Psychology- Schizophrenia

Biological explanations of schizophrenia

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  • Created by: Sarah
  • Created on: 02-06-09 09:05

Evidence from family studies

  • Schizophrenia is more common in the biological relatives of a schizophrenic, and that the closer the degree of genetic relatedness, the greater the risk
  • Kendler et al. (1985) Found that first-degree relatives are 18x more at risk than the general population


  • MZ twins have around a 48% risk of developing schizophrenia if their twin has the disorder
  • DZ twins- this drops to just 17%


  • Kety et al. (1962), the Copenhagen study, found that 14% of the biological relatives of adoptees with schizophrenia were classified with schizophrenia
  • Only 2.7% of their adoptive relatives were found to be schizophrenic
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Evaluation of genetic factors

  • Research evidence - Now very strong evidence, particularly from adoption studies, that genetics are a clear risk factor for schizophrenia
  • Degree of risk - Never 100% concordance with MZ twins. Genetics cannot offer a complete explanation
  • Not just family - Doesn't account for those who are diagnosed but have no close relatives with schizophrenia - about 2/3rds. Causes may be viruses or other things
  • Just one gene? - Possible to explain the sudden emergence of schizophrenia in terms of inherited factors. If schizophrenia is caused by a large number of genes, individuals with a few of these genes show no disorder; it is only when a large number are present that an individual become vulnerable
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Biochemical factors

The dopamine hypothesis

  • Dopamine is a neurotransmitter operating in the brain
  • Schizophrenics are thought to have an abnormally high number of D2 receptors on their receiving neurons, resulting in more dopamine binding and therefore more neurons firing.
  • Dopamine neurons play a key role in guiding attention so disturbances in this process may lead to problems of attention and thought found in people with schizophrenia (Comer, 2003).

Evidence supporting the dopamine hypothesis

Drugs called phenothiazines used to bind to the D2 receptors, effectively blocking the transmission of nerve impulses through those receptors and therefore reducing the attentional deficit found in schizophrenia

  • Low levels of dopamine activity are found in suffers of Parkinson's. Some people who were taking the drug L-dopa to raise their dopamine level developed schizophrenic-type symptoms (Grilly, 2002)
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Evaluation of biochemical factors

  • Anti-psychotic drugs are effective only for the positive symptoms. Therefore, excessive dopamine can only explain some types of schizophrenia
  • Newer atypical anti-psychotic drugs have proved more effective than traditional ones. These newer drugs affect dopamine as well as other neurotransmitters, such as serotonin. Therefore, dopamine levels alone cannot explain schizophrenia
  • The hypothesis also cannot explain that fact that schizophrenics frequently have spontaneous, lengthy periods of remission. This could be explained only by a variation in dopamine levels over time, but there is no suggestion why this might occur
  • The effects of dopamine blockers may be indirect. These drugs may influence other systems that have more impact on schizophrenic symptoms
  • Schizophrenics are not the only people who respond to anti-psychotic medication. This suggests that dopamine deficiencys are not necessarily specific to schizophrenic symptoms but to many genetic symptoms common to all mental disorders
  • This does not show cause and effect. Whether dopamine causes schizophrenic symptoms or schizophrenia causes a rise in dopamine levels
  • Current available evidence supports some form of the dopamine hypothesis. Excess dopamine activity has been clearly demonstrated in certain individuals with schizophrenia, especially in those displaying positive symptoms.
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Brain dsyfunction

Enlarged ventricles

  • The ventricles of a person with schizophrenia are on average 15% bigger than normal (Torrey, 2002)
  • People with schizophrenia who have enlarged ventricles tend to display negative rather than positive symptoms and have greater cognitive disturbances and a poorer response to traditional anti-psychotics.
  • The enlarged ventricles may be the result of poor brain development or tissue damage, and these problems can lead to schizophrenia

Specific brain abnormalities

  • Meyer-Lindenberg et al. (2002) examined brain activity in schizophrenia engaged on a working memory task. Their pre-frontal cortex showed reduced activation, reflecting their poor performance on such tasks
  • At the same time, dopamine levels were elevated, suggesting that a dysfunction of the pre-frontal cortex is linked to dopamine abnormalities
  • Structural abnormalities have been found more often in those with negative/chronic symptoms, rather than positive/acute symptoms
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Evaluation of brain dsyfunction

  • Whilst MRI studies appear to provide conclusive evidence of structural abnormalities, they do not always agree on the regions of the brain affected. Flaum et al. (1995) found no abnormalities in the temporal lobe regions, whereas Woodruff et al. (1997) found quite significant reductions in the temporal lobe
  • Does not show cause and effect
  • Studies mainly done on animals and so cannot always be generalised to humans
  • Patients with type 2 schizophrenia also have smaller amounts of grey matter and smaller temporal and frontal lobes. This supports the view that enlarged ventricles are significant only because they indicate reduced brain matter, which may be related to brain damage.
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Viral infections/birth factors

  • Schizophrenia may be associated with exposure to viruses before birth. These may remain dormant until puberty when they are activated by hormonal changes


  • A significant number of people with schizophrenia are born during winter, when exposure to viruses is higher. Mothers of schizophrenics are more likely to have been exposed to flu virus during pregnancy than mothers of non-schizophrenics
  • Work with identical twins has also established that many schizophrenics have fingerprint abnormalities compared to their non-schizophrenic twin.
  • Fingerprint develop in the second trimester of pregnancy, when the foetus is most at risk from viruses. The fingerprint abnormalities of people with schizophrenia could therefore indicate viral infection during this period, causing these abnormalities and predisposing the person to schizophrenia (Comer, 2003)
  • Throughout history, peaks in schizophrenia diagnosis have corresponded with major flu epidemics (Torrey et al. 1988)
  • A longitudional study by Dalman et al. (1999) found significant links between birth complications and later development of schizophrenia, with pre-eclampsia being the most significant risk factor.
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Evaluation of viral infections/birth factors

  • It can explain why schizophrenia appears in individuals with no family history of the disorder
  • But there is no evidence that all people with schizophrenia have been exposed to viruses. It is unlikely that birth complications are the sole cause of schizophrenia as problems such as pre-eclampsia are common and not all infants do go on to develop schizophrenia
  • Torrey et al. (1988) claimed that the link between viral infections and schizophrenia only occurs in those who are already genetically predisposed. However, if that were the case, there would be 100% concordance in MZ twins and maybe DZ twins as they share the uterus and thus exposed to the same virus.
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Diathesis-stress model

  • Even though such studies have found compelling support for the importance of genetic factors, they have also shown that schizophrenia did not always develop in those thought to be genetically vulnerable
  • People with a biological predisposition for schizophrenia may only develop into having schizophrenia if other psychological stressors are present (Gottesman and Reilly, 2003)
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Evaluation of biological explanation

  • Attempts to explain schizophrenia simply in terms of one biological cause are challenged by the fact that there are different types of schizophrenia. Patients generally display certain clusters of symptoms
  • Type 1 schizophrenia is characterized by positive symptoms, whereas type 2 is associated with negative symptoms (Crow, 1985). Paranoid schizophrenics experience delusions and hallucinations, whereas undifferentiated schizophrenics display flatness of affect. The existence of these different types suggest different causes
  • For example, enlarged ventricles are most common in type 2 schizophrenia so this explanation may only apply to this type.
  • Causes can be proximate or ultimate.
  • Proximate= immediate causes. e.g excessive dopamine
  • Ultimate= caused by something else. e.g. birth complications and poor nutrition
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