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Besides, several hypothesis are also proposed to explain the etiology of schizophrenia. Freud and Bleuler believed that schizophrenia was caused by a biologic abnormality. In the mid twenties it was believed that schizophrenia was caused by disturbances of child-rearing. A few of the researchers believed the cause of schizophrenia to be a communication deviance between the parents and the schizophrenic child. Twin studies points at the genetic links of schizophrenia. Studies have found a concordance rate of 40% in monozygotic twins and a 15% concordance in dizygotic twins.
Another breakthrough that reinforced the biologic bases of schizophrenia is the discovery of the first antipsychotic medication - Chlorpromazine in the 1950's. This has enabled many people with schizophrenia to live a better life. Psychosocial stressors influence relapse and possibly determine the timing of the first episode and may even determine whether the disorder will occur or not. It seems more and more likely that a specific set of biological predispositions is necessary (even if not sufficient) for the disease to occur.
Although the exact cause of schizophrenia is still unknown the disease seems to be partly related to increased dopamine activity in certain neuronal tracts. The dopamine hypothesis is the most widely accepted hypothesis in the development of schizophrenia. The original dopamine hypothesis proposed a hyperactivity of dopamine transmission in the limbic brain areas, especially the nucleus accumbens, but also in the stria terminalis, lateral septum, and olfactory tubercle that is responsible for the symptoms of schizophrenia.
There is some consensus among researchers that over activity of dopamine systems in the mesolimbic pathway may contribute to the 'positive symptoms' of schizophrenia, whereas problems with dopamine function in the mesocortical pathway may be responsible for the 'negative symptoms'. Evidence to support this hypothesis comes from the fact that most antipsychotics that are successful in treating schizophrenia are dopamine receptor antagonists. In addition, researchers also found that drugs that increase dopamine activity such as cocaine and amphetamines can lead to schizophrenic-like symptoms.
This paper mainly focuses on the relevance or irrelevance of the dopamine hypothesis of schizophrenia. Evidence in favor of the dopamine hypothesis of schizophreniaThere are two main points in favor of the dopamine hypothesis of schizophrenia. The first one comes from evidence that most antipsychotics that are successful in treating schizophrenia are dopamine receptor antagonists. The second evidence comes from the fact that, dugs that increase dopamine activity like cocaine and amphetamines can lead to schizophrenic-like symptoms.
Evidence for the dopamine hypothesis of schizophrenia is partly based on the observed effects of drugs such as amphetamine and cocaine. Both of these drugs increase levels of dopamine in the brain and can cause psychosis, especially after large doses or prolonged use. Amphetamine psychosis and cocaine psychosis may produce symptoms that are indistinguishable from the positive symptoms associated with schizophrenia. A review by Lieberman and colleagues demonstrated that up to 75% of patients with schizophrenia have exacerbated the signs and symptoms of their psychosis when given moderate doses of methylphenidate, amphetamine or other dopamine-like
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