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

A set of schizophrenic male monozygotic triplets is described. At age 20 years, within 8 months the three men independently developed acute fulminant schizophrenic disorders (DSM-III-R) with auditory hallucinations, bizarre delusions, and thought disturbances. There were also great similarities between the triplets with regard to the chronic intermittent course of the disorder, impairment of social adjustment, and loss of working ability. The psychoses responded rapidly to conventional neuroleptic treatment. Neuropsychological assessment demonstrated similar marked reductions of attentional, mnestic, and executive functions. Magnetic resonance imaging (MRI) showed similar borderline ventricular enlargement and widened subarachnoid spaces over frontoparietal and basal regions as well as around the pituitary gland (empty sella). All the boys also had a right-sided hearing defect with a marked reduction of the ossicular bones on the right side. Possible clues as to etiological mechanisms were the lack of reported family history for the disorder and a possible influenza infection in the mother during the first trimester. It is suggested that a DNA aberration being present or occurring at conception initiated a precise time-programmed series of events that produced the very similar schizophrenic phenotypes. Such an aberration might have been induced by an external agent, occurred spontaneously, or been inherited by a recessive mechanism. It seems possible that the psychoses, the reductions of neuropsychological functions, the morphological MRI changes, and the right-sided ossicular reductions may all be related to such a DNA alteration.
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PMID:A set of male monozygotic triplets with schizophrenic psychoses: nature or nurture? 778 6

Many people with severe schizophrenia have increased cerebral ventricular size and diffuse reduction in cortical volume; recent attention has focused on subtle malformations of the cytoarchitecture in the hippocampus and parahippocampal cortex. Sufferers also show an excess of dermatoglyphic and minor physical abnormalities, and a significant proportion had psychomotor deficits, cognitive or behavioural problems as children. Such findings suggest that the form of schizophrenia most akin to Kraepelin's original description of dementia praecox results from neurodevelopmental impairment. This may have its origin in genetic defects in the control of early brain growth, or in early environmental hazards such as prenatal exposure to maternal influenza or perinatal complications. How foetal or neonatal lesions produce hallucinations and delusions two or three decades later remains a mystery, but maturational changes in the brain may be important.
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PMID:Neurodevelopmental schizophrenia: the rediscovery of dementia praecox. 786 95

The dates of birth of patients who were admitted with schizophrenia to public hospitals in Queensland between the years 1972 and 1988 were examined for associations between risk of schizophrenia and influenza epidemics. The hypothesis that infants born between four and six months after an influenza epidemic onset have increased risk of schizophrenia was examined for the 1954, 1957 and 1959 epidemics. After the 1954 epidemic there was a significant excess of male schizophrenia births four months after the onset of the epidemic. In 1957, there was a significant excess of female schizophrenia births in the fifth month after the onset of the epidemic. The 1959 epidemic was not associated with any significant excess.
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PMID:Schizophrenia and the influenza epidemics of 1954, 1957 and 1959: a southern hemisphere study. 789 16

Based on recent quantitative EEG findings of increased slow activity in negative schizophrenia indicating organicity, it was hypothesized that neuroleptics decreasing delta/theta activity should be beneficial for schizophrenics with predominantly negative symptoms. Thus, a double-blind, clinical, psychometric and neurophysiological study was carried out in 40 hospitalized patients with unproductive schizophrenia (mean age: 31 years; ICD diagnoses: 295.0, 295.1 and 295.6) who were treated randomly either with the benzamide amisulpride (AMI; n = 19) or low doses of fluphenazine (FLU; n = 21). In the first 2 weeks the daily doses were 50 mg AMI or 2 mg FLU, respectively, from the third week on up to the sixth week 100 mg AMI and 4 mg FLU. Clinical evaluations, psychometry and EEG mapping were performed on day 1 (hours 0 and 4--acute effect), on day 14 (hour 0--subacute effect) and on day 42 (hours 0 and 4--chronic and superimposed effects). Three AMI patients discontinued therapy prematurely because of productive symptoms (days 14, 28 and 35), while in the FLU group 2 patients dropped out due to depressive symptoms (days 21, 28), 1 due to productive symptoms (day 35), 1 due to ineffectiveness (day 28), and 1 because of an akinetic crisis (day 6). Statistical evaluation demonstrated a significant improvement in the AMDP apathy and Andreasen SANS score in both groups with the patients remaining severely ill as rated by the CGI. FLU-treated patients needed significantly more anticholinergic medication than the AMI-treated group. Psychometric evaluation showed in regard to the noopsyche significant improvement after subacute, chronic and superimposed AMI, while FLU-treated patients showed significant improvement only after subacute treatment. AMI was significantly superior to FLU at the hours 0 and 4 of day 42. The thymopsyche improved after subacute, chronic and superimposed administration of both compounds with a significant superiority of AMI on days 14 and 42 (4 h postdrug). EEG mapping showed a decrease of delta/theta and increase of beta activity as well as an acceleration of the centroid after acute and superimposed AMI on day 42 as compared with baseline; FLU patients exhibited a decrease of delta/theta activity and an acceleration of the total centroid too, while alpha activity was augmented and beta activity tended to be reduced. Our study demonstrated that, in addition to the new benzamide AMI, FLU in low doses may also be regarded as a neuroleptic with activating properties and may be utilized in the treatment of schizophrenics with predominantly negative symptoms.
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PMID:Clinical, EEG mapping and psychometric studies in negative schizophrenia: comparative trials with amisulpride and fluphenazine. 791 19

