Schizophrenia: Discussion

by lucycarrick03gmailcom | Wednesday 1st of February 2023

Schizophrenia: Discussion

Get study help to learn more about schizophrenia diagnosis and key discussions surrounding the condition.


When it comes to diagnosis there is always a degree of subjectivity involved. Psychiatrists will use the existing diagnostic manuals to aid their decision making but ultimately rely on how they interpret the symptoms being described to them. Unfortunately, the diagnoses that are given to patients are not always correct and can lead to unnecessary labelling for that individual. Schizophrenia in particular is accompanied by a hard label to shift. When a patient is no longer experiencing positive symptoms their label changes to “residual schizophrenia” and when they are experiencing none/or very few symptoms it becomes “schizophrenia in remission”. People who have received a diagnosis are never truly free from this label, which can impact on all aspects of their lives. 

Schizophrenia is particularly hard to distinguish at early onset and is not always diagnosed as such until the disorder is quite severe, causing negative implications for the sufferer. It also shares similar symptoms with other mood disorders and is often co-morbid with depression as well. This again makes it difficult to identify schizophrenia as a separate disorder, and involves subjectivity of the psychiatrist to diagnose and treat it appropriately. Ultimately, the limited understanding of the cause of schizophrenia makes the diagnosis and treatment process very difficult, with the treatments not always leading to positive outcomes for the individual. 

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The genetic explanation for schizophrenia has good support from research studies. It is investigated by using family, twin and adoption studies in attempt to untangle the role of genetics and environmental causes in schizophrenia. Twin studies examine the concordance rates of schizophrenia between monozygotic twins (MZ/identical twins) and dizygotic twins (DZ/non-identical twins). This will show the strength of the genetic link, as MZ twins share 100% of the same genetics and thus should be more likely to both suffer from schizophrenia compared to DZ twins who only share 50% of their genetics. Gottesman (1991) reviewed a large number of twin and family studies and found the average concordance rates in MZ twins was 48% compared to 17% in DZ twins and 9% in siblings. These findings show that the genetic contribution towards schizophrenia is quite high but is not 100% in MZ twins and thus cannot solely be due to genetics. Also, the higher concordance rates observed in DZ twins compared to siblings imply that the environment that twins share may be increasing their risk of developing schizophrenia. The genetic contribution in siblings and DZ twins is the same (50%) so we would expect to see similar concordance rates however this is not the case. Adoption studies have also found that adopted children with a biological parent with schizophrenia are more likely to develop schizophrenia (32%) compared to control adopted children (18%) (Kety et al., 1988). 

This evidence suggests that there is definitely genetic involvement in the disorder but how exactly it is linked is not yet understood. Unlike other genetic disorders no particular gene has been identified as the cause and it is more likely that it is a number of genes that are contributing to the symptoms seen in schizophrenia. It is also apparent from the research that there is an interaction between genetics and environment causing the disorder not one factor on its own. 

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Research into the neurochemical explanation of schizophrenia tends to examine the symptoms that arise as a result of taking drugs, that either increase or decrease levels of dopamine. For example, amphetamines increase dopamine levels and symptoms of delusions and hallucinations can be seen in these individuals. However, it is very difficult to establish that dopamine is the only neurotransmitter causing these changes because recreational drugs also impact on other neurotransmitters in the brain. Another issue with conducting research in this area concerns cause and effect. As ‘post-mortem’ investigations are carried out to look at dopamine levels in the brain we cannot establish whether the increase in dopamine caused the disorder or was a symptom of the disorder. In response to this, PET (positron emission tomography) scans are now being conducted on living patients to determine the glucose activity in certain areas of the brain. These allow scientists to observe the contribution of dopamine but do not help to explain the cause of schizophrenia. This theory could be regarded as a reductionist because it oversimplifies the complex disorder of schizophrenia to simply the role of one neurotransmitter. There is not enough research support to conclude that high levels of dopamine are the unique and only cause of schizophrenia. 

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Evidence for the attention deficit theory has shown that less blood is accessible to areas of the brain that use dopamine (the Pre-frontal cortex) when schizophrenics engage in specific cognitive tasks. This implies that these areas of the brain are less active in these individuals (Frith, 1992). However, this theory is not fully supported as research has also shown that schizophrenics are no worse at focussing their attention on a cognitive task than normal people (McKenna, 1994). The research support is very limited and generally this theory is no longer considered to be a suitable explanation. 

In another experiment participants were asked to judge if the person in a photograph was real or an actor. The person in the photo was receiving a painful electric shock, which would be regarded as an emotional stimulus. The researchers found that schizophrenics were more sensitive to these images than a control group of people without schizophrenia. This suggests that there is an increase in processing of particular stimuli and supports the cognitive processing bias theory (Bentall). 

Generally research support is poor for this explanation and the issue of cause and effect makes it very difficult to establish the theories validity. Unfortunately, cognitive psychologists are unable to determine if schizophrenia is directly caused by disordered thinking or whether this comes as a result of the disorder itself. It also ignores the possibility of a third variable contributing to the development of the disorder. For example, the disorder thinking seen in someone suffering from schizophrenia could be a result of an imbalance of neurochemicals in the brain. 

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This approach to explaining schizophrenia has become less popular over the years after the introduction of more credible biological and cognitive explanations, which have greater research support. It has been criticised for a number of reasons particularly the over-emphasis on the role of a cold and non-nurturing family environment, specifically the mother as the cause of schizophrenia. It is not the case that people who have been brought up in this environment always develop schizophrenia and similarly people who have developed schizophrenia have often experienced a very caring and loving upbringing. It is much more likely that the family life can influence the development of schizophrenia but is not directly the cause. This explanation also fails to offer an effective treatment for schizophrenia, unlike other approaches, and thus demonstrates that psychodynamic theory is not the most beneficial approach to use. 

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