Sc - Biological explanations for schizophrenia Flashcards

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1
Q

Biological explanations

A

Emphasise the role of inherited factors and dysfunction of brain activity in the development of a behaviour or mental disorder.

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2
Q

Dopamine hypothesis

A

Claims that an excess of the NT dopamine in certain regions of the brain is associated with the positive symptoms of SZ.

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3
Q

Genetics

A

Inherited factors make certain individuals more likely to develop a behaviour or mental disorder.

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4
Q

Neural correlates

A

Changes in neuronal events and mechanisms that result in the characteristic symptoms of a behaviour or mental disorder.

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5
Q

What are the 2 biological explanations for SZ?

A

Genetic factors

Neural correlates

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6
Q

What genetic factors can we talk about for SZ?

A

Family studies
Twin studies
Adoption studies

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7
Q

Explain family studies as a biological explanation for SZ

A

SZ is more common among biological relatives of a person with SZ, and that the closer the degree of genetic relatedness, the greater the risk.

Gottesman’s study - children with 2 schizophrenic parents had a concordance rate of 46%, children with one SZ parent had a rate of 13%, and siblings of a SZ person had a rate of 9%.

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8
Q

What were the results of Gottesman’s family studies?

A

Gottesman’s study - children with 2 schizophrenic parents had a concordance rate of 46%, children with one SZ parent had a rate of 13%, and siblings of a SZ person had a rate of 9%.

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9
Q

Explain twin studies as a biological explanation for SZ

A

If MZ (genetically identical) twins are more similar than DZ twins (only share 50% of genes), then this suggests that the greater similarity is due to genetic factors.

Joseph (2004) calculated that the pooled data for all SZ twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins.

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10
Q

What were the results of Joseph’s twin studies?

A

Joseph (2004) calculated that the pooled data for all SZ twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins.

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11
Q

Who did family studies?

A

Gottesman

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12
Q

Who did twin studies?

A

Joseph (2004)

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13
Q

Explain adoption studies as a biological explanation for SZ

A

Difficult to disentangle genetic and environmental influences for individuals who share genes and environment so studies of genetically related individuals who have been reared apart have been used.

Tienari et al. (2000) in Finland - of the 164 adoptees who biological mothers had SZ, 11 (6.7%) also received a diagnosis of SZ, compared to just 4 (2%) of the 197 control adoptees (non-SZ mothers).

Findings showed the genetic liability to SZ had been ‘decisively confirmed’.

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14
Q

Who did adoption studies?

A

Tienari et al. (2000) in Finland

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15
Q

What were the results of the Tienari et al. adoption studies?

A

Tienari et al. (2000) in Finland - of the 164 adoptees who biological mothers had SZ, 11 (6.7%) also received a diagnosis of SZ, compared to just 4 (2%) of the 197 control adoptees (non-SZ mothers).

Findings showed the genetic liability to SZ had been ‘decisively confirmed’.

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16
Q

What neural correlates can we talk about for SZ?

A

Dopamine hypothesis

Specific brain areas

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17
Q

Link between D2 receptors and SZ

A

Schizophrenics thought to have abnormally high numbers of D2 receptors on receiving neurons.

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18
Q

What does schizophrenics having abnormally high numbers of D2 receptors on receiving neurons result in?

A

More dopamine binding and therefore more neurons firing.

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19
Q

What evidence showed the key role played by dopamine?

A

Drugs that increase dopaminergic activity and drugs that decrease dopaminergic activity.

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20
Q

What does amphetamine cause?

A

Dopamine agonist - stimulates nerve cells containing dopamine, causing the synapse to be flooded with the NT.

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21
Q

What is a drug that increases dopaminergic activity?

A

Amphetamine.

22
Q

What does excess dopamine/amphetamine do to ‘normal’ individuals?

A

‘Normal’ individuals exposed to large doses of dopamine releasing drugs such as amphetamines can develop the characteristic symptoms of a schizophrenic episode, which generally disappear with abstinence from the drug.

