Biological and Environmental Factors for Schizophrenia

biological and Environmental Factors for Schizophrenia

chronicity or other, as yet unidentified, factors. From the literature findings, it is evident that an extensive body of literature has accumulated regarding the efficacy of these interventions. Vref1 titleSchizophrenia: the biological and psychological effect m dateNovember 2013 accessdate locationNottingham, UK Reference Copied to Clipboard. Available from: p?vref1 Accessed Reference Copied to Clipboard. Brain imaging scans have shown that some areas of the brain are smaller or malformed in those with schizophrenia. Measurements of ventricular size have however, shown considerable inconsistency, with some studies finding no significant difference between subjects and non-schizophrenic controls (Bles et al, 2010 and some reporting significant differences between chronic paranoid and hebephrenic subjects and normal controls (Bales et al, 2010). Research shows it takes a combination of genetics is There Such Thing as TOO Much Defense? and your environment to trigger the disease. The viral hypothesis has received impetus from recent research into retroviruses capable of genetic transmission and causing latent disease onset. This would mean that studies using young subjects showing predominantly.

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The findings could eventually lead researchers to develop better drugs to treat the cognitive dysfunction associated with schizophrenia and possibly other mental illnesses. The truth is, doctors dont really know what causes this mental illness. Studies using absolute predominance measures to the exclusion of other symptoms reject many subjects displaying both sets of symptoms. However, the influence of neuroleptic drugs on attentional and extrapyramidal functioning could also issues that effect the African American Community contribute to the development of differential symptoms. 3 article references next: Schizophrenia Genetics: Is Schizophrenia Hereditary? Endorphins have been the subject of the most intensive study because of their association to proposed neural deficit areas both in biochemical and neuropathlogical research. It is equally probable that any such changes are caused by the disease process rather than their being causal. The reasoning behind the success of each treatment can give guidance into the psychological effects of the disease. It appears, Pletnikov says, that people with disc1 mutations associated with the psychiatric illness are faster to metabolize D-serine, which leads to a decrease in the apparently crucial transmitter.

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