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

Earlier clinical pneumoencephalographic studies showed a subgroup of schizophrenics that have small and dysplastic cerebral ventricles as well as a subgroup with a "pure defect", i.e., a slight internal brain atrophy. In echoencephalograms of pure and mixed residual schizophrenic syndrome patients, a significantly higher average transverse diameter of the third ventricle was demonstrated compared to that in patients with complete remissions. Correlations cannot be expected between certain groups of disease, e.g., epilepsy, multiple sclerosis, or schizophrenia on the whole, and pneumoencephalographic (PEG) and CT findings. Only schizophrenics with distinct signs of pure defect that had persisted for at least 3 years revealed deviations from normal by CT and PEG, but those with irreversible fixed deformations of personality structure ("Strukturverformungen" [9,10]) did not. In patients who were 50 years of age or less with psychic reactive and psychopathic personality disorders, CT showed an average third ventricle diameter of 4.2 mm (range 2-6 mm). Of 117 schizophrenics (average age 35.5 years), only 28% revealed pathological CT changes. However, of 36 schizophrenics with pure residual syndromes 69% showed pathological CT findings that always concerned the third ventricle, rarely the lateral ventricles, and in no case the cortex. The average transverse diameter of the third ventricle in this subgroup with pure defect was 7.6 mm, as compared to 4.6 mm in the subgroup of schizophrenics with complete remission. There was no increase in size with increasing years until the 50th year in schizophrenics, as well as in the control group of variations of psychic being (neuroses and psychopathic personality disorders).
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PMID:Computerized tomography studies on schizophrenic diseases. 713 78

Fifty-five schizophrenic, 24 manic and 27 control subjects, all males between 20-45 years of age, were examined for structural brain abnormalities with computerized tomography (CT) scans. Both manic and schizophrenic samples had significantly larger ventricles than the control group. Cerebral atrophy was more frequent in schizophrenia, while cerebellar atrophy was more frequent in mania. An association between increased ventricular size and cerebellar atrophy was found in mania but not in schizophrenia. Cerebral atrophy was not associated with ventricular enlargement in either disorder. Implications of these findings are discussed.
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PMID:Cortical atrophy in schizophrenia and mania: a comparative CT study. 717 17

In order to elucidate the interplay of prolactin and dopamine in schizophrenia, base-line levels of prolactin were assayed in the cerebrospinal fluid (CSF) of chronic schizophrenic patients with or without lobotomy. Cental and cortical atrophy and significantly lowered CSF prolactin levels were found in lobotomized patients in comparison to equally neuroleptic-treated non-lobotomized patients. The mean CSF prolactin level in the female patients was significantly higher than in the male patients. This study did not support the 'dopamine hypothesis' of schizophrenia, since CSF prolactin levels did not correlate with schizophrenic symptoms. The brain atrophy blocked completely the expected elevation of CSF prolactin levels induced by neuroleptics.
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PMID:Low prolactin levels in cerebrospinal fluid: an after effect of lobotomy in chronic schizophrenia. 728 16

A survey of 14 published studies found no consistent association between specific HLA antigens and schizophrenia. Since these studies lacked diagnostic or biological criteria, an investigation was undertaken using recognized diagnostic criteria and CT scan findings. Typing for HLA antigens at loci A, B and C was carried out on 130 patients. Among 92 black schizophrenic patients there was an increase of HLA-A2 which remained significant even after correcting for the number of antigens studied. When the patients for whom CT scans were available were divided according to the presence or absence of evidence of brain atrophy, there was an increase of A2 in the black schizophrenic patients without evidence of atrophy, which remained significant after multiplying by the number of antigens studied. However, there was no significant increase of A2 in those with evidence of atrophy. Similar trends held for the white population but they failed to reach significance. The need for HLA studies on biologically defined groups of schizophrenic patients is stressed.
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PMID:HLA antigens in schizophrenia:differences between patients with and without evidence of brain atrophy. 738 27

Of 50 heavy drinkers referred for nonalcoholic psychiatric problems, 56% had computerized tomographic evidence of cerebral atrophy. This contrasted with a rate of 6% in patients with schizophrenia and affective illnesses who had taken psychotropic drugs for at least ten years. Further, the severity of atrophy was greater in the group of heavy drinkers. The results support a role for computerized tomography in assessment of patients with chronic alcoholic problems.
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PMID:Computerized tomographic evidence of cerebral atrophy in heavy drinkers. 739 87

The prevalence of brain cortical sulci atrophy and central (subcortical) atrophy among Nigerian psychiatric patients is highlighted and compared with findings from developed countries. The relationship between these indices of brain atrophy and clinical parameters is also examined. Visual ratings of cortical sulci atrophy and central (subcortical) atrophy, assessed on the computed tomography (CT) image console, were compared among 50 patients with schizophrenia, 14 patients with mania and 41 healthy control subjects. The patients with schizophrenia and the patients with mania had a significantly higher prevalence of brain atrophy than normal subjects. Among the patients with schizophrenia, indices of brain atrophy were not significantly associated with disease outcome, and the presence of negative symptoms. In view of the findings from a parallel study of the same patients that psychiatric patient groups showed other evidence of CT abnormalities, the findings of this study indicate that the so-called functional psychiatric states in developing countries--as in developed countries--are probably associated with some diffuse neuropathological process.
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PMID:The correlates of cortical sulci atrophy and central atrophy in a cohort of schizophrenia and manic subjects in Nigeria. 762 89

