, and treatment as well as ethical problems of catatonia in childhood and adolescence. Although there are no accepted standardized criteria for catatonia in childhood and adolescence, catatonic features described by child psychiatrists are similar to Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV) criteria for catatonia. With respect to etiology, the motor and behavioral symptoms that are part of catatonia bear some similarities with those seen in autism. Several case reports suggest an association between catatonia and general medical conditions. Certain drugs abused by youngsters as well as prescribed medicine can induce catatonia. Regarding catatonic cases originally diagnosed as schizophrenia, it is unclear whether all of these cases should be identified as schizophrenia or whether some of them are pervasive developmental disorders that develop psychic features in adolescence. Environmental changes preceding the onset of catatonia in patients with mood disorder play a possibly important role. Examples that suggest stress-induced catatonia, although rare, also exist. A few patients exhibit features of malignant catatonia, some without taking neuroleptics and others having taken them. Benzodiazepines and electroconvulsive therapy are considered to be effective treatments for catatonic youngsters.

Adolescent↗
PubMed1994

Malignant catatonia.

The authors review catatonia, especially malignant catatonia, suggest a revised nomenclature, and establish a basis for furthering our understanding and treatment of this syndrome. After a brief historical review of catatonia, they review all available recent (1986-1991) English-language reports on malignant catatonia and summarize 5 cases of psychiatric malignant catatonia seen at their institution. Although much has been written about malignant catatonia "due to neuroleptics," malignant catatonia caused by other factors has received less attention, hindering our ability to recognize and treat non-neuroleptic-induced malignant catatonia. Catatonia, including malignant catatonia, occurs infrequently, but recognition and management are essential with a syndrome that can be life-threatening.

Adolescent↗
PubMed1997

Catatonia and other motor syndromes in a chronically hospitalized psychiatric population.

BACKGROUND: To determine the motor characteristics of chronic catatonia, catatonia and other motor disorders were systematically rated in a long-term hospitalized sample. METHOD: Chronically hospitalized psychiatric inpatients (N = 42) with a clinical diagnosis of catatonic schizophrenia (295.2X) were rated for catatonia with a novel 23-item catatonia rating scale, and for parkinsonism, dyskinesia and akathisia using standard rating scales with scale-based criteria for case definition. RESULTS: Catatonia was the sole motor syndrome in nine cases (21%), co-existed with parkinsonism in five (12%), tardive dyskinesia in four (10%), and both parkinsonism and tardive dyskinesia in 10 (24%). There was no correlation between total scores across the four rating scales. 'Rigidity' was the sole catatonic sign which overlapped with other scales. The symptom profile of catatonia in this chronic sample was similar to previous reports based on acutely ill patients. CONCLUSION: Catatonia is distinguishable from other motor disorders in chronic psychiatric patients using the 23-item catatonia rating scale. The features of chronic catatonia are described, and the distribution of catatonic signs is similar for chronic and acute catatonia.

Adult↗
PubMed2006

Catatonia in individuals with autism spectrum disorders in adolescence and early adulthood: a long-term prospective study.

The objective is to cast light on diagnosis and catastasis, course, and comorbidity as concerned with catatonia in patients with autism spectrum disorders (ASDs) with respect to long-term prospective follow-up. Eleven patients (all male) were enrolled. The mean age and the mean follow-up duration were 27.6 years (standard deviation (SD) 5.5) and 18.7 years (SD 8.7), respectively. The mean IQ was 27 (SD 16.4). Information was garnered from medical case records; current examination and observation of patients, interview of parents, and questionnaires completed by parents or other caretakers. Informed consent was obtained from the parents. Criteria for catatonia in this study were: (1) abrupt stop of movements and maintenance of immobility or bizarre posture beginning in adolescence and early adult life, (2) such a cataleptic state had continued for at least several minutes and appeared many times a day to the point of interfering with daily activities. We described two typical catatonic cases of ASDs. The average onset age was 19 years (SD 6). In all cases, our diagnostic criteria of catatonia evaluating at worse are fully compatible with those of Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-VI). In 8 out of 11, the onset of catatonia was clearly preceded by the appearance of slowness in movements accompanying the exacerbation of obsessive-compulsive symptoms. Catatonia was also found to have some connection with Tourette syndrome (3 cases), adjustment disorders (N=1), and depressive mood disorders (N=1). In one case, the manifestations of catatonia had to be distinguished from parkinsonism caused by antipsychotics. Catatonia in ASDs seems to be a chronic condition in most cases. However, there were also a few cases in which catatonia repeatedly aggravated over short spans of time. Catatonia in ASDs may be considered an epiphenomenon of ASDs or a manifestation of comorbidity in adolescence or early adulthood.