23
Q

What drugs decreases dopaminergic activity?

A

Antipsychotics.

24
Q

What do antipsychotics do to dopamine?

A

Dopamine antagonists - block the activity of dopamine in the brain.

25
Q

How do antipsychotics decrease dopaminergic activity?

A

By reducing activity in the neural pathways of the brain that use dopamine as the NT.

26
Q

What do antipsychotics do to symptoms?

A

Eliminate symptoms such as hallucinations and delusions.

27
Q

Why are antipsychotics evidence for the hypothesis?

A

The fact that these drugs (dopamine antagonists) alleviated many of the symptoms of SZ strengthened the case for the important role of dopamine in this disorder.

28
Q

What did Davis and kahn (1991) propose about positive symptoms of SZ?

A

They are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway.

29
Q

Who proposed that positive symptoms of SZ are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway?

A

Davis and kahn (1991)

30
Q

From what are the negative symptoms of SZ thought to arise?

A

From a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway).

31
Q

Who carried out a study on dopamine levels in people with SZ compared to those without?

A

Patel et al. (2010)

32
Q

How did Patel et al. (2010) compare dopamine levels in people with SZ to people without SZ?

A

Using PET scans.

33
Q

What did Patel et al. (2010) find about dopamine levels in people with SZ compared to those without?

A

Found lower levels of dopamine in the dorsolateral prefrontal cortex (DLPFC) of schizophrenic patients compared to their normal controls.

34
Q

What brain areas are known to be involved in SZ?

A

PFC
Hippocampus
Grey matter
White matter

35
Q

What is the PFC involved in?

A

Main are for executive control (i.e. planning, reasoning, and judgement).

36
Q

What research is there for a difference in the PFC of people with SZ?

A

Weinberger and Gallhofer (1997).

37
Q

What problems in SZ do deficits within the PFC and its connections with other areas of the brain (particularly the hippocampus) cause?

A

Cognitive symptoms

38
Q

Where is the hippocampus?

A

Temporal lobe

39
Q

What research is there for a difference in the hippocampus of people with SZ?

A

Conrad et al. (1991) - anatomical changes.

40
Q

What do deficits in the nerve connections between the hippocampus and the PFC correlate with?

A

The degree of working memory impairments, a central cognitive impairment in SZ (Mukai et al., 2015).

41
Q

What do Goto and Grace (2008) suggest that hippocampal dysfunction might aloso influence?

A

Levels of dopamine release in the basal ganglia, indirectly affecting the processing of information in the PFC.

42
Q

Grey matter link to SZ

A

SZ = reduced grey matter especially in temporal and frontal lobes.

43
Q

Ventricle size link to negative symptoms of SZ

A

Those with SZ, particularly those displaying negative symptoms, have enlarged ventricles (Hartberg et al., 2011).

44
Q

What is grey matter

A

Mostly dead cell bodies and unmyelinated axons.

45
Q

What are enlarged ventricles said to be a consequence of?

A

A consequence of nearby parts of the brain not developing properly or being damaged.

46
Q

What did Cannon et al. (2014) find about grey matter and ventricles in individuals at high clinical risk who developed SZ compared to those who did not develop SZ?

A

Found that individuals at high clinical risk who developed SZ showed a steeper rate of grey matter loss and a greater rate of expansion of brain ventricles compared to those who did not develop SZ.

47
Q

What are ventricles in the brain?

A

Brain cavities filled with cerebrospinal fluid.

48
Q

What is white matter?

A

Made up of nerve fibres covered in myelin.

49
Q

Where is white matter found?

A

Brain and spinal cord.

50
Q

What does myelin do?

A

Creates an insulating sheath around nerve fibres and helps to conduct information quickly through the CNS, enabling efficient information processing.

51
Q

What has research (e.g. Du et al., 2013) found about white matter in those with SZ?

A

Found reduced myelination of white matter pathways in schizophrenic patients, compared to healthy controls. This is particularly the case in the neural pathways between the PFC and the hippocampus.