Schizophrenia is a very serious condition. It is the most common psychosis. Schizophrenia affects attention, thinking, social relationships, motivation and emotion. In a serious episode, most find it hard to understand the “reality” and it challenges our basic understanding about human perceptions of the real world. Most experts believe it is not really a single disorder, but has several different causes. This could be due to the fact that it has so many different characteristics. One aspect that all types of schizophrenia share is “a break with reality”.
No single cause has been identified with schizophrenia. Biological, behavioural and social research suggests a complex interplay between factors. For example, people might have an inherited tendency towards schizophrenia that is triggered by environmental circumstances. Schizophrenia depends in part on genetic factors. Grottesman (1978) studied the likelihood of offspring developing schizophrenia. It was found that children of one schizophrenic parent was a 17% risk, children with two schizophrenic parents were 46-47% more likely to get schizophrenia, siblings were 8%, identical twin of one parent was 17%.
Putting the fact that the prevalence for the normal population is 1% it can be concluded that the cause of schizophrenia looks to be genetic. However it cannot be a full cause as it’s not 100% concordance rate for MZ twins or 50% for others. Also this is a family study, it does not take social accounts, and schizophrenia could be a learnt behaviour. The evidence that has been reported clearly indicates that schizophrenia runs in families, and the concordance rate is much higher between relatives with a higher genetic similarity. However, the fact family members who are more similar genetically tend to spend more time together, which means that environmental factors are also indicated in this evidence.
Another biological explanation is brain biochemistry. Biochemical abnormalities may be important in the development and maintenance of schizophrenia. For example, schizophrenia may be a result from excess levels of the neurotransmitter dopamine. Neurons in the brains of a schizophrenic could be oversensitive to dopamine. There is various evidence that dopamine plays a role in schizophrenia. Neuroleptic drugs that block dopamine seem to reduce the symptoms of schizophrenia. The phenothiazines are neuroleptic drugs that block dopamine at the receptors. They typically reduce many of the symptoms of schizophrenia.
Also drugs that increase dopamine activity, produce schizophrenic like symptoms in non schizophrenic people, (Davidson et al 1987). Similarly the symptoms of schizophrenic patients often become worse when they are given amphetamine which activates dopamine. Post-mortems show a marked increase in the dopamine receptor sites in comparison to others. This suggests a super sensitivity to dopamine.
However there are some problems with the dopamine hypothesis. Neuroleptic drugs block dopamine fairy rapidly, but generally fail to reduce the symptoms of schizophrenia for days or weeks thereafter. Also there is a fairly new drug, Clozapine. It is frequently more effective than dopamine in reducing schizophrenic symptoms. It should be less effective according the dopamine hypothesis. Another negative point on the dopamine hypothesis is that antipsychotic medication does not work on a number of people, even if dopamine is reduced. It has been thought that someone could be wrongly diagnosed with schizophrenia but has a different mental disorder and don’t have high dopamine.