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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↗
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↗