Biological Explanations of Schizophrenia

Erica Lai
Mind Map by Erica Lai, updated more than 1 year ago
Erica Lai
Created by Erica Lai about 5 years ago
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Psychology (Schizophrenia ) Mind Map on Biological Explanations of Schizophrenia, created by Erica Lai on 15/01/2015.

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Biological Explanations of Schizophrenia
1 Genetic Factors
1.1 Family Studies
1.1.1 e.g. Gottesman (1991)
1.1.2 Find individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives
1.1.3 Have established that schizophrenia is more common among biological relatives, and that the closer the degree of genetic relatedness, the greater the risk.
1.1.3.1 e.g. Children with 2 schizophrenic parents have a concordance rate of 46%, children with 1 schizophrenic parent 13% and siblings 9%.
1.1.3.2 However, many researchers now accept that the fact that schizophrenia appears to run in families may be more to do with common rearing patterns or other factors that have nothing to do with heredity.
1.2 Twin Studies
1.2.1 Offer a unique opportunity for researchers to investigate the relative contributions of genetic and environmental factors.
1.2.2 If monozygotic twins (100% same genes) are more concordant in terms of a trait like schizophrenia than are dizygotic twins (50% same genes) then this suggests that the greater the similarity is due to genetic factors.
1.2.2.1 Joseph (2004) calculated that the pooled data of all schizophrenia twin studies prior to 2001 shows a concordance rate for monozygotic twins of 40.4% and for dizygotic twins of 7.4%.
1.2.3 More recent, methodologically sound studies (e.g. double blind trials) have tended to report a lower concordance rate for monozygotic twins.
1.2.3.1 Twin researchers still argue that even these findings support the genetic position, because they provide a monozygotic concordance rate that is many times higher than the dizygotic concordance rate.
1.2.4 A crucial assumption underlying all twin studies is that the environments of MZ twins and DZ twins are equivalent. Therefore, the greater concordance for schizophrenia between MZ twins is a product of greater genetic similarity rather than greater environmental similarity.
1.2.4.1 Joseph (2004) criticises this. Pointed out that MZ twins are treated more similarly and encounter more similar environments. They also experience more 'identity confusion' (i.e. frequently referred to as 'twins' rather than individuals) than DZ twins. As a result, Joseph argues that the differences in concordance rates between MZ and DZ twins reflect nothing more than the environmental differences that distinguish the two types of twin
1.3 Adoption Studies
1.3.1 There are obvious difficulties of distinguishing genetic and environmental influences for individuals who share genes and environment, so studies of genetically related individuals who have been reared apart are used.
1.3.2 One of the most methodologically sound studies of this kind was conducted by Tienari et al. (2000) in Finland. Of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis of schizophrenia, compared to just 4 (2%) of the 197 control adoptees (born to non-schizophrenic mothers). The investigators concluded that these findings showed that the genetic liability to schizophrenia had been 'decisively confirmed'.
1.3.2.1 Relatively large sample size = good population validity, therefore increased usefulness
1.3.2.2 Finland, so sample is unrepresentative of the global community, therefore decreased ecological validity and generalisability (cultural bias?)
2 The Dopamine Hypothesis
2.1 Dopamine is a neurotransmitter that operates in the brain
2.1.1 Plays a key role in guiding attention, so disturbances in this process may lead to problems relating to attention, perception and thought found in people with schizophrenia (Comer (2003))
2.2 States that messages from neurons that transmit dopamine fire too easily or too often, leading to characteristic symptoms of schizophrenia
2.3 Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.
2.4 Evidence for the key role dopamine plays in schizophrenia
2.4.1 Amphetamines
2.4.1.1 a drug with special relevance for our understanding of schizophrenia
2.4.1.2 A dopamine agonist, stimulating nerve cells containing dopamine causing the synapse to be flooded with this neurotransmitter
2.4.1.3 Large doses can cause the characteristic hallucinations and delusions of a schizophrenic episode
2.4.2 Antipsychotic drugs
2.4.2.1 Many different types but they all have one thing in common, they block the activity of dopamine in the brain.
2.4.2.2 Reducing stimulation of the dopamine system, and thereby eliminating the symptoms such as hallucinations and delusions
2.4.2.2.1 by alleviating many of the symptoms of schizophrenia, it strengthened the case for dopamine being a significant contributory factor in this disorder
2.4.2.3 dopamine antagonists
2.4.3 Parkinson's Disease
2.4.3.1 Low levels of dopamine activity
2.4.3.2 Degenerative neurological disorder
2.4.3.3 found that some people who were taking the drug L-dopa to raise their dopamine levels were developing schizophrenic-type symptoms (Grilly (2002))
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