A cohort of 168 psychotic patients underwent computerised tomography (CT) during their first admission. Cortical atrophy was present in 40% of patients. The frequency of atrophy increased with age, but did not differ between patients with schizophrenia, schizoaffective disorder, bipolar disorder or psychotic depression. Other CT findings of note were present in 6.6% of patients, and included four infarctions, three arachnoid cysts, and one each of venous angioma, colloid cyst, cavum vergae and post-traumatic changes. The frequency of CT findings other than atrophy was increased in the psychotic depression group. The findings support the proposal of the onset of psychosis being an indication for CT.
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PMID:Results of computerised tomography during first admission for psychosis. 795 85

Aggressive behavior is a common feature of schizophrenia and is associated with the presence of 'soft' neurological signs. Since early age of onset of schizophrenia has been found to be associated with the negative syndrome, which according to Crow (1982) is related to structural brain abnormalities, I predicted that early age of onset may be a biological risk factor for aggressive behavior in the disease. To test this hypothesis, I investigated in 52 chronic institutionalized schizophrenic patients (mean age = 32.8 years; SD = 8.0), the association between age of onset of the disease and the severity of belligerent behavior. The age of onset was judged from the patient's histories as the age at which florid symptoms first emerged. Patients with early onset schizophrenia had a significantly higher belligerent score compared to those with later-onset schizophrenia (p < .05). These findings support the hypothesis of an association between early age of onset of schizophrenia and the risk of aggressive behavior and suggest, furthermore, that schizophrenic symptoms which emerge early may predict a higher risk of aggressive behavior. Furthermore, this study suggest that the neurochemical mechanisms which underlie the early emergence of symptoms may also predispose to aggressive behavior in schizophrenia. Specifically, since aggressive behavior has been linked to impairment of serotonergic (5-HT) functions, I propose that the timing of onset of schizophrenia may be partly associated with dysregulation of the 5-HT system. In a second study, I investigated whether schizophrenic patients with aggressive (suicide) behavior are characterized by more extensive brain damage and hence greater degree of cerebral atrophy on CT scan. The study, which involved 26 schizophrenic patients (mean age: 31.3 years; SD = 6.8), revealed that patients with aggressive behavior had a significantly greater degree of parieto-occipital atrophy on CT scan (p < .05). In contrast, ventricular size and prefrontal cortical atrophy did not distinguish aggressive from nonaggressive patients. These findings suggest that cortical atrophy may be a neuroradiological marker of aggressive behavior in schizophrenia.
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PMID:Aggressive behavior in schizophrenia: relationship to age of onset and cortical atrophy. 806 5

The diagnostic allocation and aetiological basis of paranoid psychoses with late onset is controversial. We examined the clinical features of patients with a diagnosis of paranoid psychosis and we compared their cranial computed tomography (CT) scans and electroencephalographic (EEG) recordings with findings from matched samples of patients with Alzheimer's disease and non-demented elderly controls. During a 5-year period, 81 patients (15 men and 66 women) with a diagnosis of paranoid psychosis and onset after age 50 were referred to our Institute. They represent 5.4% of the patients older than 50 admitted during the same period. More than half of these patients had first-rank symptoms. The ventricles, anterior and sylvian fissures of the paranoid group were larger than in non-demented controls but smaller than in Alzheimer's disease. The posterior dominant alpha EEG rhythm was slower than in normal aging and faster than in Alzheimer's dementia. If paranoid patients with first-rank symptoms were distinguished from the ones without, the former had less severe brain atrophy and faster posterior dominant rhythm, although they received higher doses of neuroleptics. This could be explained by the existence of at least 2 subgroups of late paranoid psychosis: late-onset schizophrenia and organic paranoid syndrome, the former characterized by first-rank symptoms and less severe brain atrophy, the latter by more severe EEG and CT scan changes with a closer resemblance to degenerative brain disease.
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PMID:Organic factors and the clinical features of late paranoid psychosis: a comparison with Alzheimer's disease and normal ageing. 806 72

Prediction of response to neuroleptics is a crucial topic since drug resistance phenomena can make the management of schizophrenia problematic and further deteriorate the outcome. Cerebral atrophy and enlarged ventricles have been suggested as the structural changes underlying negative symptoms and poor response to neuroleptic treatment. A higher percentage of non-suppressors to the dexamethasone suppression test (DST) among negative schizophrenics has been reported. Twenty-four schizophrenic in-patients, of both sexes, mean age 26.62 +/- 5.26 years, diagnosed according to DSM-III-R, with a mean duration of illness of 4.86 +/- 3.99 years, were treated with haloperidol 4-20 mg/day p.o. for 4 weeks. Clinical picture and extrapyramidal side effects were evaluated using BPRS and Simpson and Angus Scale at the beginning and end of the study. Ventricular brain ratio and basal and post-DST cortisol levels were evaluated at admission. The severity of the psychopathological picture, particularly positive symptoms at admission, were correlated to a higher amelioration at BPRS. Patients with ventricular enlargement and non-suppressors to DST showed higher variability of BPRS at baseline and more unpredictable clinical outcome than patients with normal ventricular brain ratio (VBR) and suppressors, even if a real difference in clinical outcome between patients characterized by normal or pathological parameters cannot be defined.
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PMID:Prediction of response to haloperidol in schizophrenia: neuroendocrine, neuromorphological and clinical variables. 819 79


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