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The descriptions of catatonia are complex and unclear. More than 40 different signs and symptoms have been included, but coma is not among them. Recently, a case report of coma in relation to catatonia was presented. We report two further cases where coma was a part of this syndrome of disturbed motility. They were successfully treated with ECT. Consequently, we suggest that catatonia may be a differential diagnosis of coma.
A 16-year-old girl, who carried a diagnosis of schizoaffective disorder, presented with symptoms consistent with excited catatonia/delirious mania. We believe this is the first report of excited catatonia in a child under the age of 18. Her catatonic symptoms responded to low-dose oral lorazepam (higher doses led to worsening of her clinical status). This case highlights the importance of considering catatonia in the differential diagnosis of agitated delirium, even in pediatric populations, and it underscores the need for more data about the pathogenesis and treatment of catatonia.
A series of four clinical cases suggests that catatonic disorder due to a chronic neurologic condition does not respond as reliably to electroconvulsive therapy (ECT) as functional catatonia does. Cases reported in the medical literature show a similar pattern. Presumably this form of catatonia is intrinsically less responsive to ECT, although the possibility remains that a more intense quality of treatment and prophylaxis is needed. Conversely, catatonia resistant to ECT suggests an underlying medical condition.
OBJECTIVE: We describe a case of psychogenic malignant catatonia resulting in permanent cognitive impairment. BACKGROUND: Catatonia is a neuropsychiatric syndrome characterized by catalepsy, negativism, mutism, muscular rigidity, and mannerisms, often accompanied by autonomic instability and fever. Little is known about the long-term cognitive consequences of the syndrome. METHOD: Medical history includes neurologic examination, neuropsychological evaluation, electroencephalographic data, magnetic resonance imaging, sodium amytal interview, and treatment with electroconvulsive therapy. RESULTS: Selective deficits in executive function and an anterograde amnesia were evident a week post-ECT treatment and continued to be present at follow-up after 2 years and 8 months. CONCLUSION: The permanent cognitive impairments are considered in the context of catatonia as a frontal lobe syndrome.
Logorrhea, verbigeration and echolalia persisted unremittingly for 3 years, with occasional short periods of motoric excitement, in a patient with mild intellectual handicap suffering from chronic schizophrenia. The speech catatonic symptoms, previously refractory to various antipsychotics, responded promptly to lorazepam, a benzodiazepine with documented efficacy in the treatment of acute catatonia but not chronic catatonia. It is suggested that pathways in speech production were selectively involved in the genesis of the chronic speech catatonic syndrome, possibly a rare form of chronic catatonia not previously described.
This report describes the case of a 61-year-old female schizophrenic patient with status post-frontal lobotomy some 35 years ago with prominent paranoid delusions. This woman developed severe catatonia under medication with a serotonergic/dopaminergic neuroleptic, risperidone, at a dose of up to 5 mg daily. The catatonic disorder was dose-dependent and subsided immediately after switching the medication to another atypical antipsychotic, clozapine. Given the negative history for catatonia in this patient, the temporal coincidence of administration of risperidone and catatonia is a novel finding.
A retrospective case control study was performed using the records of 60 catatonics, 189 noncatatonic schizophrenics, 262 schizophreniform disorder cases, 122 manics, 203 depressives and 134 surgical controls. This study suggests that perinatal distress and a history of severe infectious disease in childhood are more common among subjects with catatonia. Rheumatic fever is particularly common among the histories of catatonic patients. Although these findings did not occur in all cases of catatonia in the study, they may indicate a risk factor for some types of catatonia.
The authors describe a case of the catatonia syndrome associated with disulfiram therapy. Although useful in the management of chronic alcoholism, disulfiram is being increasingly associated with a wide spectrum of side effects and untoward medical sequelae, which now include catatonia. The authors note that catatonia is a clinical syndrome associated with multiple medical conditions as well as psychiatric disorders.
Although catatonia has traditionally been thought of as a type of schizophrenia, the author presents studies indicating that catatonia may be at least as common in bipolar disorder as it is in schizophrenia. He points out that changing definitions of schizophrenia and affective disorder require a reassessment of catatonia and its incorporation in modern diagnostic systems. The discussion represents material presented at the Affective Disorders Advisory Committee of the American Psychiatric Association Work Group to Revise DSM-III.
Lethal catatonia, a life-threatening febrile neuropsychiatric disorder, was widely reported in this country and abroad before the introduction of modern psychopharmacologic treatments. A comprehensive review of the world literature indicates that although the prevalence of lethal catatonia may have declined, it continues to occur, now reported primarily in the foreign literature. Lack of recognition probably accounts for the scarcity of recent American reports. Furthermore, lethal catatonia is a syndrome rather than a specific disease and may develop in association with both functional and organic illnesses. Familiarity with the clinical features and varied etiologies is essential for effective management of this catastrophic reaction.
