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At least 19 recordsLinked to original sources
PubMed1985

Neuroleptic catatonia and its relationship to psychogenic catatonia.

Neuroleptics are among those pharmacological agents that can cause a nonpsychogenic catatonic state. Neuroleptic malignant syndrome (NMS) is marked by a change in state of consciousness, ranging from withdrawal through stupor to coma. In addition, it is characterized by autonomic dysfunction, hyperthermia, mutism, and rigidity. It is included in the differential diagnosis of the catatonic syndrome. Evidence is reviewed to suggest that agents responsible for improving NMS act on the dopamine (DA) gamma aminobutyric acid (GABA) connections in the mesostriatal and mesolimbic systems and also in the hypothalamus. In addition, based on symptomatology, pathophysiology, and therapeutic mechanisms, the relationship between nonpsychogenic neuroleptic-induced catatonia and psychogenic catatonia is examined.

Anti-Anxiety Agents↗
PubMed1997

Clozapine withdrawal catatonia and neuroleptic malignant syndrome: a case report.

Catatonia as a clozapine withdrawal syndrome has not been documented. We report a case of excited catatonia with fever, autonomic instability, and delirium--a picture of malignant catatonia (lethal catatonia) after abrupt clozapine withdrawal. The use of conventional neuroleptics transformed the excited malignant catatonia into a stuporous state resembling neuroleptic malignant syndrome (NMS). Such a transformation of excited lethal catatonia into NMS has been described in the literature, providing support for the hypothesis that NMS is a variant of catatonia. Opinions, however, have been conflicting whether lethal catatonia and NMS are indistinguishable. We argue that NMS may be regarded as a neuroleptic-induced retarded (stuporous) subtype of malignant catatonia, clinically indistinguishable from nonneuroleptic retarded malignant catatonia but different from the excited form. To differentiate between the two subtypes of malignant catatonia would help resolve the controversy. The nosological status of excited catatonia, a poorly studied condition, remains unclear. The two subtypes of catatonia may differ in pathophysiology and responses to treatment. Clinicians should be alert to catatonia as a possible clozapine withdrawal phenomenon, and excited catatonia deserves more research attention.

Adult↗
PubMedDate not supplied

[Catatonia: resurgence of a concept. A review of the international literature].

Catatonia was first described in 1874 by Kahlbaum as being a cyclic disease mixing motor features and mood variations. Because most cases ended in dementia, Kraepelin recognized catatonia as a form of dementia praecox and Bleuler included it within his wide group of schizophrenias. This view influenced the psychiatric practice for more than 70 years. But catatonia was recently reconsidered and this because of the definition of more precise diagnosis criteria, the discovery of a striking association with mood disorders, and the emphasis on effective therapeutics. Peralta et al empirically developed a performant diagnostic instrument with the 11 most discriminant signs among catatonic features. Diagnostic threshold is three or more signs with sensitivity of 100% and specificity of 99%. These signs are: immobility/stupor (extreme passivity, marked hypokinesia); mutism (includes inaudible whisper); negativism (resistance to instructions, contrary comportment to whose asked); oppositionism, other called gegenhalten (resistance to passive movement which increases with the force exerted); posturing (patient adopts spontaneously odd postures); catalepsy (patient retains limb positions passively imposed during examination; waxy flexibility); automatic obedience (exaggerated co-operation to instructed movements); echo phenomena (movements, mimic and speech of the examiner are copied with modification and amplifications); rigidity (increased muscular tone); verbigeration (continuous and directionless repetition of single words or phrases); withdrawal/refusal to eat or drink (turning away from examiner, no eye contact, refusal to take food or drink when offered). Using this diagnostic tool, prevalence of catatonic syndrome appears to be close to 8% of psychiatric admissions. Other signs are also common but less specific: staring, ambitendance, iterations, stereotypes, mannerism, overactivity/excitement, impulsivity, combativeness. Some authors complete this description by adding an affective dimension which is considered specific. Clinical forms are differentiated according to evolution: acute, chronic and periodic forms exist; and symptomatology: excited catatonias have a best prognostic than retarded catatonias. Malignant catatonia is the most studied form because of its severity and high rate of mortality (25%); catatonic patients develop autonomic disturbances with labile blood pressure, hyperthermia, diaphoresis, etc. Malignant catatonia requires ECT intervention in emergency. While catatonias due to general medical conditions are well admitted (first concerned are neurologic etiologies) and concern 14,1% of catatonias, psychiatric comorbidity remains a problem. The documented decline in the proportion of patients with schizophrenia diagnosed as catatonic is congruent with the fact that most studies highlight the strong association between catatonia and mood disorders. However, customary clinical practice continues to over value diagnostic of schizophrenia because catatonic symptoms are recognized as schizophrenic and schizophrenia corresponds to a pharmacological target. Other authors stress that on average 20 to 40% of catatonias are idiopathic. Conceptual proximity between catatonic symptomatology and extrapyramidal syndrome could give some ways for neurobiological grasp of the trouble; mesolimbic and mesostriatal dopaminergic imbalance in a frontal lobe-basal ganglia-brainstem system is supposed to be involved. Treatment procedure could be standardized as follows: 1) Withhold neuroleptic medication. Those drugs are proven to be lethal when catatonic symptoms are developed; 2) Investigations to exclude treatable physical disorders (including standard blood laboratory tests, urinary drug screening, electroencephalogram and brain computerized tomography); 3) Trial of lorazepam. This therapeutic is safe and 80% effective. We propose to administer an initial oral 2,5 mg challenge; catatonic signs are rated after the first hours. If necessary, the patient could receive 3 mg/day with a 6-day full dose treatment and then, treatment would progressively be reduced; 4) If the patient failed to respond to lorazepam, ECT are needed; 5) Earlier use of ECT is recommended if autonomic instability or hyperthermia appears and malignant catatonia is suspected. In conclusion, catatonia has always had an unstable and blurred place in the psychiatric nosography since its first description. It has been incorporated within the group of schizophrenias and underdiagnosed for a long time, but has been predominantly associated with mood disorders for the last ten years. Psychopathological considerations, particularly on cognitive and affective status of catatonic patients, should clarify the nosologic discussion.