Adolescent↗
PubMed1991

Catatonia in autistic disorder: a sign of comorbidity or variable expression?

Catatonia, once solely attributed to schizophrenia, is now thought to be associated with many disorders. Autistic disorder shares some symptoms with catatonia, namely, mutism, echopraxia/echolalia, and sterotypes. Catatonia in autism may therefore be a variant of the autistic condition. However, organic deficits and psychiatric disorders, such as bipolar disorder, have also been deficits and psychiatric disorders, such as bipolar disorder, have also been linked with the manifestation of catatonia. Individuals with autism presenting with these comorbid conditions may therefore be at increased risk for catatonia. Little is written of the association of autism and catatonia to clarify the possibility of catatonia as a variant or a sign of a comorbid condition. The authors discuss three autistic patients and suggest specific etiologies for the symptoms of catatonia which presented in these cases. The therapeutic and diagnostic importance of comorbid disorders in autism is stressed.

Adult↗
PubMed2002

Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology.

Catatonia was originally described as a psychomotor syndrome in the 19th century by Kahlbaum including motor, affective and behavioral symptoms. Later, at the beginning of the 20th century, catatonia was rather considered as the motoric manifestation of schizophrenia. Accordingly, neuropathological research focused predominantly on those neuroanatomical substrates, i.e. the basal ganglia being primarily involved in the generation of movements. Even though some authors observed minor alterations in the basal ganglia, consistent findings in these subcortical structures could not be obtained. Since neuroleptics can induce catatonic-like symptoms i.e. neuroleptic malignant syndrome (NMS), there has been a recent re-emergence in clinical and scientific interest in catatonia. However, exact psychopathological and pathophysiological characterization of both NMS and catatonia remains unclear.Clinically, catatonia and NMS show more or less similar motor symptoms i.e. akinesia. These may be accounted for by dysregulation in cortical-subcortical circuits between motor/premotor cortex and basal ganglia i.e. the so-called "motor loop". While in NMS the "motor loop" may be dysregulated by neuroleptic blockade of subcortical striatal D-2 receptors one may rather assume cortical gaba-ergic alteration in catatonia. The premotor/motor cortex and consecutively the "motor loop" may be dysregulated by gaba-ergic abnormalities in orbitofrontal cortex. Gaba-ergic cortical dysfunction may account for affective and behavioural abnormalities in catatonia which cannot be observed as such in NMS. Consequently, one may characterize catatonia as a cortical "psychomotor syndrome" while NMS may rather be regarded as subcortical "motor syndrome".

Catatonia↗
PubMed2002

Exposure to prenatal infections, genetics and the risk of systematic and periodic catatonia.

The meaning of heterogeneity in schizophrenia and the impact of genetic and environmental factors on etiology are a matter of continuous debate in psychiatric research. Different clinical and birth history variables were investigated in a sample of 68 patients with chronic catatonic schizophrenia according to DSM III-R, classified into Leonhard's systematic schizophrenia (n = 32) and periodic catatonia (n = 36). Parental transmission of the disease was evident in 44% of the periodic catatonia cases compared to one case in systematic catatonia (3%; p = 0.0003). In systematic catatonia, 34% of the index cases were exposed to prenatal infections compared to 8% in periodic catatonia (p = 0.008). Using logistic regression analysis exposure to gestational maternal infections predicted diagnosis of systematic catatonia at p = 0.008, and parental psychosis predicted diagnosis of periodic catatonia in the index cases at p = 0.0001. The latter finding is substantiated by the recent mapping of a periodic catatonia-susceptibility locus on chromosome 15q15 with evidence for autosomal dominant transmission. These findings support the hypothesis that distinct schizophrenia phenotypes are based on different etiological mechanisms.