Lethal catatonia, a syndrome described several decades before the advent of neuroleptic drugs, has been regarded by many investigators as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, published case reports of the two syndromes indicate differences in 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. Because lethal catatonia often requires neuroleptic treatment and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics, their early clinical differentiation is important.
Since steroid-induced psychoses often appear as mood disorders and since catatonia may be associated with psychotic mood disorders, the possibility exists for a steroid-induced psychotic mood disorder to present with associated catatonia. In a computer review of the medical literature, however, I found no such cases in adult patients. This report is presented as a possible case of steroid-induced catatonia in a 62-year-old woman following treatment with melphalan, prednisone, and cimetidine for multiple myeloma of the IgA class with associated mild hypercalcemia.
The phenomenon of catatonic-like states in people with autistic spectrum disorders is discussed in the context of current knowledge about catatonia as it occurs in severe mental illness and, less frequently documented, in conjunction with developmental disorders. The existing literature on catatonic-like states in people with autistic spectrum disorders is summarized, and it is suggested that such states are not directly comparable with the existing concepts of catatonia. A concept of 'autistic catatonia' is outlined in terms of both its phenomenology and its possible aetiological and maintaining factors. A case study is presented that examines this phenomenon from a cognitive neuropsychological perspective, together with implications for everyday management. The implications of this work for both research and clinical practice are discussed.
A retrospective case-control study was performed using the records of 59 catatonics, 59 non-catatonic schizophrenics, 59 manics, 59 depressives and 59 surgical controls. The findings suggest that prior brain injury and physical illness at onset of psychosis are much more common in subjects with catatonia. While these findings do not account for all cases of catatonia, they may indicate an aetiology for some phenotypic cases of catatonia.
A historical review of Kahlbaum's Catatonia is presented. He attributed the condition to organic cerebral disease. It is now best considered as a neuropsychiatric syndrome due to a wide variety of organic disease processes, manifest in catelepsy in a setting of an abnormal mental state, most commonly an affective disorder. Chronic catatonic states were common sequelae of encephalitis lethargica; this disease has now disappeared in epidemic form with a resulting fall in the incidence of catatonia in psychiatric hospitals. Acute catatonia, due to medical and particularly pharmacogenic causes, continues to occur in current psychiatric practice.
Catatonia is commonly encountered in psychiatric and medical practice but is under-recognized. It occurs in association with a wide range of disorders and drugs. Psychiatric education and textbooks mistakenly only consider catatonia as a subtype of schizophrenia. This article, the first of two, reviews the development of the concept of catatonia, its epidemiology, clinical features and pathophysiology.
This is the second of two articles reviewing catatonia. In the first, catatonia was described as an under-recognized syndrome with a potentially fatal outcome. It was suggested that treatment with neuroleptics may exacerbate the syndrome. The differential diagnosis, management and prognosis of catatonia are reviewed below.
Reserpine-induced catatonia is a widely accepted animal model of Parkinson's disease. In the present study, reserpine (5 mg/kg i.p.) and alpha-methylpara-tyrosine (AMPT) (200 mg/kg i.p.) induced catatonia in mice 20 h and 1 h before the experiment, respectively, as assessed using the rota-rod and bar tests after reserpine treatment. There was a significant decrease in fall-off time in the rota-rod test and a significant increase in time spent on the bar in the bar test as compared to the untreated control mice. Combination therapy with L-DOPA (100 mg/kg i.p.) and carbidopa (10 mg/kg i.p.) was less effective in reversing catatonia as compared to higher doses of L-DOPA (200 mg/kg i.p.) and carbidopa (20 mg/kg i.p.), which showed intense hyperactivity in reserpinized mice. Pretreatment with nitecapone (30 mg/kg i.p.), a COMT inhibitor, or selegiline (10 mg/kg i.p.), a MAO-B inhibitor potentiated the motor stimulant actions of subthreshold doses of the L-DOPA (100 mg/kg i.p.) and carbidopa (10 mg/kg i.p.) combination. Amantadine (40 mg/kg i.p.), but not bromocriptine, potentiated the effects of L-DOPA treatment. The NMDA antagonistic action of amantadine may have beneficial effects. It is concluded that COMT and MAO-B enzymes play an important role in the metabolism of dopamine and administration of a COMT or MAO-B inhibitor may prove to be a better adjunct to L-DOPA therapy than a dopamine receptor agonist in Parkinson's disease.