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

Many observers have noted similarities between dreams, hallucinogenic drug states, and schizophrenia. In the present article, certain fundamental areas of convergence between the three states are described. Consideration is given to the hallucinogenic drug model of psychosis: the reasons for its initial attractiveness, and the reasons for its current disfavor. The concept of ego boundaries is defined, examined, and applied to the three states. In these states, the ego's capacity to average or synthesize various self-representations into a continuous, coherent self is compromised--leading to an impairment of the reality-oriented secondary process, and the emergence of the florid attributes of the primary process. This can account for many of the familiar characteristics of the three states. Current neurophysiological theories of dream and hallucinogenic drug states are presented, with emphasis upon serotonin neurotransmission. Serotonin appears to play a prominent role in the regulation of these states. The analogy contained in the present article suggests that serotonin may play a role in regulating schizophrenic states as well.
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PMID:Dreams, hallucinogenic drug states, and schizophrenia: a psychological and biological comparison. 613 48

The independent status of schizoaffective psychosis is reviewed in relation to 6 hypotheses, using pattern of inheritance, treatment response, course and outcome, and platelet 5-HT uptake as discriminating variables. The 'coincidence of 2 diseases' hypothesis would predict an annual frequency of some 2 per 10(8), compared with the observed 2 per 10(5). The 'variant of schizophrenia' hypothesis has been supported from patient groupings weighted in favour of chronicity, but little else. The 'variant of affective psychosis' hypothesis has been supported in the manic sub-group by evidence of lithium response, and outcome better than schizophrenia (but worse than mania). However in the depressed sub-group, despite responsiveness to ECT, a tendency towards chronicity is observed in a substantial proportion. The 'provisional diagnosis' hypothesis is supported by heterogeneity of outcome, and the presence of both schizophrenia and affective disorder in families of schizoaffective patients, prompting a distinction between 'mainly schizophrenic' and 'mainly affective' groupings. Evidence for the 'third psychosis' hypothesis is mainly genetic, suggesting a small aetiologically distinct subgroup which breeds true. The authors conclude with an 'interacting process' hypothesis where distinct diseases can cause, or interact to cause, the same symptoms via some final common pathway of psychological dysfunction.
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PMID:The nosology of schizoaffective psychosis. 614 98

Biological studies of the relationships between the schizoaffective disorders, the affective disorders, and schizophrenia suggest that no simple reductionist model is supported by currently available data. Thus, both affective and schizoaffective patients but not schizophrenics, manifest abnormalities such as decreased platelet serotonin (5-HT) uptake, blunted clonidine-induced increase in serum growth hormone, shortened latency of rapid eye movement (REM) sleep, and increased REM density. However, there are some types of studies which show greater similarity between schizoaffective and schizophrenic patients than between schizoaffectives and affectives--e.g., increased cerebrospinal fluid (CSF) norepinephrine levels, increased platelet 5-HT content, and decreased prostaglandin E1-stimulated adenylate cyclase activity. Other types of studies show abnormalities common to all three groups of psychoses--e.g., eye tracking dysfunction, elevated CSF concentration of gamma-aminobutyric acid, and neuromuscular abnormalities. There are also abnormalities that have been reported to be present in only one type of the psychoses. Although none of these findings have been so unequivocally demonstrated that they can be considered to be firmly established, they do suggest that it is premature to conclude that the schizoaffective disorders are subtypes of the affective disorders. The possibility of a continuum model of the psychiatric psychoses of unknown etiology merits further consideration. Further biological studies of a broad range of psychiatric psychoses with inclusion of the schizoaffective categories appear indicated.
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PMID:Biological studies of schizoaffective disorders. 642 46

To explore the possible role of serotonin (5-HT) in the etiology of schizophrenia, platelet 5-HT concentrations were determined in 41 schizophrenic (and schizoaffective, mainly schizophrenic) patients diagnosed by the RDC and 34 normal controls. There was a significant difference between the patient and control groups with the 16 paranoid, 11 undifferentiated, and 8 schizo-affective depressed patients having significantly higher mean platelet 5-HT concentrations than the controls. An analysis of variance considering the effect of race, sex, and diagnosis demonstrated a significant difference between black patients and black controls but no significant difference between white patients and white controls. Within the patient sample, platelet 5-HT concentrations were positively correlated with severity of auditory hallucinations (on the PSE) and negatively correlated with lack of insight (on the PSE) and conceptual disorganization (on the BPRS). In a subsample of 21 patients, there was no relationship between platelet 5-HT and CT findings of either enlarged ventricles or cortical atrophy.
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PMID:Platelet serotonin levels in schizophrenia: relationship to race and psychopathology. 661 45

