Psya4 - P - Biological Explanations Of Schizophrenia

Front 1

Biological explanations of Schizophrenia

GENES
AO1

Back 1

Genetic factors in S have supported by family, twin and adoptee studies .
FAMILY HISTORY STUDY - Zerbin-Rudin (1972) calculated the ‘risk’ for individual for relatives who suffer from S. They found a 40-68% risk if you are the child of two parents down to a 1-4% risk if you are the niece/nephew. Their results indicated that as genetic relatedness increased, so did the risk of developing S.
TWIN STUDIES - GOTTESMAN (1987) - Concordance rates for MZ twins were 44%; DZ twins were 12%.
ADOPTEE STUDIES - TIENARI (1969) - found 7% of adopted children whose mother had S also went on to develop it, compared to only 1.5% of the control group (whose mother didnt have it).

Front 2

Biological explanations of Schizophrenia

GENES
AO2

Back 2

+ TRIANGULATION - Different methods all indicate a role for genes in the development of S.
- NO 100% CONCORDANCE RATE - If S was purely genetic, then MZ twins should be 100% concordant, BUT could this discordance be due to issues in the diagnosis of S rather than the genetic explanation being wrong?
- IMPOSSIBLE TO SEPARATE NATURE AND NURTURE - Families and twins tend to share environments and so the increased heritability seen could also be the product of mimicking role models rather than shared genes?
- DIAGNOSTIC CRITERIA CHANGING OVER TIME - impedes our ability to accurately conduct family history studies, especially as they rely on retrospective data. Do most people have a good knowledge of the familes mental health history? Nah!

Front 3

Biological explanations of Schizophrenia

GENES
AO2 Conclusion

Back 3

* Althought the evidence for genes intially seems supportive, methodological flaws really limit the support this explanation gets BUT just because the research techniques are flawed doesn't mean the genetic explanation itself is wrong.
* Most modern researchers are now trying to identify an actual gene, although as yet there have been much research identifying specific genes, no findings have been succesfully replicated.

Front 4

Biological explanations of Schizophrenia

DOPAMINE
AO1

Back 4

In some individuals with S, high levels of neurological activity have been noted where Dopamine is a major neurotransmitter, such as the nerve tracks leading from the limbic system to the frontal lobes (thought processes and integration) and the temporal lobes (storage of auditory and visual experience) of the brain. This explanation suggests that messages from neurons that transmit dopamine fire either too often or too quickly causing overstimulation and ultimately S symptoms such as hallucinations or delusions.

Front 5

Biological explanations of Schizophrenia

DOPAMINE
AO2

Back 5

+ Drugs which increase dopamine in the brain, e.g. cocaine and amphetamines, often produce S-like behaviours in ‘normal’ individuals (Angrist et al 1974).
+ L-dopa, used to treat Parkinson’s disease, also increases dopamine, can result in S behaviours.
- Atypical antipsychotics reduce dopamine but they also reduce serontonin levels suggesting the dopamine hypothesis is inadequate as other neurotransmitters appear to be implicated in S.
- Dopamine Hypothesis only really explains the positive symptoms seen in S; to explain negative, we have to look for explanations like structural abnormalities.

Front 6

Biological explanations of Schizophrenia
STRUCTURAL ABNORMALITIES
Description of structural abnormalities and supportive research
AO1

Back 6

Structural abnormalities have been observed in the brains of individuals with Schizophrenia. Enlarged ventricles, cortical atrophy and reversed cerebral asymmetry are some.
+ Andereasen (1988) studied the MRI scans of some individuals with schizophrenia and found their ventricles were 20% to 50% larger than individuals without schizophrenia.
+ Reversed cerebral asymmetry might explain why language (normally found on the left hemisphere) is impaired (e.g. poverty of speech) in individuals in S.

Front 7

Biological explanations of Schizophrenia
STRUCTURAL ABNORMALITIES

AO2

Back 7

- Not all individuals suffering from S have structural abnormalities. They are more associated with negative symptoms of schizophrenia, so might support Schneider's suggestion that positive and negative symptoms of S are actually different disorders and have different aetiologies.
- Structural abnormality research can be quite contradictory. Coplov found a significant overlap in the size of ventricles of individuals with S and control subjects. Suggesting that an enlarged ventricle size is not always an indicator of S. In fact some researchers suggest that this structural abnormality may be the result of taking antipsychotic medication.
- Leucotomies, an early psychosurgical treatment for S. Modern imaging techniques like MRI might support structural differences, the leucotomy did not effect any of the structures in the brain noted above.

Front 8

Biological explanations of Schizophrenia

OVERALL CONCLUSION

Back 8

+ Biological explanations tend to be a great deal more coherent than psychological explanations, but part of their success must rely on the production of effective treatments, especially atypical antipsychotics.
+ S being a biological based disease may also help reduce the stigma of mental illness, but it may also lead to genetic screening for a S gene, an ethically contentious issue.