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)

Serum-cortisol response to the 1 mg overnight dexamethasone suppression test was investigated in 86 patients with unipolar primary depressive illness and 80 non-depressed controls (45 with mania and 35 with schizophrenia). The depressed patients were assigned to one of three genetic subtypes according to the family psychiatric history. Resistance to suppression of serum-cortisol by dexamethasone was found in 37 of 86 (43%) depressives and none of the 80 controls. Non-suppression distinguished the three genetic subtypes of depression, being found in 23 of 28 (82%) patients with familial pure depressive disease (F.P.D.D.), 13 of 35 (37%) patients with sporadic depressive disease (S.D.D.), and 1 of 23 (4%) patients with depression spectrum disease (D.S.D.). The three genetic subtypes were further distinguished by the age of onset, with S.D.D. the oldest, and by the number of previous depressive episodes, with F.P.D.D. the most. Severity of depression did not separate the three subtypes. This is the first report of a distinct neuroendocrine abnormality which supports an objectively defined classification of unipolar primary depressive illness. It is suggested that unipolar primary depressive illness is three or more separate illnesses, each with a potentially distinctive mode of inheritance, pathophysiology, neurochemistry, clinical course, and treatment response.
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PMID:Genetic subtypes of unipolar primary depressive illness distinguished by hypothalamic-pituitary-adrenal axis activity. 8 87

The hypotheses of relative cholinergic underactivity in Huntington's disease, tardive dyskinesia, mania, and schizophrenia were pharmacologically investigated, using physostigmine and choline chloride. Intravenous physostigmine improved the involuntary movements of all of four patients with tardive dyskinesia and three of six patients with Huntington's disease. Physostigmine infusion also decreased manic symptoms in six of nine patients with mania, but had no beneficial effects in three patients with schizophrenia. Precursorloading with choline chloride may increase brain acetylcholine levels and central cholinergic activity. In patients with movement disorders a transient improvement during physostigmine infusion predicted a positive response to a trial of oral choline chloride. One manic patient may have been improved by choline chloride, however choline chloride did not improve symptoms in four of six schizophrenix patients. Chronic treatment with oral choline chloride increases plasma levels of choline during administration and for approximately 48 hr after discontinuation of treatment. A single 5-g dose of choline chloride also transiently raises plasma choline levels. These results with physostigmine support the hypotheses of cholinergic underactivity in Huntington's disease, tardive dyskinesia, and mania. Agents which might chronically increase cholinergic activity such as choline chloride should be further tested in these disorders.
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PMID:Pharmacological investigations of the cholinergic imbalance hypotheses of movement disorders and psychosis. 14 24

Acetylcholinesterase (AChE) was measured in the cerebrospinal fluid (CSF) of patients with a diagnosis of Huntington's disease, depression, schizophrenia, or mania and also in the CSF of normal subjects. No significant differences in CSF AChE were found between any diagnostic group and normal subjects. Furthermore, the administration of choline chloride, physostigmine, or probenecid did not significantly alter CSF AChE. No diurnal variation in CSF AChE activity was apparent. These findings, combined with the unclear relationship of brain AChE to CSF AChE, suggest that this measurement does not reflect the relative cholinergic underactivity presumed to exist in some neuropsychiatric conditions.
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PMID:Cerebrospinal fluid acetylcholinesterase in neuropsychiatric disorders. 15 94

Narrow definitions of schizophrenia increase homogeneity at the expense of leaving unclassified many patients with shizophrenic symptoms. Family history and follow-up studies indicate that many such patients ought to be classified with those having affective disorders. This study determines morbid risks for affective disorder and schizophrenia in first degree relatives of patients with chart but not research diagnoses of schizophrenia. Comparisons with morbid risk figures for relatives of individuals satisfying research criteria for depression, mania or schizophrenia indicate that the 'non-Feighner schizophrenia' group is probably too heterogenous to be classified entirely as affective disorder or as schizophrenia.
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PMID:Should 'non-Feighner schizophrenia' be classified with affective disorder? 16 80

Inpatient admissions to all psychiatric hospital beds in England and Wales in 1970-73 were studied by month of admission for eight diagnostic groups. The admission rates for schizophrenia showed a pronounced seasonal variation, with a maximum in summer. The seasonal pattern for schizophrenia was very similar to the one shown for mania, although somewhat less marked. The admission rates for neurosis and for the large group of 'all other non-psychotic mental illness' showed little evidence of seasonal variation as there was could largely be explained by social factors. In schizophrenic and manic patients, the pattern of seasonal admissions (peak months July and August) is similar to the pattern reported for their births (peak months February and March). This is consistent with the hypothesis of an abnormal seasonal pattern of parental conception as the cause of the abnormal birth pattern.
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PMID:Seasonal variation in admissions of psychiatric patients and its relation to seasonal variation in their births. 26 89

