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)

Enzymes concerned with neurotransmitter metabolism were measured postmortem in 50 regions from the brains of 11 chronic schizophrenics, 2 patients with senile dementia, 1 depressive, and 18 controls. Enzymes studied were tyrosine hydroxylase, dopa decarboxylase, glutamic decarboxylase, choline acetyltransferase (CAT), and acetylcholinesterase. The schizophrenic group had high CAT activities in the hippocampus, caudate, putamen, and nucleus accumbens; the other patients from the same hospital did not. A compensatory response to long- or short-term drug usage is considered, but correlations are hard to establish in the group studied. An alternative hypothesis proposes that the high levels are a compensatory response to defective cholinergic receptors in the affected areas. On this hypothesis, and by analogy with chorea, dopaminergic antagonists would act in schizophrenia by helping to reestablish cholinergic-dopaminergic balance.
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PMID:Possible changes in striatal and limbic cholinergic systems in schizophrenia. 4 82

1. The treatment of schizophrenic symptoms has not the same efficacy in acute and chronic phases of the disease and on the various target symptoms of schizophrenia. 2. The ideal antipsychotic drug might have different properties, sometimes contradictory, to be effective both on paranoid and hebephrenic symptoms which seem to be a mirror image of the same disorder. 3. Basic perspectives in the chemotherapy of schizophrenic psychoses must be founded on better methodological considerations in clinical trials, on a better use of antipsychotic drugs with the help of pharmacokinetic data and computerized EEG and also on new neurochemical findings. 4. Recent data on the mode of action of neuroleptics open up new therapeutic classes of drugs. Such are GABA-like drugs and, more recently, beta-blockers.
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PMID:Perspectives in chemotherapy of schizophrenic psychoses. 4 63

1. Progress in 25 years' history of the neuroleptics is briefly reviewed. 2. Development of certain butyrophenones more directly effective in "minus" symptoms of schizophrenia and introduction of depot neuroleptics is discussed. 3. Extrapyramidal motor side effects (EPMS) are still a serious problem in the treatment. 4. Clozapine does not have EPMS. This drug could therefore become the starting point of a series of less hazardous antipsychotic drugs. 5. The neuroleptics can be used as tools for exploration of the etiopathogenesis of schizophrenia. Some important pharmacological mechanisms, i.e. their antidopaminergic activity, are briefly outlined.
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PMID:Treatment of schizophrenia. 4 64

Whole blood, plasma, or serum levels of various components were measured in fasting, drug-free control subjects and drug-free schizophrenic patients. Compared to normal controls, chronic schizophrenic patients showed increased alpha2-globulins and decreased plasma cholinesterase activity and ceruloplasmin activity, and acute schizophrenic patients showed decreased alpha2-globulins. Compared to chronic patients, acute schizophrenics showed decreased alpha2-globulins and IgA. Compared to normal controls of similar age, chronic schizophrenic patients weighed less, were shorter, and had smaller body surface area. The acute schizophrenic patients were significantly younger than the normal subjects or chronic schizophrenics but there was no difference in the other physical measurements. The present study indicates no gross disturbances in the blood variables studied. That some differences are statistically significant from controls is of scientific interest, but of no clinical value in the diagnosis of schizophrenia.
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PMID:Blood protein fraction comparisons of normal and schizophrenic patients. 4 63

The possible mechanisms that underlie symptom formation in childhood schizophrenia are discussed. A body of research evidence has been reviewed in which dissociation in relation to information processing was examined for its possible consequence in the formation and expression of symptomatology. Schizophrenic children have been found to exhibit dissociation of integrative processes among the sense systems at a level which is several years below normal expectation, and they usually fail to improve as age increases. The clinical manifestations of schizophrenia are considered to be the consequence of the conflict, distortion, and deprivation that derive from failure in information processing. These consequences can best be understood within a developmental framework which encompasses the different age-stages of function. This approach to the understanding of symptom formation is discussed in relationship to other evidence which suggests that primary neurological abnormality is present in schizophrenic children. Thus the identification of abnormality of intersensory integrative function may increase our understanding of etiology as well as of the mechanisms of symptom formation in schizophrenic children.
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PMID:Symptom formation as an expression of disordered information processing in schizophrenic children. 4 49

The examination of 32 children with Kanner's syndrome of early infantile autism permits to assume that this syndrome in some of the cases is expressed only by inborn anomalies which correspond to constitutional psychopathy in adults. In most of the cases this syndrome forms the initial expression of child schizophrenia. In separate cases disorders very similar to Kanner's syndrome may be seen after the first olliterated attack during early childhood (up to 3 years). A comparative study of the same indices of development of 268 children with an early onset of schizophrenic process in spite of some differences confirms that Kanner's syndrome is very close to childhood schizophrenia. An analysis of genealogical data shows genetical relations of Kanner's syndrome with child schizophrenia.
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PMID:[Kanner's syndrome and childhood schizophrenia]. 5 49

The model psychosis associated with amphetamine overdosage is known to bear a close resemblance to acute paranoid schizophrenia. Amphetamine is chemically similar to the endogenous sympathomimetic amine, phenylethylamine, which possess many of its pharmacological properties. It is suggested that some cases of schizophrenia may be associated with an abnormal phenylethylamine response, either from increased concentrations of the amine or from abnormal receptor sensitivity to it.
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PMID:Does phenylethylamine cause schizophrenia? 5 86

A representative sample (R.S.) of 79 subjects living in Edinburgh common lodging houses was compared with a clinical series (C.S.) of 44 patients from the same type of resisence. C.S. patients were more likely to be out of work, to be under 55 years of age, and to have been married as some time. They had spent much shorter times in lodging houses, in Edinburgh and at their current address. Alcoholism was rather more often diagnosed in the C.S., and personality disorder much more often. Schizophrenia tended to be found more in the R.S. The C.S. obtained higher Personal Illness and 'Character Disorder' scores. It is concluded that those subjects presenting to the psychiatric services are a highly selected group quite unrepresentative of homeless single persons in general.
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PMID:The homeless person and the psychiatric services: an Edinburgh survey. 5 3

Catatonia is often automatically assumed to be a subtype of schizophrenia. This paper proposes that it be considered as a syndrome with various possible causes. Physicians are advised to be aware of potentially serious organic illnesses which may underlie the catatonic syndrome.
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PMID:The catatonic syndrome. 5 26

The antipsychotic actions and extra-pyramidal side-effects of neuroleptic drugs are strongly correlated with their ability to block central dopaminergic transmission. It is argued that the former are more closely related to actions on dopaminergic mechanisms in the "mesolimbic dopamine" system, and the latter to similar actions in the striatum. Although the amphetamine psychosis closely resembles paranoid schizophrenia and may be due to excess dopamine release, clinical, biochemical, and endocrine studies suggest that dopaminergic overactivity is not a necessary concomitant of schizophrenic illnesses. It is suggested that the primary defect in schizophrenia does not lie in the dopamine neuron. It remains to be excluded that the receptors, particularly in the mesolimbic dopamine areas, become supersensitive, or that there is a deficit in a system which normally acts in antiagonism to the to the mesolimbic dopamine system.
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PMID:Dopamine and schizophrenia. 6 Jun 35


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