Benzodiazepines↗
PubMed2003

Catatonia in psychiatric classification: a home of its own.

OBJECTIVE: The authors assess the present position of catatonia in diagnostic classification systems and consider the merits of designating catatonia as a separate diagnostic category with defined criteria. METHOD: Following the logical steps to establish diagnostic validity when the etiology of a syndrome is unknown, the authors review the literature on the features that delineate catatonia as a syndrome, the prevalence and response to treatment of catatonia, and the conditions that are associated with catatonia. RESULTS: Catatonia is a well-defined syndrome that can be reliably ascertained. Although more than 40 motor signs of catatonia are known, the presence of two prominent features for 24 hours or longer is sufficient to identify the syndrome. Catatonia is found in about 10% of acutely ill psychiatric inpatients and is more commonly observed in persons with mood disorder than in those with schizophrenia. It is found in many conditions and presents mainly as retarded-stuporous or excited-delirious forms. Catatonia responds to specific treatments, including sedative anticonvulsants (barbiturates and benzodiazepines) and ECT. CONCLUSIONS: Catatonia can be distinguished from other behavioral syndromes by a recognizable cluster of clinical features. Catatonia is sufficiently common to warrant classification as an independent syndrome. It can be reliably identified, has a typical course when appropriately treated, responds to specific treatments, and is worsened by other treatments. It is associated with many pathophysiologic processes and most often with mood disorder. These findings, which are consistent with established methods of defining distinct diagnostic groupings, support consideration of catatonia as an individual category in psychiatric diagnostic systems.

Adolescent↗
PubMed1995

Somatic treatment of catatonia.

OBJECTIVE: The authors reviewed the recent literature regarding the treatment of catatonia as a syndrome of multiple etiologies. Given the historical and clinical association of catatonia with schizophrenia, the authors' examined the assumption that the first-line treatment of catatonia is antipsychotic medication. METHODS: Articles published between January 1, 1985 and December 31, 1994 were located using the Paperchase medical literature search system. Additionally, references from those identified articles were examined for possible inclusion in this review. To be included in this review, articles had to be written in English and report specific symptoms of catatonia to determine, retrospectively, if DSM-IV criteria for catatonia were met. RESULTS: Seventy publications met inclusion criteria and reported on a total of 178 patients and included 270 separate treatment episodes. Most of the articles were case-reports, although a few case-series were identified. Multiple causes of catatonia were identified in these reports. The most commonly reported treatment for catatonia was with benzodiazepines which were effective in 70 percent of the cases, with lorazepam demonstrating the highest frequency of use and a 79 percent complete response rate. Electroconvulsive therapy (ECT) was also efficacious (85%) and was more likely to provide a positive outcome in cases of malignant catatonia. Antipsychotics demonstrated poor efficacy. CONCLUSIONS: Catatonia is a nonspecific syndrome with multiple etiologies. Treatment of catatonia should be based on the underlying cause when it is identifiable. Lorazepam appears to offer a safe, effective first-line treatment of catatonia. ECT should be considered when rapid resolution is necessary (e.g., malignant catatonia) or when an initial lorazepam trial fails.

Anti-Anxiety Agents↗
PubMedDate not supplied

Catatonia and the neuroleptics: psychobiologic significance of remote and recent findings.

The previously common occurrence of catatonic schizophrenia and catatonic symptoms among schizophrenic patients has diminished sharply; catatonic symptoms now occur more frequently in association with severe affective disorders or with general medical conditions. Catatonia is generally viewed as a peculiar and puzzling syndrome and attracts limited attention. Yet significant catatonic symptoms tend to be present in close to 10% of patients admitted to psychiatric inpatient facilities. The dynamic significance of catatonia can be recognized by considering the original biologic role of catatonia in schizophrenia as an opposite to the paranoid disorder. Szondi viewed catatonia as an attempt at self-healing of the paranoid psychosis with its threatening total expansion, by extreme constriction of the ego. The previously predominant primary association of catatonia with schizophrenia has been eclipsed as neuroleptics have supplanted the endogenous self-healing attempt of catatonia, preventing the occurrence of catatonic symptoms in schizophrenia. Neuroleptics in fact duplicate or approximate the symptoms of catatonia by producing mental immobilization, hypokinesis (parkinsonism and dystonia), hyperkinesis (akathisia), and pernicious catatonia in the modern guise of the neuroleptic malignant syndrome (NMS). Patients with past or present catatonic symptoms are particularly vulnerable to NMS, and treatment of catatonia requires avoidance of neuroleptics and the use of benzodiazepines or electroconvulsive therapy (ECT). The extreme negativism and constriction of consciousness in catatonia suggest a primary role of the frontal lobes, with secondary involvement of the extrapyramidal system and its movement disorders. In an attempt to integrate clinical, psychologic, neuropharmacologic, and neurochemical findings, a modern dynamic neuropsychiatry must appreciate the major significance of catatonia.

Antipsychotic Agents↗
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↗
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↗