Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bromperidol therapeutic efficacy, and tolerance was studied by means of a 3-month open trial on 25 chronic psychotic female inpatients from a room at San Juan ward for medium to extensive length of stay, The Braulio A. Moyano National Psychiatric Hospital, Buenos Aires. This drug was administered orally on a single 10- to 35 mg night dose. No effect whatsoever was observed on periodic catatonia. However, its being well-tolerated and effective on chronic psychotic patients, coupled to the "bonus" of a single daily dose, turns BP into a suitable alternative drug for Haloperidol when dealing with schizophrenia, and delusions with no deficitary evolution.
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PMID:[Clinical experience with bromperidol in chronic psychoses]. 307 Oct 92

Karl Ludwig Kahlbaum was the first to describe catatonia in 1868. There has been a tendency to consider catatonia as a psychiatric disease despite many case reports demonstrating a wide range of medical and neurological as well as psychiatric causes. We present our accumulated experience of the catatonic syndrome. Most cases (36%) were associated with affective illness but five cases (20%) had a defined organic disorder. A significant minority had no identifiable cause and there was only one case of schizophrenia. The idiopathic and affective groups had a high incidence of recurrent catatonic episodes and many had a family history of a similar problem. The prognosis was excellent, except for the few patients who presented with the acute and rapidly progressive form of the syndrome which led to acute renal failure.
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PMID:The syndrome of Karl Ludwig Kahlbaum. 376 Sep 5

Mutism is a common manifestation of both psychiatric and neurologic illness. Psychiatric disturbances associated with mutism include schizophrenia, affective disorders, conversion reactions, dissociative states, and dementias. Neurologic disorders producing mutism involve the basal ganglia, frontal lobes, or limbic system structures. In psychiatric and neurologic conditions, mutism is often associated with other signs of catatonia. The authors review the literature on mutism, including psychiatric, neurologic, toxic-metabolic, and drug-induced causes. Methods to discriminate among the many causes of mutism in the clinical setting are discussed, and 22 new cases of mutism are reported to emphasize the wide differential diagnosis.
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PMID:Mutism: review, differential diagnosis, and report of 22 cases. 377 29

The unique situation that the Norwegian 1891 census included information on consanguineous relation between spouses and that first admissions to psychiatric hospitals by diagnosis were available for the years 1921-40, formed the basis for the present study. There are similarities between the pattern of inbreeding and admission rates in our rural communities, but we were unable to demonstrate any significant correlation. This is interpreted as due to selective avoidance in the choice of a marriage partner, particularly between near relatives. Good neighbourhood knowledge was an important factor in our sparsely populated communities with a marriage pattern distinguished by extreme geographical proximity of residence of spouses. The considerably lower proportion of first cousin matings than expected among parents of psychiatric in-patients 1926-55, illustrates the lower psychiatric morbidity in offspring of consanguineous parentage. Admissions 1921-40 comprised only functional psychoses with a predominance of schizophrenia (greater than 80%), which today is diagnosed in less than 10%. A decline in incidence rate is not likely, whereas changing diagnostic practice is probably a main factor. The near disappearance of catatonia and hebephrenia could be related to the introduction of psychotropic drugs and the accompanying improvement in hospital treatment. The epidemiology of schizophrenia is unchanged with a significant excess in lower social classes. This could in part be due to schizophrenic phenocopies related to the unchanged social differential in infant mortality and morbidity (including a particular season of birth effect), in part to the prevalence of adverse environment postnatally. The considerably greater male marital differential has probably a social cause, whereas male earlier onset of disease and more severe course of the disease are discussed in relation to the new concept of progressive sexual brain differentiation.
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PMID:Inbreeding and schizophrenia. 379 75

For the continued availability of electroconvulsive therapy (ECT) in clinical practice on equal footing with other treatments, and without judicial interference, the following points are essential: ECT should be used or not used on the basis of scientific evidence and not because of public opinion or antipsychiatric propaganda. There should be no hesitation to use ECT in conditions where its omission would mean prolonged suffering, risk of suicide, or death from other causes (deep melancholic syndromes, acute lethal catatonia, psychogenic confusion). ECT should not be used where the effect is short-lived or must be paid at the price of an organic syndrome (schizophrenia, paranoid states, organic confusions). Efficiency should be optimal (oxygen, superficial narcosis, absence of benzodiazepines, generalized tonic-clonic seizures of at least 30-sec duration, maintenance treatment with antidepressive drugs). Safety should be optimal, not only for life but also for cerebral functioning (anesthesiological management, unilateral nondominant stimulation, pulse wave stimuli, appropriate number of treatments, not too closely spaced). The mechanism of action should be the object of further investigation. Such research will open possibilities for finding drugs that can compete with ECT.
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PMID:Use and misuse of electroconvulsive treatment. 402 14

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.
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PMID:DSM-III implications of the diagnoses of catatonia and bipolar disorder. 407 15

Questionnaires were completed by 73 volunteers with a history of probable schizophrenia, and by 67 patients admitted to the accident wards of a general hospital. A high incidence of sensory distortions was recorded in the schizophrenic group compared with the controls, distortions of brightness contrast being the most common. Many schizophrenic patients reported that such distortions were reduced or removed early in treatment. Patients who reported visual distortions also tended to report visual hallucinations. The results are discussed with reference to the hypothesis that perceptual malfunction may underlie some other schizophrenic disorders such as delusions or catatonia.
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PMID:Perceptual changes in schizophrenia: a questionnaire survey. 408 Aug 89