Averaged cortical evoked potentials from single clicks were recorded from 51 patients and controls. The patient group consisted of 40 subjects with a diagnosis of 'nuclear' schizophrenia, and 11 subjects with diagnoses including mania, anxiety neurosis and personality disorder. Changes in auditory evoked cortical responses (AECR's) were most marked in clinically stable, dysphoric, chronic schizophrenics. These subjects showed reproducible, low amplitude, 'untidy' responses in which the amplitude of the primary peak was lower than the amplitude of later peaks. Chronic schizophrenics who were rated as being depressed, showed a more 'normal' AECR. AECR changes during the memorising of nonsense syllables demonstrated a functional separation between early and later peaks of the AECR. It was postulated that the AECR changes in schizophrenia and during memorising result from pathological patterns of cortical desynchronisation produced by altered mid-brain activity different from that of anxious arousal, and that the clinical 'steady-state' of chronic schizophrenia is reflected in the 'steady-state' desynchronisation changes in the AECR.
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PMID:Computer analyses of auditory evoked cortical potentials in schizophrenic subjects. 27 6

The excretion of the hallucinogen dimethyltryptamine (DMT) and its precursor N-methyltryptamine (NMT) was studied among 74 recently admitted psychiatric patients and 19 normal persons. Both compounds were detected in 24-hour urine samples from all subjects. Dimethyltryptamine excretion was greatest in schizophrenia, mania, and "other psychosis" and tended to decline as clinical state improved. Psychotic depressives excreted smaller amounts of DMT more akin to those excreted by neurotic and normal subjects. Urinary NMT excretion was unrelated to psychiatric diagnosis. Ratings on the Present State Examination (PSE) also indicated that increased excretion of DMT was associated with psychotic rather than neurotic psychopathology. Forty-three percent of the variance in urinary DMT levels could be explained in terms of six of the 38 PSE syndromes. Syndromes suggesting elation, perceptual abnormalities, and difficulty in thinking and communicating were most correlated with raised urinary DMT excretion.
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PMID:Increased excretion of dimethyltryptamine and certain features of psychosis: a possible association. 28 76

Present clinical and research methods of differential diagnosis of schizophrenia and affective psychoses rely very heavily on presenting symptoms and signs, especially in acute psychosis. We have reviewed studies bearing on this issue, including studies of the phenomenology of psychotic illness, outcome, family history, response to treatment with lithium carbonate, and cross-national and historical diagnostic comparisons. We conclude that most so-called schizophrenic symptoms, taken alone and in cross section, have remarkably little, if any, demonstrated validity in determining diagnosis, prognosis, or treatment response in psychosis. In the United States, particularly, overreliance on such symptoms alone results in overdiagnosis of schizophrenia and underdiagnosis of affective illnesses, particularly mania. This compromises both clinical treatment and research.
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PMID:Diagnosis in schizophrenia and manic-depressive illness: a reassessment of the specificity of 'schizophrenic' symptoms in the light of current research. 35 52

Systems of psychiatric diagnosis have been regularly criticized for their low reliability and their inability to fit accurately the kinds of patients coming for treatment. To explore the reasons for these problems, this study utilizes a new method, the biplot, for defining groups of similar patients and the relationships of these groups to key symptom clusters. Using this technique to analyze data from a representative sample of first admissions for psychiatric disorder, results showed: a) symptom clusters representing the classical diagnostic categories, mania, schizophrenia, neurotic depression, and psychotic depression, were readily identified; b) however, only a few patients were clustered near these traditional syndromes. These findings suggest that although syndromes do exist that fit traditional diagnostic categories, the vast majority of patients fall between these syndromes, having characteristics from several of them. For most patients, forcing the diagnostician to choose among the categories requires an arbitrary decision that may contribute to dissatisfaction in the diagnostician who recognizes how misleading the diagnosis can be.
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PMID:Do psychiatric patients fit their diagnoses? Patterns of symptomatology as described with the biplot. 36 91

The authors describe three patients with delusional unipolar depression whose delusional thinking worsened markedly following administration of tricyclic antidepressant drugs. The patients had met Research Diagnostic Criteria for major depressive episode and had no evidence of schizophrenia or mania. Since tricyclic antidepressants are known to exacerbate psychosis in schizophrenic patients, it is sometimes suggested that the exacerbation of psychotic thinking in depressed patients indicates schizophrenia. The authors suggest that such an exacerbation does not in itself indicate schizophrenia but may occur in patients with an affective disorder who are prone to depressive delusions. The authors discuss the use of antipsychotic medication in this patient group and present a neurochemical hypothesis to explain the interaction of the drug with the illness, which results in exacerbation of psychotic thinking.
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PMID:Exacerbation of psychosis by tricyclic antidepressants in delusional depression. 42 46


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