The relationship between DSM-III schizophrenia, major affective disorders, and the psychotic disorders not elsewhere classified (PDNEC) can be explored through studies which attempt to determine whether these disorders can be differentiated from one another and normal controls by biological measures. Preliminary results of an ongoing project which utilizes measures of blood platelet monoamine oxidase (MAO), serotonin (5-HT) uptake, and 5-HT content, and the apomorphine-induced increase in growth hormone (GH) to accomplish these goals are reported here. DSM-III major affective disorders (bipolar disorder and major depression) can be differentiated from normal controls by the V max of platelet 5-HT. Platelet 5-HT V max of bipolar disorder, depressed type, is significantly different from that of schizophrenia and PDNEC. Elevated platelet 5-HT content is present in black schizophrenic patients compared to black normal controls. Platelet MAO was increased in a small group of schizophreniform female patients. There was no difference in the apomorphine-induced GH response between any of the diagnostic groups. If confirmed in a larger series of patients, these results tend to identify the PDNEC more closely with schizophrenia than the major affective disorders.
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PMID:Biological studies of DSM-III psychotic disorders. I. Platelet measures and apomorphine-induced growth hormone response. 675 71

Platelet uptake of serotonin (5-HT) was studied in drug-free groups of normal controls, depressives and schizophrenics. The Michaelis constant was significantly higher in both the schizophrenics and the depressives than in the controls. The Vmax did not differ significantly between the three groups. Uptake velocity at low substrate concentrations was significantly lower in the schizophrenic group and showed a similar trend in the depressives. There were no significant differences in Km or Vmax when depressives wee subclassified as unipolar and bipolar. There were no significant correlations between 5-HT uptake kinetics and severity of illness. These findings raise the possibility of a structural defect inthe 5-HT reuptake system in the major psychoses that reduces the affinity of the carrier for the amine. This alteration, if present in central serotonergic neurons, may play a role in the etiology and pathogenesis of depression and schizophrenia.
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PMID:Altered platelet serotonin uptake kinetics in schizophrenia and depression. 713 68

The behavioural consequences of daily beta-phenylethylamine (PEA) administration for a period of 6 weeks have been examined. Rats first showed signs of the 5-HT behavioural syndrome after a single injection of PEA (50mg/kg) or 7 daily injections of PEA (25mg/kg). The syndrome reached peak intensity after 3 weeks treatment and was prevented by pre-treatment with 5-HT antagonists mianserin and methysergide or the neuroloptic clozapine but relatively unaffected by pre-treatment with haloperidol. These data provide strong evidence for an effect of PEA on brain 5-HT mechanisms. Because of the similarity between PEA and amphetamine and the suggestion that PEA may be involved in the aetiology of schizophrenia, it is proposed that the mechanisms of action of PEA be reassessed taking into account its ability to affect 5-HT systems in addition to catecholaminergic systems.
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PMID:Behavioural effects of acute and chronic beta-phenylethylamine administration in the rat: evidence for the involvement of 5-hydroxytryptamine. 732 83

