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)

A 36 year-old female patient with schizophrenia and Tourette syndrome is described. Clinical course, present neurological and psychopathological state, results of psychological testing, computed tomography and MR tomography of the skull, EEG and evoked potentials are reported. Results of neurochemical analysis of CSF and plasma are presented. Possible relationships between Tourette syndrome and schizophrenia are discussed with particular reference to neurochemical findings.
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PMID:[Schizophrenic psychosis in a patient with Gilles de la Tourette syndrome]. 290 4

The biological enigma of schizophrenia has led, on the basis of thin evidence, to widen the field of clinical research to a study of endomorphines in this disease. Too many different methods of measuring the levels of opiate peptides in the CSF have been used so that it is not possible to analyse the results statistically. Clinical trials of agonists and antagonists to the opiate receptors have once again emphasised the biochemical heterogeneity of schizophrenics but have not allowed any confirmation that the endorphinical system plays any part in the genesis or symptomatology of schizophrenia. The presence of sub-groups who respond positively to experimental treatment can lead to the hope, despite the uncertainties of their mode of pharmacological action, to the next advance in the routine treatment of schizophrenia.
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PMID:[Endomorphines in schizophrenia]. 303 7

Electrophoretic studies of human CSF proteins from patients with diseases of the NS are reviewed. Various 1-DE methods are of similar value in identifying the non-specific OBs, which are helpful in the diagnosis of MS and recurrent GBS. In early and subclinical MS, OBs are of prognostic value, with IEF gels having the greater resolution. Silver-stained 2-DE gels provide the equivalent information to the OBs on 1-DE gels, with even greater sensitivity, and yield additional disease-associated protein data. Two proteins have proven to have diagnostic value in CJD and other changes that are still being evaluated have been identified in Parkinson's disease, GBS, Alzheimer's disease, schizophrenia and Herpes simplex encephalitis. The vastly improved CSF protein information obtained with silver-stained 2-DE gels heralds both a change from the relatively limited applications with 1-DE methods and also the need to adopt this approach in the routine clinical laboratory.
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PMID:Cerebrospinal fluid protein analysis in diseases of the nervous system. 306 25

1. CCK-peptides are distributed throughout the whole brain with the exception of the cerebellum. 2. There is strong evidence that they act as neuromodulators on the noradrenergic, opioid and mainly dopaminergic system. 3. CCK reduces food-intake. However, tolerance occurs, when chronically given. Thus, potential benefits in the treatment of obesity seem unlikely. 4. CCK increases threshold and tolerance to electrically and thermally induced cutaneous pain. CCK yields relief of pain in colic and ischaemic pain. 5. To date, results about CCK-content in CSF and post-mortem-brain in various psychiatric and neurological diseases related to the dopaminergic system are equivocal. 6. Treatment studies do not provide evidence for beneficial effects of CCK-peptides in schizophrenia.
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PMID:Cholecystokinin. 307 40

Validity and interpretation of neuroradiological findings in schizophrenics are still discussed controversially. This applies also to some adjacent functional diagnostic techniques, which could possibly give support to neuroradiology, as post-mortem histopathological examination, electrophysiological recording, and positron-emission tomography. One of the causes for the inconclusive findings could be the patient- and control-group sampling, which is despite standardized diagnoses still heterogeneous in factors determining ventricular size. This heterogeneity applies also to the adjacent functional-diagnostic studies. A prevalence of enlarged ventricules of about 10% in schizophrenics is largely assumed, the measurements within the normal range tending to be somewhat higher than in the control-groups as well. Inconsistently a relation is reported between enlarged CSF-spaces on one side and unfavourable premorbid adjustment, chronic course of the illness, and predominance of negative symptoms on the other side. The CT findings in twin- and family studies stress also the etiological impact of brain morphology on schizophrenia. Size and width of ventricles in schizophrenics seem to be determined genetically as well as environmental. Most recently findings of unusual laterality or blurring of physiological lateral organization in the central nervous system gain growing interest. In this area brain-morphological findings are supported and supplemented by electrophysiological and PET-findings. For interpretation most authors at present refer to the hypothesis of 2 subgroups of schizophrenia, with and without dementing factors. The author suggests the view, that there is a common feature in all the heterogeneous and contradictory biological findings: They generally indicate a loss of cerebral organization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current status of brain morphologic and related functional diagnosis in schizophrenic patients]. 395 20

