Introduction
Schizophrenia is a serious, debilitating and complex disorder causing disconnected or altered thought processes and a loss of contact with reality. Professor Eugen Bleuler first coined the term ‘schizophrenia’ on 24th April 1908. (Ashok, Baugh, & Yeragani, 2012) Despite common misconceptions about schizophrenia meaning split personality Bleuler (1908) emphasised that splitting of physic functioning is an essential feature of schizophrenia. Schizophrenia can have a chronic or acute onset and affects an individual’s moods, feelings, thoughts, behaviour and perception as well as the ability to communicate. The symptoms of schizophrenia can be either positive, appearing to reflect an excess of distortion of normal function, or negative, appearing reflect a loss of normal function. The onset of schizophrenia can be acute or chronic, usually occurring between the age of 15 and 45 years old, often earlier in males than females. The lifetime risk of being diagnosed with schizophrenia is 1%.
The biological approach to psychopathology
There are several possible biological explanations for the development of schizophrenia; these include trauma and brain injury, infection such as maternal flu during pregnancy, biochemistry such as altered levels of hormones or neurotransmitters and the genetic explanation. It is widely known that brain injuries and trauma often have an impact on an individuals long term physical and mental health depending on the areas of the brain affected. There is evidence to suggest that it is not just maternal flu but movement and positioning of twins whilst in the womb that can influence the chances of an individual developing schizophrenia, this is supported by research carried out by Van Os et al (1997) who found that in identical twins, the schizophrenic child often have abnormalities within their fingerprints compared to their non-schizophrenic twin (Berman, Flanagan, & Frost, 2005).
One of the main biological explanations for the development of schizophrenia is genetics. A large amount of meta-analysis has been carried out with strong evidence to suggest that genetic factors play a major contributory role in the development of schizophrenia. Kety et al (1994) conducted a longitudinal study involving 311 children with 207 children born to mothers with a diagnosis of schizophrenia and 104 children born to mothers with no diagnosis of schizophrenia. The study showed a strong genetic element with 16.2% of children from mothers with a diagnosis of schizophrenia going on to develop schizophrenia themselves. (Cardwell, Clark, Meldrum, & Wadely, 2009) However, this study also concluded that 1.9% of children born to mother’s with no diagnosis of schizophrenia also went on to develop schizophrenia, this could be as a result of skipping generations or indicate that there is also an element of environmental factors that also contribute to a person developing schizophrenia.
A further study in support of the genetic explanation was carried out by Janicak et al (2001), this study identified that Monozygotic or identical twins (MZ) who share 100% DNA have a 48% risk of developing schizophrenia with this percentage falling to around 17% in Dizygotic or non-identical twins (DZ) who share 50% DNA. (Berman, Flanagan, & Frost, 2005). However, although this study, carried out by Janicak et al (2001) provides evidence in support of the genetic explanation, if it was solely genetics that caused schizophrenia, the concordance rate in MZ twins would be 100%. Twin studies also fail to consider factors such as social class.
The biological explanation provides evidence to classify schizophrenia as being a serious medical illness and therefore attributes a ‘no blame’ attitude. The fact that there is a genetic element to schizophrenia means that the awareness amongst families of individuals with a family history of schizophrenia can be more aware of the risks and seek treatment/symptom management early. A positive outcome of this approach is that there is plenty of research has been undertaken therefore increasing the knowledge and understanding of schizophrenia; this enhances treatment techniques and outcomes. A disadvantage of the biological approach is the stigma attached to mental illness potentially leading to the isolation and regression of an individual with schizophrenia therefore escalating symptoms, potentially leading to them causing harm to themselves or others. The biological approach is also deterministic in that it implies it is inevitable that an individual with certain genetics will develop schizophrenia however they only increase the risk of an individual developing schizophrenia.
The cognitive approach to psychopathology
With a lot of symptoms of schizophrenia impacting an individual’s cognition this would indicate that there is a cognitive explanation. One cognitive explanation for the development of schizophrenia is ‘Distortion Reality’, as proposed by Frith & Done (1988). It is suggested that schizophrenic individuals experience ‘alien control symptoms’ as a result of poor self-management. (Stirling, Hellewell, & Quraishi, 1998) Frith (1992) also suggested that schizophrenic individuals are unable to differentiate between the actions of external forces and those that are generated internally, compared to non-schizophrenic individuals. Quite often as a result schizophrenic individuals mistake their own ‘inner voice’ for someone or something in the external environment trying to communicate with them. This encourages a further lack of control and self–management.
There is also the suggestion of a stress trigger element to the onset of schizophrenia by Brown and Birley (1968). Brown and Birley (1968) concluded that around 50% of those diagnosed with schizophrenia suffer some kind of traumatic or major life event around 3 weeks prior to a schizophrenic episode and around 12% experiencing a traumatic or major life event around 9 weeks prior to a schizophrenic episode (Berman, Flanagan, & Frost, 2005). This would also fit with the diathesis-stress model.
In comparison to the biological approach the cognitive model would allow for individual differences in symptoms experienced by individuals and go some way in explaining the variations of schizophrenia in contrast to all suffers simply having the schizophrenic genes (Lawton & Willard, 2015). Even though the cognitive evidence does not appear to explain the initial onset of schizophrenia is, there is further neurological evidence to suggest that cognitive processes are different in individuals with schizophrenia compared to those without schizophrenia. The fact that some symptoms of schizophrenia can be treated through cognitive behavioural therapy (CBT) also supports the cognitive approach.
Conclusion
In contrast to the biological approach the cognitive approach explains the cognitive symptoms of schizophrenia however it does not provide adequate explanation for they’re being a purely cognitive role in the onset of schizophrenia. The biological and cognitive approaches are very reductionist on there own suggesting that an element of both approaches are involved in the onset of schizophrenia. A study carried out by Tienari et al (2004) looked at children born from mothers with schizophrenia who have been raised in an adopted environment and concluded that adopted children raised in a stable, healthy family were only at 5.8% risk of developing schizophrenia whereas children raised in a dysfunctional family have a 36.8% risk of developing schizophrenia. This not only supports the biological model in that there is a genetic link but also environmental factors that children born to mothers diagnosed with schizophrenia and raised within a dysfunctional environment are more likely to develop schizophrenia. In conclusion the causes of schizophrenia are not widely understood, however there is empirical research and evidence to support both the biological and genetic explanation of the onset of schizophrenia as well as an element of cognitive and behavioural impact. Therefore making the diathesis-stress model a more likely explanation combining both a biological and a psychological/stress trigger, ultimately a genetic abnormality leading to biochemical abnormalities with neurotransmitters which can result in psychological and physiological predisposition.