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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[Catatonia: resurgence of a concept. A review of the international literature]. 1250 60

No reports have yet been published on catatonia using latent class analysis (LCA). This study applied LCA to a large, diagnostically homogenous sample of patients with chronic schizophrenia who also presented with catatonic symptoms. A random sample of 225 Chinese inpatients with DSM-IV schizophrenia was selected from the long-stay wards of a psychiatric hospital. Their psychopathology, extrapyramidal motor status and level of functioning were evaluated with standardized rating scales. Catatonia was rated using a modified version of the Bush-Francis Catatonia Rating Scale. LCA was then applied to the 178 patients who presented with at least one catatonic sign. In LCA a four-class solution was found to fit best the statistical model. Classes 1, 2, 3 and 4 constituted 18%, 39.4%, 20.1% and 22.5% of the whole catatonic sample, respectively. Class 1 included patients with symptoms of 'automatic' phenomena (automatic obedience, Mitgehen, waxy flexibility). Class 2 comprised patients with 'repetitive/echo' phenomena (perseveration, stereotypy, verbigeration, mannerisms and grimacing). Class 3 contained patients with symptoms of 'withdrawal' (immobility, mutism, posturing, staring and withdrawal). Class 4 consisted of 'agitated/resistive' patients, who displayed symptoms of excitement, impulsivity, negativism and combativeness. The symptom composition of these 4 classes was nearly identical with that of the four factors identified by factor analysis in the same cohort of subjects in an earlier study. In multivariate regression analysis, the 'withdrawn' class was associated with higher scores on the Scale of Assessment of Negative Symptoms and lower and higher scores for negative and positive items respectively on the Nurses' Observation Scale for Inpatient Evaluation's (NOSIE). The 'automatic' class was associated with lower values on the Simpson-Angus Extrapyramidal Side Effects Scale, and the 'repetitive/echo' class with higher scores on the NOSIE positive items. These results provide preliminary support for the notion that chronic schizophrenia patients with catatonic features can be classified into 4 distinct syndromal groups on the basis of their motor symptoms. Identifying distinct catatonic syndromes would help to find their biological substrates and to develop specific therapeutic measures.
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PMID:Schizophrenia with prominent catatonic features ('catatonic schizophrenia') III. Latent class analysis of the catatonic syndrome. 1899 97

Neuroleptic Malignant Syndrome (NMS) is unusual but could be a lethal reaction associated with neuroleptic drugs. It occurs in almost 0.07-2.2% of patients under treatment with neuroleptics. There are some medical treatments that may also be helpful for its treatment, including dopamine agonists, muscle relaxants, and electroconvulsive therapy (ECT). We present this case to alert the clinicians to the potential for inducing afebrile NMS.Our case is a 41-year-old man with a history of schizophrenia showing signs and symptoms in accordance with NMS, 2 weeks after receiving one dose of 12.5 mg fluphenazine decanoate, abruptly following the 3rdsession of ECT. The patient presented with decreased level of consciousness, muscular rigidity, waxy flexibility, mutism, generalized tremor, sever diaphoresis and tachycardia which progressed during the previous 24 h. Laboratory data indicated primarily leukocytosis, an increasing level of creatinine phosphokinase and hypokalemia during the next 72h.In patients receiving antipsychotics, any feature of NMS should carefully be evaluated whether it is usual or unusual particularly in patients receiving long acting neuroleptics.
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PMID:Afebrile Neuroleptic Malignant Syndrome associated with Fluphenazine decanoate: A case report. 2295 96

Catatonia has been defined as a cluster of signs and occurs secondary to or as a subgroup of schizophrenia, mood disorders or organic syndrome. This study specifically examined the distinct variety of catatonia that did not meet any standard psychiatric diagnostic criteria on globally recognised psychiatric rating tools and compared the clinical features with the catatonia that occurred in association with a diagnosis of schizophrenia. The inpatients in a tertiary psychiatric ward in Ahmedabad, India, between 2002 and 2005 who presented with two or more catatonic signs present for more than 24h period were assessed on Structured Clinical Interview for DSM IV tool. Those with catatonic signs that met diagnostic criteria for schizophrenia (n=21) were compared, with those without any disorder called Idiopathic catatonia (n=13), on measures of Bush Francis Catatonia Rating Scale (BFRCS), Brief Psychiatric Rating Scale (BPRS) and Scale for Assessment of Negative Symptoms (SANS). The scores on duration of illness (U=14.00; p<0.001) and mean BPRS (t=6.76; df=32; p<0.001) were significantly higher in schizophrenia group. The Idiopathic group had significantly higher scores on mean total BFCRS (t=-3.50; df=32; p=0.001) and also on subscores of negativism (p=0.02), waxy flexibility (p=0.02), mitgehen (p<0.05) and ambitendency (p=0.01). The results indicate that the Idiopathic catatonia present early in their course and have fewer general psychopathologies; however have higher number and severity of catatonic signs. The study also supports the current concept that there does exists, a distinct variety of catatonia that probably has its own course and prognosis, which need further consideration and more studies to explore this.
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PMID:A comparative study of "Idiopathic catatonia" with catatonia in schizophrenia. 2305 Oct 79

Catatonia, originally described by Karl Kahlbaum in 1874, may be regarded as a set of clinical features found in a subtype of schizophrenia, but the syndrome may also stem from organic causes including vascular parkinsonism, brain masses, globus pallidus lesions, metabolic derangements, and pharmacologic agents, especially first generation antipsychotics. Catatonia may include paratonia, waxy flexibility (cerea flexibilitas), stupor, mutism, echolalia, and catalepsy (abnormal posturing). A case of catatonia as a result of acute renal failure in a patient with dementia with Lewy bodies is described. This patient recovered after intravenous fluid administration and reinstitution of the atypical dopamine receptor blocking agent quetiapine, but benzodiazepines and amantadine are additional possible treatments. Recognition of organic causes of catatonia leads to timely treatment and resolution of the syndrome.
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PMID:Renal failure in dementia with lewy bodies presenting as catatonia. 2346 22

Catatonia is a psychomotor syndrome associated with several psychiatric and medical conditions. Psychomotor signs range from stupor to agitation, and include pathognomonic features such as verbigeration and waxy flexibility. Disturbances of volition led to the classification of catatonia as a subtype of schizophrenia, but changes in nosology now recognise the high prevalence in mood disorders, overlap with delirium, and comorbidity with medical conditions. Initial psychometric studies have revealed three behavioural factors, but the structure of catatonia is still unknown. Evidence from brain imaging studies of patients with psychotic disorders indicates increased neural activity in premotor areas in patients with hypokinetic catatonia. However, whether this localised hyperactivity is due to corticocortical inhibition or excess activity of inhibitory corticobasal ganglia loops is unclear. Current treatment of catatonia relies on benzodiazepines and electroconvulsive therapy-both effective, yet unspecific in their modes of action. Longitudinal research and treatment studies, with neuroimaging and brain stimulation techniques, are needed to advance our understanding of catatonia.
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PMID:Structure and neural mechanisms of catatonia. 3119 92