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PubMed2005

Clinical and cost-effectiveness of electroconvulsive therapy for depressive illness, schizophrenia, catatonia and mania: systematic reviews and economic modelling studies.

OBJECTIVES: To establish the clinical effectiveness and cost-effectiveness of electroconvulsive therapy (ECT) for depressive illness, schizophrenia, catatonia and mania. DATA SOURCES: Electronic bibliographic databases. The reference lists of relevant articles and health services research-related resources were consulted via the Internet. REVIEW METHODS: Identified studies were examined to ascertain whether they met the inclusion criteria for the review. The study quality of relevant articles was assessed using standard checklists and data were abstracted using standardised forms into a database. Where relevant, results from studies were pooled for meta-analysis. Two economic models were developed primarily based on evidence from the clinical effectiveness analysis and limited quality of life studies. RESULTS: Two good-quality systematic reviews of randomised evidence of the efficacy and safety of ECT in people with depression, schizophrenia, catatonia and mania were identified. Four systematic reviews on non-randomised evidence were also identified, although only one of these could be described as good quality. There was no randomised evidence of the effectiveness of ECT in specific subgroups including older people, children and adolescents, people with catatonia and women with postpartum exacerbations of depression or schizophrenia. The economic modelling results for depression did not demonstrate that any of the scenarios had a clear economic benefit over the others, mainly because of the uncertainty surrounding the clinical effectiveness of the different treatments and the quality of life utility gains. Sensitivity analysis surrounding the cost of ECT and the quality of life utility values had little effect on the overall results. The results of the model for schizophrenia adapted to include ECT suggest that clozapine is a cost-effective treatment compared with ECT. For patients who fail to respond to clozapine, ECT treatment may be preferred to the comparative treatment of haloperidol/chlorpromazine. CONCLUSIONS: Real ECT is probably more effective than sham ECT, but as stimulus parameters have an important influence on efficacy, low-dose unilateral ECT is no more effective than sham ECT. ECT is probably more effective than pharmacotherapy in the short term and limited evidence suggests that ECT is more effective than repetitive transcranial magnetic stimulation. Tricyclic antidepressants (TCAs) may improve the antidepressant effect of ECT during the course of treatment. Continuation pharmacotherapy with TCAs combined with lithium in people who have responded to ECT reduces the rate of relapses. Overall, gains in the efficacy of the intervention depending on the stimulus parameters of ECT are achieved only at the expense of an increased risk of cognitive side-effects. Limited evidence suggests these effects do not last beyond 6 months, but there is no evidence examining the longer term cognitive effects of ECT. There is little evidence of the long-term efficacy of ECT. ECT either combined with antipsychotic medication or as a monotherapy is not more effective than antipsychotic medication in people with schizophrenia. More research is needed to examine the long-term efficacy of ECT and the effectiveness of post-ECT pharmacotherapy, the short-term and longer term cognitive side-effects of ECT, and the impact of ECT on suicide and all-cause mortality. Further work is needed to examine the information needs of people deciding whether to accept ECT and how their decision-making can be facilitated. More research is also needed on the mechanism of action of ECT. Finally, the quality of reporting of trials in this area would be vastly improved by strict adherence to the Consolidated Standards of Reporting Trials recommendations. Economic analysis may identify areas in which research would be best targeted by identifying parameters where reducing the level of uncertainty would have the most effect in helping to make the decision on whether ECT is a cost-effective treatment.

Adolescent↗
PubMed1999

[Acute life-threatening catatonia].

Malignant catatonia is a rare, life-threatening syndrome that occurs in connection with somatic as well as psychiatric disorders, in particular with functional psychosis. Key symptoms are catatonic features combined with elevated muscle tone, hyperthermia, vegetative instability, and pathological laboratory values. Benzodiazepines, dantrolene, and ECT have been reported to be an effective treatment of malignant catatonia, whereas classic neuroleptics and anticholinergic drugs are contraindicated. If antipsychotic treatment is required, clozapine is generally used. In this article we describe a case of malignant catatonia in a 52 year old female patient and discuss the clinical picture, the treatment, and the time course of the syndrome.

Anti-Anxiety Agents↗
PubMed1999

Malignant catatonia-induced respiratory failure with response to ECT.

