b) There are many explanations for the onset of schizophrenia one of these is the neurological ones.
Towards the end of the 1800s it was discovered that people diagnosed with schizophrenia had some sort of brain damage. It was thought by Kraepelin that it was this brain damage that led to symptoms of the illness.
With the help of MRI scans we now have more accurate knowledge of these abnormalities. Most psychologists have now found that schizophrenic sufferers have abnormally enlarged ventricles in the brain. Some found decreased brain weight, others smaller volumes in certain parts of the brain, etc. Young (1991) found that schizophrenics had more symmetrical brains than controls. He also found that the degree of structural abnormality correlated with the severity of the illness, and many other psychologists have found that structural abnormalities are more common in those with chronic/negative symptoms, which is generally thought to be the more severe of the two types.
Nopoulos and colleagues examined gender differences and found that men seemed to generally express more severe symptoms, and support from this comes from the significantly larger ventricles found in affected males than affected females.
Cannon et al (1994) found that ventricular enlargement was greater in those that were at a genetically higher risk and those that experienced birth complications.
All evidence of structural brain abnormalities supports the view that Kraepelin had more than a century ago, that these brain abnormalities are the cause of schizophrenia.
However the normal age of onset is after adolescence, therefore if abnormalities in the brain come before the symptoms schizophrenia would be a developmental disorder
Weinberger (1998) criticises the fact that although there is a lot of research there is no conclusive evidence to prove if brain damage causes schizophrenia or if schizophrenia cause brain damage. The main problem in trying to find this conclusive evidence is that scans are being carried out on people who are already diagnosed, this way it is not likely that we are going to find out which occurred first, the structure abnormality or the symptoms.
There is a study however that supports the idea that abnormalities cause the illness. Castner et al (1998) subjected foetus monkeys to brain-damaging x-rays and found that the monkeys were normal throughout their childhood, but at puberty they developed symptoms of schizophrenia, such as hallucinations. However it is perhaps inappropriate to extrapolate such results to humans.
An alternative explanation is the season of birth explanation. Since as early as the 1920s a pattern has been observed in the time of year that most schizophrenia sufferers are born. A very large proportion of people diagnosed with the illness are born in winter and early spring (Hope-Simpson 1981). An explanation suggested that the prevalence of Influenza A had something to do with it. It is thought that if the pregnant mother contracts the virus when she is 25 – 30 weeks pregnant, this is when the foetus is most vulnerable because of the accelerated growth in the cerebral cortex at this time. There are two main opinions of what happens after this, the first suggests that the virus gestates until the child reaches puberty when it is activated, the second proposes that there is a gradual degeneration of the brain that eventually leads to schizophrenia. This hypothesis is supported by abnormalities revealed by MRI scans.
Crow (1984) even suggested that the virus somehow becomes integrated into the genes, with may then be passed down to other generations. Weiss (1988) supports this theory by stating that retroviruses can now be transcribed onto DNA.
Further support for the viral hypothesis comes from correlations between flu epidemics and peaks in schizophrenia (Torrey 1988). Hare reports higher incidence of schizophrenia with urbanisation, which brought about many infectious diseases. However urbanisation also brought about more hospitals that probably brought about more diagnoses.
Torrey et al (1988) suggested that the link between viral infection and schizophrenia only occurs in those who are already genetically predisposed.