In the present study several drugs that are predominantly agonists of kappa receptors were tested in rhesus monkeys prepared with deep and surface brain electrodes. The administration of two benzomorphan derivatives and of ethylketocyclazocine induced acute behavioral effects resembling catatonia concomitant with generalized spike and slow-wave electroencephalographic activity at widespread brain sites, that lasted for about 1 hr. After administration of one to three doses of these agonists (the benzomorphan derivatives to five monkeys and the ethylketocyclazocine to two monkeys), chronic recording changes developed, characterized by continuous high-amplitude spiking activity focal at the anterior septal region and periaqueductal gray of the mesencephalon. They increased in intensity with the passage of time, the monkeys having been followed as long as 5 months without further drug administration. Light microscopy and electron microscopy showed no structural abnormalities in the monkey brains at the sites of altered recordings, although occasional dendritic atrophy was noted at all cortical and subcortical brain sites examined. Chronic recording changes did not develop in a monkey that received U-50,488H on eight occasions. And none of the electrode-implanted monkeys that served as controls (having received no kappa agonists) developed recording changes. The sites affected by the active kappa agonists were those at which abnormal activity has been correlated with psychotic behavior. The ability of the kappa agonists to induce a lasting physiologic change without corresponding structural change at those focal sites implicated in schizophrenia may prove a useful probe in further investigations into the cause of schizophrenia and its ultimate treatment.
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PMID:Kappa opiate receptor agonists: effects on behavior and on brain function and structure in rhesus monkeys. 608 18

Two patients who developed the neuroleptic malignant syndrome (NMS) are described, and pertinent literature is reviewed. A 30-year-old man developed NMS, apparently as a result of haloperidol treatment of chronic undifferentiated schizophrenia. Treatment with cooling blankets, acetaminophen, dantrolene sodium, and bromocriptine mesylate decreased abnormal vital signs, but catatonia continued. After 30 treatments with electroconvulsive therapy over a one-month period, the patient's catatonia was resolved, and he was discharged on no medication with the schizophrenia in remission. The second patient was a 22-year-old woman who developed NMS after five weeks of therapy with haloperidol and thiothixene for an acute episode of abnormal behavior. She did not respond to therapy with cooling blankets, acetaminophen, antibiotics, and amobarbital sodium. Dantrolene sodium therapy produced no improvement except for some relief of muscular rigidity. Electroconvulsive therapy (22 treatments over one month) successfully decreased the patient's elevated liver enzymes and leukocyte count, but periodic temperature elevations and catatonia continued. Prompt diagnosis and treatment of NMS are essential, as the mortality rate is 20%. Acute lethal catatonia and malignant hyperthermia are considered in differential diagnosis. Both central and peripheral pathophysiologic mechanisms are probably involved in NMS, and most cases are seen in patients with psychiatric illness. Onset of NMS does not seem related to duration of neuroleptic therapy and, in susceptible persons, additional factors may be required to trigger onset of NMS. Symptoms, including diffuse muscular rigidity, akinesia, and fever, develop within 24-72 hours. Neurologic symptoms may develop or worsen, and leukocytosis and elevated levels of liver enzymes occur. Death can result from respiratory or cardiovascular failure, and rhabdomyolysis can lead to acute renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection and management of the neuroleptic malignant syndrome. 614 37

To elucidate the significance of beta-endorphin in human cerebrospinal fluid (CSF), CSF levels of beta-endorphin-like immunoreactivity (beta-EP-LI) in various diseases were determined by a specific radioimmunoassay and compared with simultaneously determined ACTH-like immunoreactivity (ACTH-LI) levels in CSF. CSF beta-EP-LI and ACTH-LI in the control group, consisting of 5 normal subjects and 19 patients with nonendocrine diseases, were 22.2+/-1.3 and 14.6+/-0.4 fmol/ml, respectively. CSF levels of these peptides in patients with schizophrenia (n = 19) and acromegaly (n = 10) were not significantly different from those in the control group. Patients with Cushing's disease (n = 7) had significantly lower CSF beta-EP-LI and ACTH-LI levels than those in the control group. Four of them showed a parallel increase in CSF beta-EP-LI and CSF ACTH-LI levels after the complete removal of pituitary microadenomas (P < 0.05). Gel chromatography of CSF beta-EP-LI from a normal volunteer, a control patient, and one patient each with catatonia, Nelson's syndrome, Cushing's syndrome (adrenal adenoma), and acromegaly gave similar patterns consisting of three peaks with the elution positions comparable to those of authentic beta-endorphin, beta-lipotropin, and possibly their precursor molecule. Gel chromatographic patterns of CSF beta-EP-LI and ACTH-LI were compared in a normal volunteer. The first peaks of beta-EP-LI and ACTH-LI eluted at the same position and the second peak of ACTH-LI coincided with the elution position of authentic ACTH.CSF beta-EP-LI and ACTH-LI levels determined every 5 min over a period of 80 min in three normal volunteers did not show moment-to-moment variability.A significant correlation (r = 0.75, P < 0.001) was seen between CSF beta-EP-LI and ACTH-LI levels in normal subjects and patients studied (n = 73). This suggests that beta-endorphin and ACTH in human CSF share the common regulatory mechanism in normal and pathologic conditions.
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PMID:Immunoreactive beta-endorphin and adrenocorticotropin in human cerebrospinal fluid. 625 11


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