A 47-year-old acutely psychotic schizophrenic man was diagnosed with malignant catatonia. Because of a history of neuroleptic malignant syndrome (NMS), traditional neuroleptics were avoided, and the patient had been treated with reserpine for a period of 10 years. Symptomatically, severe agitation alternated with severe retardation. The syndrome progressed, despite early termination of any neuroleptic medications, to marked catatonic rigidity and dehydration. Worsening was associated with transfer to a medical intensive care unit, intubation, and subsequently a tracheostomy. Dantrolene and bromocriptine were unhelpful. Lorazepam produced muscular relaxation and resulting decreases in creatine phosphokinase levels but elicited no other improvement. Eleven bilateral electroconvulsive treatments, however, resolved the respiratory impairment and catatonia and improved the psychosis. This report highlights the efficacy of ECT in lethal catatonia despite respiratory impairment and tracheostomy.

Catatonia↗
PubMed1999

Severe catatonia and neuroleptic malignant syndrome: report of 3 cases.

Catatonia is a syndrome characterized by motor rigidity or stupor, negativism, mutism and inappropriate or bizarre posture. Without proper management, patients may have significant morbidity and mortality from stupor, coma and death (lethal or malignant catatonia). Neuroleptic malignant syndrome (NMS) is characterized by a sudden appearance of motor rigidity, fever, autonomic effect, increased white blood cell count, serum creatinine phosphokinase, liver enzymes, and myoglobin. The mortality rate is 15 per cent to 25 per cent or even higher when depot form of neuroleptic is used. We report a patient with severe catatonia and two cases of NMS. Death was encountered with one of the latter.

Adult↗
PubMed2001

Adverse outcome with delay in identification of catatonia in elderly patients.

All three patients to show catatonia at a teaching veterans' hospital over a 1-year period were over 60 years old. Each experienced delays of 2-5 months in identification of catatonia and adverse events attributable to the delay (e.g., pulmonary embolus, physical restraint, pneumonia, mislabeling as "advanced dementia," Do Not Resuscitate orders, and death). These outcomes suggest that geriatric patients with unrecognized catatonia are at high risk for major adverse events.

Aged↗
PubMed2003

[Malignant catatonia as paradigm of neuropsychiatric disease].

Catatonia is a large neuropsychiatric syndrome with multiple etiologies (psychiatric disorder, cerebral structural lesion, systemic disease, secondary to drugs and toxic agents) and varied clinical manifestations (cognitive and behavioral disorders, motor and speech disorders and vegetative disorders). The presence of disautonomy means a situation having vital risk, that requires immediate therapeutic intervention. A 22 year old woman was admitted due to a picture of stupor, fever, maintained postures, rigidity, seizures and tachycardia and hypertension episodes; this picture initiated four weeks earlier, with psychotic and affective symptoms and she slowly developed speech and motor activity impairment. Initially, she had been treated with neuroleptics, anticholinergics and antidepressants. The CT, MRI and CSF studies were normal. The EEG revealed diffuse slow waves and right frontotemporal paroxystic activity Laboratory determinations showed elevation of CK, coinciding with the vegetative disorder phase. The picture resolved progressively in two months, after receiving 19 sessions of electroshock therapy. In all the patients, and above all in those who receive neuroleptics, with symptoms suggesting catatonia, the presence of disautonomy should be considered as an alarm situation, which would make it necessary to discontinue the neuroleptics and to adopt special control. Electroshock therapy is the most effective therapeutic option in the situation of malignant catatonia.

Adult↗
PubMed2004

[A patient with probable dementia with Lewy bodies, who showed catatonia induced by donepezil: a case report].

We report a 75-year-old Japanese woman with probable dementia with Lewy bodies (DLB). At the age of 64, she showed left hand resting tremor, and gradually developed bradykinesia, and rigidity. She was diagnosed as having parkinsonism and took medication. At the age of 70, she showed hallucination and dementia. As she had developing cognitive dysfunction and hallucination and parkinsonism, she was diagnosed to have probable DLB. At the age of 75, after administration of donepezil, she showed severe psychosis and worsened parkinsonism, and was admitted to hospital. On neurological examination, she showed severe rigidity and akinesia, and behavioral immobility like "waxy flexibility" or motiveless resistance to maintenance of rigid posture against attempts to be moved. The phenomena, she presented as motor abnormalities, were thought to be catatonia. In consideration of clinical course, her catatonia and worsened parkinsonism was thought to be induced by donepezil and she was stopped the administration of donepezil. After treatment with trihexiphenizil, she had improvement of motor abnormalities and worsened parkinsonism. It is important to recognize that donepezil may induce catatonia on the patients of parkinsonism with severe dementia.