Serum and CSF prolactin (PRL) concentrations were determined during eight weeks of fluphenazine medication in 28 patients with acute symptoms of schizophrenia. In both sexes a good correlation between the serum and CSF PRL values was found (r = 0.57, p less than 0.01). Throughout the entire study, first admission (FA) patients had significantly higher levels of serum and CSF PRL than the re-entry (RE) schizophrenics (0.05 greater than p less than 0.001). In addition, in FA patients, a gradual increase of the serum and CSF PRL concentrations was observed, whereas in the RE group an adaptive secretion pattern of PRL could be detected. In both patient groups, female patients exhibited significantly higher PRL serum and CSF levels than the male patients (0.05 greater than p less than 0.001). The tolerance phenomenon in the RE groups was more marked in the female than in the male patients. No correlation between clinical outcome and PRL response to fluphenazine treatment was observed. The prognostic significance of the differences in the PRL secretion pattern is discussed.
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PMID:Serum and cerebrospinal fluid prolactin patterns during neuroleptic treatment in schizophrenic patients. 401 74

Neuroleptic treatment of schizophrenia reduces CSF cyclic AMP in clinical responders after a mean of 8 weeks of treatment. This is consistent with continued effective dopamine receptor blockade by these drugs. Rat striatal 3H-spiroperidol binding sites increase more after 10 weeks of haloperidol therapy than after 3 weeks, suggesting that physiological equilibrium has not yet been reached by 3 weeks. The rat striatal receptor affinity for 3H-spiroperidol is decreased after 10 weeks but not after 3 weeks. The decreased affinity represents a new phenomenon that may be important in explaining long-term continuing neuroleptic effectiveness despite the increased receptor number. The decreased affinity of rat dopamine binding sites for 3H-spiroperidol after 10 weeks of neuroleptic treatment is consistent with the reduced human CSF cyclic AMP after a similar period of neuroleptic treatment.
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PMID:Does neuroleptic blocking of dopamine receptors continue after chronic treatment? 610 67

A recently proposed hypothesis to explain schizophrenia is based on reports of reduced concentrations of glutamic acid in the cerebrospinal fluid (CFS) of schizophrenic patients. This hypothesis suggests that there may be a dysfunction of glutamatergic neurons in schizophrenia, with either a degeneration of these neurons, or their failure to release glutamate as a neurotransmitter. Direct measurement of glutamate levels in CSF and autopsied brain of schizophrenic patient showed no differences from glutamate levels in suitable adult control subjects. The data presented here do not offer support for the new hypothesis.
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PMID:Normal cerebrospinal fluid and brain glutamate levels in schizophrenia do not support the hypothesis of glutamatergic neuronal dysfunction. 612 7

Dopamine beta-hydroxylase (DBH), the enzyme that converts dopamine to norepinephrine, was measured in the CSF of 30 schizophrenic patients and 27 normal controls. The CSF DBH activity in the patients was not significantly different from that in controls. Levels of CSF DBH activity in individual patients were highly constant over time and were not influenced by clinical state or neuroleptic treatment. Low levels of DBH in CSF did significantly relate to good social and sexual functioning, good prognosis, less symptoms between hospitalizations, and excellent clinical response to neuroleptic treatment. We speculate from these data that low brain DBH activity may produce a type of vulnerability to psychotic decompensation and thereby influence the clinical course, although it does not cause schizophrenia, in general. Low CSF DBH activity may delineate a "reactive" subgroup from the heterogenous population of patients with diagnoses of schizophrenia.
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PMID:CSF dopamine beta-hydroxylase in schizophrenia. 613 15

The effect of naloxone on CSF [Met5]enkephalin level and on the suppression of psychotic symptoms associated with schizophrenia was studied. Seven patients were treated with naloxone at a dose of 0.4 mg/day for seven days and six were treated with saline for the same period. Of the seven patients receiving naloxone, three showed signs of improvement. In the saline group, only one case of obvious improvement was observed. The mean CSF [Met5]enkephalin level before and after treatment in both the naloxone and saline group did not change significantly. However, there was a highly significant correlation (r = -0.73, P less than 0.01) between the increase of [Met5]enkephalin level and the decrease in psychotic symptoms.
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PMID:Cerebrospinal fluid [Met5]enkephalin level in schizophrenics during treatment with naloxone. 613 59


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