Adult↗
PubMed2006

Case reports with a child psychiatric exploration of catatonia, autism, and delirium.

This chapter starts with some remarks on the conceptual history of catatonia, which begins with Kahlbaum and continues with Kraeplin, Bleuler, and Leonhard. The Diagnostic and Statistical Manual, 4th ed., Text Revision, criteria for catatonia and the multicausal origin of the disorder are discussed. So, not only schizophrenia and mood disorders associated with catatonia, which is the primary form, are introduced but also an extensive list of somatic disorders-resulting in secondary catatonia-along with the work of Gelenberg and Wing. Next, two very difficult cases, of boys with autism, catatonia, and one of them with mental retardation as well, are presented. Major textbooks, PubMed, and Medline were used for a select literature search. The results show the main and really relevant but scarce data concerning primary and secondary catatonia. In the discussion the topics are this dearth in knowledge, the concept of catatonia and its similarities with delirium, and the relation catatonia-autism, and where to find the data. The conclusions summarize the main points and end with a gentle reminder, or is it an appeal?

Adolescent↗
PubMed2001

ECT for prolonged catatonia.

OBJECTIVE AND BACKGROUND: Electroconvulsive therapy (ECT) is highly effective for acute catatonia but its use in prolonged catatonia is not well established. We report three cases of prolonged catatonia with medical complications or comorbidities treated by ECT. METHOD: Case reports. RESULTS: A 24 year-old woman developed fever and autonomic instability after parenteral neuroleptics. Catatonia and autonomic signs persisted for 14 weeks. After minimal improvement from lorazepam, 15 bilateral ECTs led to resolution. A 26-year-old woman with a history of lupus erythematosus, complicated by lupus cerebritis with lesions in the cortex and basal ganglia and a communicating hydrocephalus, was catatonic for 9 weeks. Lorazepam produced marginal improvement. A series of 14 bilateral ECTs led to improved mobility, speech, and interaction, but the response was less robust than Case 1. A 40-year-old man with mental retardation and intermittent psychosis developed severe neuroleptic malignant syndrome and remained catatonic for 4 months. After lorazepam produced minimal improvement, his catatonia resolved with 20 bilateral ECTs. CONCLUSIONS: ECT may improve prolonged catatonia with complex medical comorbidities, but may require many treatment sessions. Gross cerebral pathology may predict a less robust response. As for acute catatonia, ECT may resolve prolonged catatonia after benzodiazepines have failed.

Adult↗
PubMed2001

Emergence of catatonia during ECT.

Emergence of catatonia during electroconvulsive therapy (ECT) is unexpected, as catatonia responds well to ECT. We report four cases with onset of catatonia during ECT. Four inpatients with affective disorders (three without prior catatonia) developed catatonia by Bush-Francis criteria during a course of ECT. All four patients had been taking benzodiazepines, which were stopped 5-15 days before ECT. Two became catatonic after ECT no. 4, one after ECT no. 1, and one after ECT no. 10. The episodes of catatonia resolved promptly with the resumption of benzodiazepines. Two patients completed a course of ECT, whereas two received neuroleptics and/or antidepressants without further ECT. All showed improvements in their affective and psychotic symptoms. The cases illustrate the appearance of catatonia during a course of ECT and suggest recent cessation of benzodiazepines as a risk factor. Benzodiazepines relieve the catatonia, and ECT may be continued.

Adult↗
PubMed1996

Catatonia in depression: prevalence, clinical correlates, and validation of a scale.