Aged↗
PubMed1992

[Electroconvulsive therapy in treatment of acute life threatening catatonia in toxic epidermal necrolysis (Lyell syndrome)].

Toxic epidermal necrolysis (Lyell syndrome) developed in a 43-year woman treated with carbamazepine, perazine, and sulpiride for recurrent manic bipolar disorder. Five days after withdrawal of all psychotropic medication her psychiatric illness was exacerbated and a syndrome of lethal catatonia developed which was promptly treated with unilateral electroconvulsive therapy (ECT). Rapid remission of lethal catatonia after the first ECT treatment and of her affective disorder within days was achieved. According to clinical observations of the preneuroleptic era, early improvement of lethal catatonia following ECT may have been supported by concurrent high dose corticosteroid therapy for toxic epidermal necrolysis.

Adult↗
PubMed2006

[A young woman with a labile mood, hyperactivity, hyperthermia and exhaustion: symptoms of lethal catatonia].

A 22-year-old woman went through a period with a labile mood that first turned into psychotic hyperactivity and was then followed by hyperthermia and exhaustion. This was accompanied by diminished consciousness, sinus arrhythmia and respiratory insufficiency. With a working diagnosis of 'lethal catatonia' she was treated by electroshock and later also with the antipsychotic agent quetiapine. After a few electroshock treatments her vital functions improved and ultimately, the patient recovered. Lethal catatonia is characterised by acute excitation, catalepsy, autonomic instability and fever, which can lead to death. The syndrome often starts with mood instability, which turns into hyperactivity accompanied by hyperthermia and exhaustion. The creatine kinase, blood-sedimentation rate and leukocyte count are often raised. Lethal catatonia must be distinguished from the neuroleptic malignant syndrome, serotonin syndrome and encephalitis. The pathophysiology is unclear, but most reports suggest a hypodopaminergic state. The syndrome is associated with affective disorders and schizophrenia. Early recognition is made difficult by the low frequency of appearance, diversity in nomenclature, and strong resemblance to other syndromes.

Adult↗
PubMed1988

[The clinical position of catatonia].

Revising the principal historical and clinical data available allows catatonia to be considered a kind of brain reaction unrelated to schizophrenia in restricted sense--i.e. to dementia praecox. Owing to the probabilities there are that malignant manifestations be developed, it is the author's opinion that it should be included into general medicine instead. Many cases including several catatonic attacks do not follow the usual course of dementia praecox. Moreover, true catatonic attacks frequency is quite low in chronic schizophrenia known as "catatonic schizophrenia". Thus, it seems necessary that relationships between catatonia, and spasmodic hysterical and epileptic symptoms be reevaluated accordingly. Electroconvulsive therapy is a very useful treatment, not only in simple catatonia attacks (which is a well-known application) but also on different malignant manifestations likely to arise during attacks.

Catatonia↗
PubMed1984

Effects of amine pretreatment on ketamine catatonia in pinealectomized or hypophysectomized animals.

The present studies were designed to clarify the role of catecholamines and pineal idolamines on ketamine-induced catatonia in the intact, pinealectomized or hypophysectomized chick and rat. In the pinealectomized chick, pretreatment with dopamine increased the duration of catatonia (DOC) after ketamine, but pretreatment with norepinephrine did not. The pineal indolamines exhibited mixed actions. Serotonin and N-acetyl serotonin which augmented ketamine DOC, did not do so in the absence of the pineal gland, whereas melatonin potentiated the ketamine DOC in both the intact and pinealectomized chick. Ketamine was more potent in the hypophysectomized chick and the circadian rhythm noted in the intact chick was absent; furthermore, melatonin did not augment the ketamine DOC whereas dopamine continued to do so. This study did not demonstrate a species difference regarding the role of the amines on the pineal in spite of the immature blood-brain barrier in the young chick and the intact barrier in the rat. In addition, these data indicate a direct role of the pituitary in the augmentation of ketamine DOC induced by melatonin. Furthermore, dopamine appeared to act on systems more closely involved with the induction of ketamine catatonia rather than directly on the pituitary.

Amines↗
PubMed1995

[Favourable effect of zolpidem on catatonia].

According to the literature, electroconvulsive therapy and benzodiazepines, especially lorazepam, are recommended for the treatment of catatonia. We report the case of a 56-year-old woman with catatonia resistant to electroconvulsive therapy and benzodiazepines. Treatment with zolpidem led to durable improvement. This case suggests that zolpidem should be tested in catatonia since side effects are minimal.

