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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Considerable evidence exists linking dopamine with schizophrenia. Other neurotransmitters including acetylcholine, serotonin and gamma-aminobutyric acid (GABA) are also being implicated. Neurotransmitters act via receptors on brain cells and evidence suggests that antipsychotic drugs exert their therapeutic actions and produce side effects by receptor blockade.
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PMID:Mayo Seminars in Psychiatry: dopamine and schizophrenia--a review. 3 63

This paper reviews the present status of the transmethylation and the dopamine hypotheses of schizophrenia and presents recent data on the definitive identification and measurement of the endogenous hallucinogen, dimethyltryptamine (DMT) in human cerebrospinal fluid and urine. Elevated levels are found in some cases of schizophrenia and of liver disease. Evidence is discussed showing that DMT may be a normal neuroregulatory agent which is responsive to stress or emotional reactions.
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PMID:Biochemistry and the schizophrenias. 3 48

Long-term administration of antipsychotic drugs to animals induces super-sensitive mesolimbic postsynaptic dopamine receptors. It is possible that a similar process can occur in man. Following a reduction in the dose of antipsychotic medications, or their complete discontinuation, mesolimbic dopamine receptor supersensitivity could be reflected in rapid relapse of schizophrenic patients, the development of schizophrenic symptoms in patients with no prior history of schizophrenia, or in the necessity for ever-increasing doses of long-acting depot fluphenazine to maintain a remission.
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PMID:Is there a limbic system equivalent of tardive dyskinesia? 3 41

Two catecholamine-containing pathways, the locus ceruleus system and the dopamine neurons arising from the ventral mid-brain, may be involved in reward. Dopamine neurons function as a system for energizing the organism's responses and directing them toward significant environmental stimuli, but the functions of the locus ceruleus system remain obscure. It appears increasingly likely that neuroleptic drugs exert their anti-psychotic effects in acute schizophrenia by blocking dopamine receptors, although the time course of the effect suggests that the mechanism is more complex than a simple reversal of a neurohumoral imbalance. Evidence from postmortem studies suggests that, at least in the chronic state, dopamine turnover is not increased, but that there may be an increase in postsynaptic receptor density in some cases, including some patients who apparently had not received medication in the year before death. The evidence is consistent with Olds and Travis' conjecture that "counteraction of positive feedback processes subserving positive reinforcement mechanisms may be a key to control of certain psychotic episodes".
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PMID:Catecholamine reward pathways and schizophrenia: the mechanism of the antipsychotic effect and the site of the primary disturbance. 3 90

Numerous studies have been reviewed concerning the relationship of the catecholamines and indoleamines to depression and its treatment with antidepressant drugs. The profusion of data on the subject suggests the amines may be implicated in the disease, however no convincing hypothesis is available which unites the two. A similar situation seems to exist concerning the antipsychotic agents, dopamine and schizophrenia. The evidence appears to be overwhelming relating dopamine in the action of these agents and yet serious inconsistencies have been reported suggesting the need for a revision of the hypothesis regarding the mode of action of antipsychotic agents.
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PMID:Antidepressant and antipsychotic agents. 4 Nov 88

The hypothesis that schizophrenia results from overactive dopaminergic influences suggests that reducing dopamine synthesis may increase the clinical effects of dopamine receptor blocking neuroleptic drugs. The neuroleptic potentiating role of alpha-methyl-paratyrosine (AMPT), a tyrosine hydroxylase inhibitor, was compared with haloperidol and placebo in a double-blind cross-over trial. Both AMPT and haloperidol increased the anti-schizophrenic effect of neuroleptic treatment in reduced dose compared with placebo (P less than 0.05), though two patients relapsed during the AMPT period. Both drugs slightly increased extrapyramidal symptoms, but the effect was greater with haloperidol. The limited antipsychotic effect and the potential for aggravating neurological symptoms suggest that the combination of AMPT and neuroleptics does not offer a superior advantage to treating schizophrenia. AMPT, however, may still be used as a research tool in elucidating pathogenetic mechanisms.
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PMID:Neuroleptic-potentiating effect of alpha-methyl-p-tyrosine compared with haloperidol and placebo in a double-blind cross-over trial. 4 13

