Outline and Evaluate Aetiologies of Schizophrenia






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Schizophrenia is a mental disorder characterised by a breakdown of thought processes and impaired emotional responses.  It is not known for certain what the exact cause of schizophrenia is - there is no definitive answer. There are many possible explanations for the disorder which can be placed into two categories; physiological (biological) and  psychological (sociocultural). 

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Biologists use twin studies to explain schizophrenia as a genetic disorder. By comparing the concordance rates in twins and the likelihood of one twin developing  schizophrenia if the other has the disorder, they can tell if schizophrenia is genetic. It is assumed if the concordance rates are high, the twins have a genetic predisposition to schizophrenia.

Gottesman and Shields (1972) examined records of 57 schizophrenics between 1948-1964. 40% were MZ and 60% DZ. Twins followed for 13 yrs to see if pair discordant. Results showed probability of twin having schizo if it's twin had the disorder was 42% in MZ and 9% in DZ. Such evidence supports notion that schizo is genetic as MZ twins who share all of genes are more likely to develop disorder if twin has it.

In addition, Gottesman reviews another 40 studies in meta analysis and finds higher concordance rates- 48% in MZ and 17% in DZ.  

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Further, Heston (1970) found if one MZ twin has schizo, the other has 90% probability that other will develop some sort of mental disorder! Indicates link between genetics and mental illness.

Concordance rates show a correlation but does this prove cause/effect relationship- environmental factors? Some research suggests schizo is not genetic but environmental - prenatal complications in the womb. Consequently, evidence may suggest that schizo is a multifactoral disorder and both can play a role.

As we cannot usually separate the effect of environment on MZ twins, it is plausible.  Concordance rates not 100%, actually too low to be significant (under 50%).

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Suggests excessive amounts of neurotransmitter dopamine causes schizo. This causes neurons to fire and transmit messages excessively.

It was found that dosages of dopamine given to people already suffering from schizo would worsen their symptoms. This suggests dopamine contributes to symptoms of schizo. 

Further evidence shows the link. The drug L-Dopa is  used to treat Parkinson's. Works by blocking the dopamine receptors to prevent neurons from firing. As Parkinson's caused by lack of dopamine, it was found when given to individuals with no history of schizo, it can produce schizophrenic symptoms. Suggests excess dopamine can cause schizo. 

Post-mortems on schizophrenics showed they had 6x the number of dopamine receptors than healthy individuals. Highly suggests dopamine is involved in schizo.            

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Although these figures support the dopamine hypothesis, they are correlational. The precise role played by each is unclear- cannot show cause/effect. Don't know if raised dopamine levels CAUSE schizo or if they are RESULT of disorder. 

Kasper (1999) found problems with hypothesis. Newer drugs more effective than older ones ie.clozapine although they block fewer dopamine receptors. Specifically, clozapine works by blocking serotonin NOT dopamine, suggesting it is serotonin that has a greater effect on schizo than dopamine. Thus, there is a problem with the notion of dopamine being main neurotransmitter associated with development of schizo.

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Suggest that distorted thought processes cause schizo and as a result, there is poor information processing= positive symptoms associated with schizo. 

Frith (1992) argued symptoms such as delusions of control and hallucinations occur because individuals with schizo have problems with self-monitoring and fail to keep track of own intentions, giving rise to belief they are under alien control. Further argues, schizophrenics lose ability to understand other people's mental states and Theory of Mind- explaining why some paranoid schizos are suspicious of others intentions.

Hemsley also suggests schizo is caused by failure to activate schemas and draw info together. Inability to attend attend selectively, results in sensory overload

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McGuigan (1966) tested auditory hallucinations, found that larynx of patients with schizo was often active during time they claimed to be experiencing hallucinations. Suggests they mistook their own inner speech for that of someone else. Also found to have reduced activity in parts of the brain involving inner speech. Shows explanation for hallucinations.

John (2001) findings also confirm individuals with schizo hallucinations have impaired verbal self monitoring.  Such explanations plausible- cognitive provides reasonable account of positive symptoms of schizo like hallucinations (most puzzling aspect of disorder). However, these explanations don't account for negative symptoms ie. withdrawal.

Again, causality of explanation also unclear, do not know if cognitive problems trigger schizo or if an effect of schizo. It is not clear why symptoms there in the first place. What is causing the faulty processes that result in the symptoms? More descriptive than explanatory of the disorder itself.

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Another explanation is expressed emotion within the individuals environment causes schizo.

Brown (1972) suggested that families that display high level of expressed emotion towards an individual ie. hostility, criticism and over-concern increase the stress levels in patient beyond their coping mechanisms, makes patient susceptible and triggers schizophrenic episodes. He found that relapse more likely where family has high levels of expressed emotion. 58% compared to 10% in those where expressed emotion is not present.

Taimer (1988) also found strong relationship between relapse and living with a relative who shows expressed emotion. Suggests schizophrenics relapse in environments with expressed emotion.

However, once again issue of cause. Possibility that individuals in poor psychological shape are more likely to provoke expressed emotion from members of their family but this can emerge after the individuals diagnoses as family members struggle to adjust to the situation. The studies also only deal with relapse, NOT the actual development of the disorder, nor does it provide explanation for schizophrenia in its first stages as focus is on relapse.

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Diathesis stress model proposes that schizophrenics have a biological predisposition to the disorder and subsequently it is stressful life events that trigger the psychotics symptoms associated with schizo. This model combines biological and psychological explanations and is plausible as it suggests there is not one specific explanation for schizo but that it is multifactoral. This may be the most effective way to combine all these explanations.

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