OBJECTIVES: To examine the clinical correlates of catatonia in depression, to validate a scale for catatonia, and to assess the validity of the DSM-IV criteria of the catatonic features specifier for mood disorders. METHODS: A series of 79 consecutive patients with depression and 41 patients with Parkinson's disease without depression were examined using the modified Rogers scale (MRS), the unified Parkinson's disease rating scale (UPDRS), and the structured clinical interview for DSM-III-R (SCID). RESULTS: Sixteen of the 79 depressed patients (20%) had catatonia. Depressed patients with catatonia had significantly higher scores on the MRS than non-catatonic depressed patients matched for severity of depression, or non-depressed patients with Parkinson's disease matched for severity of motor impairment. Depressed patients with catatonia were older, had a significantly higher frequency of major depression, more severe cognitive impairments, and more severe deficits in activities of daily living than depressed non-catatonic patients. The DSM-IV criteria of catatonia separated depressed catatonic patients from patients with Parkinson's disease matched for motor impairment, with a specificity of 100%. Catatonic signs did not improve after apomorphine. CONCLUSIONS: catatonia is most prevalent among elderly patients with severe depression. The study showed the validity of the MRS for the diagnosis of catatonia in depressed patients, as well as the specificity of the DSM-IV criteria of the catatonic features specifier.

Aged↗
PubMed1998

[A study on late catatonia--the psychopathological study of its symptoms, courses, subtypes, and treatments].

It was discussed at the beginning of this century whether to categorize "late catatonia" in "manic-depressive disorder", in "schizophrenia", or to consider itself as another clinical entity. Sommer was the first to make a clinical report on "late catatonia"; however Kraepelin had reported on cases with very similar symptoms prior to Sommer, and called them "involutional melancholia" or "presenile psychosis". Followed by a couple of decades, Jacobi's clinical report gave "late catatonia" the impressions as having a very poor prognosis. It was then stated by M. Bleuler that approximately 30% of "late schizophrenia" was well-fitted into "late catatonia". According to Huber who carried out a survey utilizing the same criterion for "late schizophrenia" some 30 years later, no such concordance was found. Hence, it may be said that some kind of change in symptoms has occurred. Symptom-transitions of 16 "late catatonia" subjects were analysed in detail. "Late catatonia" is a symptomatic concept with characteristic progressive symptoms: Stage 1 (prodrome and primary depression), Stage 2 (anxiety, irritation), Stage 3 (hallucination, delusion), Stage 4 (catatonia), and the residual stage. "The complete type" which progresses to Stage 4 stepwise, may end up developing "malignant catatonia". In this case, it may be life threatening unless suitable treatment is carried out. This disease may be divided into 2 types of clinical courses; a multi-phasic course with intermittent remission, and a mono-phasic course which is chronic. Transition to the residual stage may occur at any point. In practice, there are 3 other subtypes; these three are called "the abortive types" (anxious/irritated type, depressive/delusional type, residual type). These cases are most typically considered as depression with severe anxiety and irritation, and in case flattening of affect becomes the major symptoms, it is often misdiagnosed as "organic dementia". Considering treatment, the majority was nonrespondent to neuroleptics, especially those at stage 4; however, ECT (electroconvulsive therapy) was observed to be effective in some cases.

Aged↗
PubMed2001

Genetic predisposition and environmental causes in periodic and systematic catatonia.

The nosological heterogeneity of catatonic schizophrenia was the focus of a family study involving 139 catatonic patients. The clinical dichotomization of catatonia into periodic catatonia and systematic catatonia revealed good inter-rater reliability and stability of the diagnoses at follow-up. Analysis of the cumulative morbidity risk among first-degree relatives gave an excessive familial aggregation of homogenous psychoses in periodic catatonia with a risk of 26.9%. The mode of inheritance was consistent with an autosomal dominant model. In contrast, first-degree relatives of probands with systematic catatonia had a morbidity risk of 4.6%. Subsequent investigations pointed to a potential association of systematic catatonia to exposure to midgestational infections in the index cases and linked these sporadic disorders to disturbances of fetal neurodevelopment. The periodic catatonia, an unequivocally genetically transmitted illness, is at present under investigation in a genome-wide linkage analysis.

Catatonia↗