Catatonia↗
PubMed1977

Catatonia and systemic lupus erythematosus.

Catatonia has generally been assumed by many physicians to be a subtype of schizophrenia. Numerous cases have been reported in the literature associating catatonia with other psychiatric and also medical illnesses. The present report describes a patient with Systemic Lupus Erythematosus (SLE) who presented in a catatonic state. A brief differential diagnosis of catatonia is also included.

Adult↗
PubMed1977

Catatonia and malignant syndrome: a possible complication of neuroleptic administration. Report of a case involving haloperidol.

An unusual, acute extrapyramidal reaction, which resulted from treatment with haloperidol and which was unresponsive to standard anticholinergic treatment and indistinguishable on clinical grounds from acute catatonia, is described. Because the etiology of this reaction was not appreciated, progressive, life-threatening physiological deterioration ensued accompanied by unremitting neuromuscular symptoms, a clinical picture resembling both "lethal catatonia" and the rare "neuroleptic malignant syndrome." The literature on these conditions is reviewed and various problems in differential diagnosis are discussed. It is proposed that some cases of the neuroleptic malignant syndrome and perhaps lethal catatonia may represent the evolution of severe extrapyramidal reactions.

Adult↗
PubMed2001

Acute and long-term treatment of catatonia with risperidone.

Catatonia is a rare but difficult-to-treat disorder. Here, we report on the case of a schizophrenic patient who developed several episodes of severe catatonia after suffering from adequately treated Lyme disease with encephalitis. The catatonic stupor was not responsive to typical neuroleptics and benzodiazepines. After the medication was changed to risperidone, there was a dramatic and persistent improvement of the patient's condition. Two relapses during the follow-up period over five years were caused by dose reductions. Risperidone might be a promising drug in the treatment of acute catatonia and in preventing further episodes.

Acute Disease↗
PubMed1998

Parent-of-origin effect and evidence for differential transmission in periodic catatonia.

In a family study involving 83 probands with periodic catatonia a subtype of DSM IIIR schizophrenia, we reported an age-specific morbidity risk of 26.9% in first-degree relatives with homotypical psychoses and genetic anticipation indicating a possible major gene effect. Paternal transmission was associated with a trend for a younger age at onset in probands compared to that observed in the case of maternal transmission (P = 0.099). If this can be confirmed in a larger sample and then replicated, there would be evidence for the occurrence of a parent-of-origin effect. Such an observation may indicate that a paternally imprinted locus acts on periodic catatonia. Among the non-genetic mechanisms that may modify the penetrance of the disease, paternal affection did lead to a decrease in male offspring (P = 0.007) and maternal affection showed an increased frequency of non-affected male offspring (P = 0.021). We therefore propose that parent-of-origin effects as well as prenatal mortality and psychosocial factors need further investigation in the periodic catatonia subtype of schizophrenia.

Adolescent↗
PubMed2005

Systematic mutation analysis of KIAA0767 and KIAA1646 in chromosome 22q-linked periodic catatonia.

BACKGROUND: Periodic catatonia is a familial subtype of schizophrenia characterized by hyperkinetic and akinetic episodes, followed by a catatonic residual syndrome. The phenotype has been evaluated in two independent genome-wide linkage scans with evidence for a major locus on chromosome 15q15, and a second independent locus on chromosome 22qtel. METHODS: In the positional and brain-expressed candidate genes KIAA0767 and KIAA1646, we searched for variants in the complete exons and adjacent splice-junctions as well as in parts of the 5'- and 3'-untranslated regions by means of a systematic mutation screening in individuals from chromosome 22q-linked pedigrees. RESULTS: The mutation scan revealed 24 single nucleotide polymorphisms, among them two rare codon variants (KIAA0767: S159I; KIAA1646: V338G). However, both were neither found segregating with the disease in the respective pedigree nor found at a significant frequency in a case-control association sample. CONCLUSION: Starting from linkage signals at chromosome22qtel in periodic catatonia, we screened two positional brain-expressed candidate genes for genetic variation. Our study excludes genetic variations in the coding and putative promoter regions of KIAA0767 and KIAA1646 as causative factors for periodic catatonia.

Case-Control Studies↗
PubMedDate not supplied

[Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome: a case report].

Lethal catatonia is often regarded as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, the two syndromes reveal differences in the mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Early clinical differentiation is important, because lethal catatonia often requires neuroleptic treatment, and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics.

Adult↗