SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
The number of cases of catatonic schizophrenia has decreased in the past 50 years, but a few patients with the syndrome are still seen. The author describes the excited and withdrawn types of catatonia, reviews some organic and psychiatric conditions that resemble them, and gives suggestions for making the differential diagnosis. He discusses the use of the barbiturate interview, ECT, and phenothiazines in treatment, using case examples.
An 81 year old depressed female is described who developed catatonic-like behaviours while on the combination of the monoamine oxidase inhibitor phenelzine, and the neuroleptic haloperidol. Alternative etiologies, and the roles of the individual agents are discussed. It is suggested that whenever there is evidence of drug-induced catatonia, consideration should be given to stopping all medications.
OBJECTIVE: To evaluate the relationships of symptoms of catatonic schizophrenia to 77 symptoms relevant for diagnosing schizophrenia and to socioanamnestic variables. METHOD: Data from a sample of 112 Canadian patients diagnosed with schizophrenia according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) were evaluated via phi correlation coefficients. RESULTS: Forty-five (40.2%) of our 112 patients had catatonic symptoms, either at the time of this study or in the past. However, only weak correlations (phi < 0.31) to other symptoms relevant for diagnosing schizophrenia were found, and no significant correlations to socioanamnestic variables were found. CONCLUSION: Symptoms of catatonia appear to be independent of the key symptoms of schizophrenia.
A woman aged 20, first presenting with what appeared to be hysterical blindness as part of the syndrome of hysterical pseudo-dementia, soon showed the picture of speech-prompt catatonia, one of the subtypes of chronic schizophrenia described by Karl Leonhard. However, within a short time the neurological, EEG and laboratory findings indicated that the condition was one of subacute sclerosing panencephalitis.
A case of apparent 'lethal catatonia' in a 14-year-old girl is described; similarities with earlier descriptions are identified, although the precise cause of death in this case remains somewhat obscure.
Five consecutive cases of the NMS are presented, in all of which a catatonic state preceded the onset of the condition. Catatonia would appear to represent a highly significant risk factor for the NMS and a possible causal link between the two disorders is suggested.
Separate episodes of both catatonia and the so-called 'neuroleptic malignant syndrome' (NMS) occurred within the same patient. The only evidence for NMS in this case was prior administration of a neuroleptic and the presence of generalised muscular rigidity. It is suggested that it is misleading to view these conditions as separate diagnostic entities and that NMS is probably more correctly incorporated into the catatonic disorders.
A 12-year-old Indian boy presented to a psychiatric unit with catatonia. He was subsequently diagnosed to have Wilson's disease. Symptoms improved on treatment with penicillamine, zinc sulphate, and benzodiazepines.
BACKGROUND: Lethal catatonia and neuroleptic malignant syndrome (NMS) have been suggested to have a common neurochemical cause. We hypothesise that both conditions may be due to a sudden and massive blockade of dopamine neurotransmitters. METHOD: NMS was diagnosed in psychotic in-patients treated with neuroleptics if four features were present: diffuse severe rigidity, altered level of consciousness, hyperpyrexia and autonomic instability. RESULTS: Over three years, five NMS cases were diagnosed. Two presented with catatonic features and were diagnosed as acute reactive psychosis. Their neuroleptic doses were small, arguing for a particular sensitivity in these two cases. CONCLUSION: The sensitivity of two patients with catatonic features who developed NMS with small doses of neuroleptics supports a common neurochemical basis for the two conditions.
We studied autonomic function in a 34-year-old woman who had episodes of catatonia, hypertension, and tachycardia. In one of these episodes, epinephrine and norepinephrine levels were extremely high. Catecholamine clearance was normal. Platelet alpha 2-adrenergic receptors were normal in number and affinity. Results of the phenylephrine infusion test suggested that these episodes were due to central activation of the sympathetic nervous system.
The clinical manifestations, differential diagnosis, and treatment of the neuroleptic malignant syndrome and neuroleptic-induced catatonia are discussed. A case is presented in which the catatonic-like behavior and extrapyramidal sequelae of the neuroleptic malignant syndrome responded to combined treatment with anticholinergics and levodopa/carbidopa. Differential diagnosis and theories regarding the development of these neuroleptic-induced disorders are reviewed.
The presentation concerns 10 observations of lucid catatonia and protracted remission. Among the group of schizophrenia these cases constitute only 0.8% of all cases. They are characterized by a prevalence of negative signs and catatonic disorders which can be alloted to the anergic pole and are seen during the entire development of the disease. The most striking feature of such cases is their "outpatient" development of the process. The protracted remissions (15-37 years) are characterized by an expressed defect without positive symptoms.
A new concept of diagnostic and rating scales as well as a model of standardized examination in catatonia treatment are presented.
OBJECTIVE: In this case study, the significance of perfusion abnormalities in catatonia is examined. BACKGROUND: Recurrent catatonic symptoms are frequently observed in psychiatric disorders, but the predictors of relapse of the catatonic symptoms remain unknown. Perfusion abnormalities have been reported during catatonic states; however, little is known about brain functioning of catatonic patients during remission. METHOD: A catatonic patient was evaluated by clinical interview, behavioral examination, and functional neuroimaging (single photon emission computed tomography) to determine diagnosis and brain perfusion. RESULTS: The patient exhibited persistent hypoperfusion of the basal ganglia even after achieving symptomatic remission. CONCLUSIONS: These findings predict a secondary cause and may predict a chronic course.
The author shows the evolution of catatonia term throughout Medical Science History, from the Grecians, French and German High Schools, DSM-IV and ICD-10, and its actual position in the Argentine Psychiatry.
We describe a patient who was ill for more than 15 years. She was treated predominantly as a neurological case because of multiple motor signs. The diagnosis of catatonia was considered at the time when she was hospitalized in a psychiatric hospital after a suicidal attempt. The "therapeutic blindness", which was obviously present during 15 years of her illness, is discussed: the ICD--10 is perhaps misleading regarding this diagnosis while it associates it too tightly only to schizophrenia.
Six papers have reported the efficacy of lorazepam in alleviating catatonic symptoms that have psychogenic causes. The authors report five new cases of catatonia; three patients responded favorably and two failed to respond to lorazepam. Investigation of the nonresponders revealed the presence of pernicious anemia in one and postpartum psychosis in the other. These findings demonstrate that lorazepam has an important role in the treatment of catatonic symptoms. Its effects appear to be specific for psychogenic catatonic states and for conditions in which biogenic amines, specifically dopamine and gamma-aminobutyric acid, play a part. The authors stress intramuscular administration of lorazepam for patients in catatonic states because this route provides the psychiatrist with immediate results that assist with early diagnosis and treatment.
Many years ago the author, jointly with a psychologist, described a patient who, in spite of her alleged idiocy, showed an exceptional musical capacity. However, in the meantime the author has recognized and described early childhood catatonics and, as a consequence of this new knowledge, he has to admit an error. Even according to our then findings it would have been identifiable that, as has been confirmed now by follow-up, the patient is suffering from catatonia, starting in infancy. The high musical performance, then arousing our greatest astonishment, is now explicable, for childhood schizophrenics do not develop general mental deficiency but only specific circumscribed deficits.