We tested the hypothesis that second-trimester exposure to influenza is a risk factor for schizophrenia in the child. The dates of birth of Dutch schizophrenic in-patients were examined for any effect of the 1957 A2 influenza epidemic. Individuals who were in their second trimester of foetal life at the peak of the epidemic were at no greater risk of developing schizophrenia than controls. As the present study has a larger sample size than all previous European studies, and is supported by a large study in the USA, it provides strong evidence against the hypothesis that second-trimester exposure to influenza is a risk factor for schizophrenia.
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PMID:Evidence against maternal influenza as a risk factor for schizophrenia. 786 95

We reported previously that residents of Greater Helsinki, Finland, whose mothers were exposed to the 1957 influenza epidemic during their second trimester of gestation had a significantly elevated risk of developing adult schizophrenia. The majority of the replication studies to date have not determined whether the mothers actually contracted an infection or the stage of gestation based on mother's last menstruation. We read prenatal clinic records of the mothers of the Helsinki-born schizophrenia subjects to determine timing of infection, as noted by the prenatal clinic obstetric nurse at a time close to the actual infection. Schizophrenia subjects who were exposed in the second trimester had a significantly higher rate of definite influenza infection (86.7%) in that period compared to those who were exposed during the first and third trimesters (20.0%). These results are interpreted with caution because of the small number of cases.
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PMID:Prenatal influenza infections and adult schizophrenia. 808 30

The authors present data from the Republic of Croatia on schizophrenia rates in a birth cohort prenatally exposed to the 1957 A2 influenza epidemic and in comparison (unexposed) birth cohorts. The rate of schizophrenia did not differ significantly between the exposed and unexposed cohorts.
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PMID:Schizophrenia and prenatal exposure to the 1957 A2 influenza epidemic in Croatia. 809 42

In a retrospective study, 16 of 80 mothers of chronic DSM III-R schizophrenics reported having had a serious infectious disease during pregnancy. Eleven of the infections had occurred during the second trimester. Influenza and the common cold with fever were frequent. Ten of 80 female controls also recalled having had an infectious illness during pregnancy. Compared to the controls, mothers of schizophrenics reported more infectious illness during pregnancy, particularly during the fifth month of gestation (p < 0.05). Mothers of familial and of sporadic DSM III-R schizophrenics reported equal frequencies of infections in pregnancy. In contrast, when Leonhard's classification of psychoses was applied, significant differences appeared. Infections during pregnancy were scarcely found in unsystematic schizophrenics (mainly genetically determined according to Leonhard). In systematic schizophrenics (mainly exogenously determined according to Leonhard), a significantly higher frequency of infectious diseases was reported for the second trimester as compred both to controls (p < 0.01) and to unsystematic schizophrenics (p < 0.001). Infections during the fifth month of gestation were exclusively reported in systematic schizophrenics. Thus, in the systematic forms of schizophrenia infections during the second trimester and particularly during the fifth month of gestation seem to play an important role in the etiology and seem to be of causal importance for the various cytoarchitectural abnormalities detected in the central nervous system of schizophrenics.
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PMID:[Pregnancy infections in mothers of chronic schizophrenic patients. The significance of differential nosology]. 817 58

The authors compared the risk of schizophrenia in Dutch birth cohorts that were or were not exposed during the second trimester of gestation to the 1957 A2 influenza epidemic. Exposed birth cohorts did not have a higher risk of schizophrenia. These findings suggest that, in some populations, there is no relation between prenatal exposure to influenza and risk of schizophrenia.
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PMID:No relation between risk of schizophrenia and prenatal exposure to influenza in Holland. 818 6

The schizophrenic syndrome may represent a stereotyped response by the developing brain to various insults, including micro-organisms. We review studies that have examined the association between schizophrenia and infectious agents, and examine the current evidence for the hypothesis that exposure to influenza during fetal life increases the risk of later schizophrenia. A prenatal autoimmune basis for some cases of schizophrenia is proposed.
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PMID:Schizophrenia: prenatal influenza and autoimmunity. 825 Nov 51


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