Considerable evidence has accrued in the last two decades to support the hypothesis that alterations in serotonergic neuronal function in the central nervous system occur in patients with major depression. These findings include the following: (a) reduced cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of serotonin (5-HT) in drug-free depressed patients; (b) reduced concentrations of 5-HT and 5-HIAA in postmortem brain tissue of depressed and (or) suicidal patients; (c) decreased plasma tryptophan concentrations in depressed patients and a profound relapse in remitted depressed patients who have responded to a serotonergic antidepressant when brain tryptophan availability is reduced; (d) in general, all clinically efficacious antidepressants augment 5-HT neurotransmission following chronic treatment; (e) clinically efficacious antidepressant action by all inhibitors of 5-HT uptake; (f) increases in the density of 5-HT2 binding sites in postmortem brain tissue of depressed patients and suicide victims, as well as in platelets of drug-free depressed patients; (g) decreased number of 5-HT transporter (determined with [3H]imipramine or [3H]paroxetine) binding sites in postmortem brain tissue of suicide victims and depressed patients and in platelets of drug-free depressed patients. In our studies, this reduction in platelet 5-HT transporter binding is not due to prior antidepressant treatment of hypercortisolemia and is not observed in mania, Alzheimer disease, schizophrenia, panic disorder, fibromyalgia, or atypical depression. In a pilot study, this deficit predicted treatment response to an experimental antidepressant. These findings support the hypothesis that alterations in 5-HT neurons play a role in the pathophysiology of depression.
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PMID:Role of serotonin in the pathophysiology of depression: focus on the serotonin transporter. 1949 50

In this study, we investigated whether risperidone, a serotonin-S2A (5-HT2A)/dopamine-D2 (D2)-receptor antagonist, inhibits phencyclidine (PCP)-induced stereotyped behaviors in comparison with haloperidol and ritanserin. Moreover, we also attempted to investigate the effects of these antipsychotics on the contents of dopamine, serotonin (5-HT) and their metabolites in rat striatum and frontal cortex. In rats, PCP (5 mg/kg, i.p.) caused hyperlocomotion and stereotyped behaviors, including sniffing, head-weaving, backpedalling and turning. Both resperidone (0.8-2.4 mg/kg, p.o.) and haloperidol (0.3-1.0 mg/kg, p.o.) inhibited these behaviors, except for backpedalling, in a dose-dependent manner. PCP (10 mg/kg, i.p.) produced hyperlocomotion and stereotyped behaviors, including rearing, sniffing head-twitch, backpedalling and turning. Risperidone (0.8-2.4 mg/kg, p.o.) inhibited both hyperlocomotion and PCP-induced behaviors, except for backpedalling, while ritanserin (3-10 mg/kg, p.o.) inhibited only the head-twitch. These results suggest that risperidone may have an antipsychotic effect on schizophrenia as well as PCP psychosis in humans by exerting a mixed 5-HT2A/D2 antagonism. Neurochemically, the increasing effects of risperidone on the content of DOPAC and the ratio of DOPAC to dopamine in the striatum were lower than those of haloperidol. These findings may support the view that the extrapyramidal side effects of risperidone are lower than those of haloperidol in clinical situations.
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PMID:Effects of risperidone on phencyclidine-induced behaviors: comparison with haloperidol and ritanserin. 753 32

Serotonin-dopamine antagonists (SDAs) offer the possibility of improved treatment of schizophrenia compared with conventional neuroleptics and have superior safety profiles. Clinical trial data have so far been published for only three SDAs to date, namely, risperidone, sertindole, and olanzapine. Of these, extensive data are available only for risperidone, showing that at doses of 4 to 16 mg/day, it is superior to haloperidol at 10 to 20 mg/day. Furthermore, risperidone, 6 and 16 mg/day, significantly improved negative/symptoms, whereas 20 mg/day of haloperidol was ineffective. Risperidone also appears to cause fewer extrapyrimidal symptoms (EPS) than haloperidol, 10 or 20 mg/day. Similar advantages of risperidone over perphenazine have also been found. A clinical trial of sertindole showed that, at 20 mg/day, it was equivalent to haloperidol, 16 mg/day, and caused fewer EPS. Olanzapine, a chemical derivative of clozapine, has also been shown to be superior to haloperidol (10 to 20 mg/day) at doses of 7.5 to 17.5 mg/day. In addition, at doses of 12.5 to 17.5 mg/day, olanzapine was found to have a significantly superior effect on negative symptoms over haloperidol, 10 to 20 mg/day. Doses of up to 17.5 mg/day of olanzapine also caused fewer EPS than haloperidol, 10 to 20 mg/day. There was no evidence of any leukopenia in patients treated with olanzapine in this small study (N = 335). The low EPS liability of these SDAs, combined with their efficacy, suggests that SDAs should become the mainstay of treatment for schizophrenia.
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PMID:Clinical efficacy of serotonin-dopamine antagonists relative to classic neuroleptics. 753 85


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