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  • Gender differences in schizophrenia  (2)
  • Springer  (2)
  • Berlin, Heidelberg :Springer Berlin / Heidelberg,
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 238 (1988), S. 63-72 
    ISSN: 1433-8491
    Keywords: Aetiology of schizophrenia ; Epidemiology of schizophrenia ; Disease concept of schizophrenia ; Continuous model of vulnerability to schizophrenia ; Gender differences in schizophrenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The psychotic syndrome at the core of schizophrenia appears to be invariable across cultures. The risk of morbidity also seems to vary very little from country to country and over medium periods of time. Moreover, apart from gender differences in first onset, the cumulative lifetime risk is the same in females and males. A similar epidemiological pattern is only found in pathological conditions that are characterized by a precisely defined section of a psychopathological dimension with a continuous distribution in the population, e.g. severe mental retardation being the extreme section of normally distributed IQ values. The interpretation of schizophrenic psychosis as the extreme section of a psychopathological dimension or disposition that is almost evenly distributed in all populations is supported by the fact that milder psychiatric disorders occur more frequently before the onset of the psychosis and in close relatives of schizophrenic patients. The psychopathological heterogeneity of these disorders argues against the assumption of a manifest psychopathological dimension with a continuous transition from the schizophrenic psychosis to the “normal” schizothymic personality. More probable is a continuously distributed latent vulnerability to schizophrenia — with or without a threshold effect — which in severe degrees disposes to the uniform reaction pattern of the schizophrenia syndrome. Smaller degrees of vulnerability are associated with an increased risk for milder patterns of disturbances, which are also more strongly determined by environment and personality and therefore are rather heterogeneous. These assumptions lead to other epidemiological and genetic models than Kraepelin's early concept of a disease entity does.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 241 (1991), S. 65-68 
    ISSN: 1433-8491
    Keywords: Schizophrenia ; Onset of schizophrenia ; Gender differences in schizophrenia ; Oestradiol effect on dopamine receptor sensitivity ; Vulnerability threshold in schizophrenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a representative sample of 392 first hospital admissions for schizophrenia from a population of 1.5 million we assessed the “true” age of onset by a semistandardized interview “IRAOS”. We demonstrated that the mean age at onset of the disease is 3–4 years higher in females than in males, with the lifetime risk being exactly equal. In males, the rates of onset show a steep increase — starting from school age and reaching their maximum value in the age group 15–24 years — followed by a steady decrease. Females reach the first peak with a clear delay between 20 and 29 years. After the decrease, a second smaller peak is observed consistently in females within the age group 45–49 years and over. After having excluded competing explanations, we hypothesized that the effect of oestradiol on the dopaminergic system enhances the vulnerability threshold, which is lowered again during the menopause. Alternatively, we assumed that testosterone reduces the vulnerability threshold and thus furthers the earlier onset of the disease in males. We tested the hypotheses in three animal models by examining the effect of gonadal hormones on haloperidol-induced catalepsy and on apomorphine-induced stereotypies in both neonatal and adult rats. No clear influence by testosterone was shown. Oestradiol caused a significant reduction of both dopamine-agonist and dopamine-antagonist induced behaviour. The effects were stronger in neonatal rats. Since oestradiol caused the dopamine (DA) receptor affinity for sulpiride to be reduced by a factor of 2.8, we assumed that the behavioural changes due to oestradiol were accounted for by a down-regulation of DA receptor sensitivity. The higher age at onset and the second peak of onsets after menopause in females may therefore be due to a functional effect and possibly also to an additional structural effect of oestrogens already exerted on the development of the brain.
    Type of Medium: Electronic Resource
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