Cerebrospinal fluids (CSF) from 35 patients with senile or presenile dementia and from 13 patients with schizophrenia and related syndromes were examined in cell cultures with the aim to isolate Herpesvirus hominis 1 (HVH 1) or other viruses. Serum and CSF antibodies to HVH 1 and/or interferon in the patients indicated a recent HVH 1 antigenic or viral activity. In the CSF of two senile demented patients and of one patient with schizoaffective psychosis, agents of low virulence, causing a cytopathic effect in 3 or 4, but not more, subsequent passages were detected and identified as HVH 1 by immunofluorescence. A focus of cells containing HVH 1 antigen at the cell membrane and in cytoplasm was visualized by immunofluorescence in an explant from nucleus amygdalae from 1 of 6 patients with schizophrenia and related syndromes examined. In the original biopsy materials, various virus-like structures were found in nuclei and cytoplasm of astrocytes and neurocytes and in axons in the neuropil.
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PMID:Latent herpesvirus hominis 1 in the central nervous system of psychotic patients. 4 36

Dopamine and its metabolites homovanillic acid and dihydroxyphenylacetic acid, noradrenaline, serotonin and its metabolite 5-hydroxyindoleacetic acid, and tryptophan and its metabolite kynurenine have been assayed in 9 schizophrenic and 10 control brains, together with the monoamine-related enzymes tyrosine hydroxylase monoamine oxidase, dopamine-beta-hydroxylase, and catechol-o-methyl-transferase. In schizophrenic brains dopamine, noradrenaline and serotonin were significantly increased in some areas of corpus striatum, but there were no significant changes in enzyme activity or monoamine metabolite concentrations in any of the brain areas examined. The findings are not consistent with theories that serotonin or noradrenaline stores are grossly depleted or noradrenaline neurones have degenerated, or that monoamine oxidase activity is abnormal, in schizophrenia, and provide no direct support for the hypothesis that dopamine neurones are overactive.
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PMID:Monoamine mechanisms in chronic schizophrenia: post-mortem neurochemical findings. 4 9

A general introduction is given and followed by a review of recent literature under the following subheadings: electrodermal activity, cardiovascular activity, smooth pursuit eye movement, electroencephalogram, and evoked potentials. An attempt is made to assess the clinical significance of the findings reported in each area and to indicate directions for future investigation. The feasibility of defining homogeneous subgroups in schizophrenia using psychophysiological parameters is also considered. The review concludes with the recommendation that peripheral psychophysiological studies entailing (1) comprehensive recording of brain electrical activity and (2) behavioral experimentation on variables thought to be influenced by schizophrenia (e.g., sustained attentional ability) are promising directions for future research. Relationships between behavioral and psychophysiological variables determined by such studies (and possibly subgroupings) may then become the basis for neurophysiological-neurochemical investigations of specific abnormalities underlying such relationships and subgroups.
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PMID:Recent studies of psychophysiology in schizophrenia. 4 41

Schizophrenia and certain forms of idiopathic mental retardation may result from covert immune complex disease of the basal lamina of the choroid plexus, a process already known to cause covert transport dysfunction in similar structures of, for example, skin, bowel, kidney, and endocrines. Plexial attack could lead to cerebrospinal fluid contamination and then, via an "open" ependyma, to neurotransmitter dysfunction in the periventricular limbic brain. The immune complex mechanism implies polygenic induction, direct or autoimmune, of immune sensitivity to exogenous agents and is thus compatible with the genetic picture in schizophrenia. Candidate agents include viral coat peptides and cereal grain glutens. The glutens are known to cause immune complex skin and bowell disease variants, and some empirical evidence links them to schizophrenia. Only newer immunofluorescence methods can detect the pathology, which is otherwise silent. Systemic lupus erythematosus provides a model since it is a genetic immune complex disease strongly associated with schizophreniform psychoses, exhibits choroid plexial immunofluorescence but no central nervous system pathology by ordinary methods, and may be triggered by viruses.
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PMID:Covert transport dysfunction in the choroid plexus as a possible cause of schizophrenia. 4 42


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