Paper 3 - Schizophrenia - Biological And Neural Explanations Flashcards

1
Q

What are the 3 Biological Explanations?

A

Genetic Vulnerability
Dopamine Hypothesis
Neural Correlates

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2
Q

What are the different sub categories of Genetic Vulnerability

A

Family studies
Twin studies
Adoption studies
Candidate Gene

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3
Q

Explain family studies?

A

Gottesman (1991) Family studies
His findings showed that the greater the degree of genetic relatedness, the greater risk of developing schizophrenia
But identical twins were only about 48% so there is still a great environmental impact

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4
Q

Explain twin studies?

A

Twin studies
Gottesman and shields (1962) found that the concordance rate for schizophrenia in MZ twins was 48% compared for 17% for DZ twins
Suggesting that schizophrenia has a genetic basis
Joseph (2004) showed a concordance rate of 40.4% for MZ and 7.4% for DZ

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5
Q

Explain the first adoption study?

A

Heston (1966) compared 47 adopted children whose biological mothers had schizophrenia with a control group with no family history of schizophrenia
0 in the control group was diagnoses with schizophrenia 16% of the offsprings of the sample were diagnoses

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6
Q

explain the second adoption study?

A

Tienari (2000)
Found that 11% of 164 adoptees whose mothers had schizophrenia also had schizophrenia

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7
Q

Explain the candidate Gene?

A

Schizophrenia is thought to be polygenic (many genes make up the disorder)
Ripke (2014) completed a study combining all data from a genome wide study of schizophrenia
37000 patients were compared to 113,000 controls
108 separate genetic variations were associated with an increased risk of schizophrenia

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8
Q

What is the word for many genes being the cause of something?

A

Polygenic

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9
Q

What is important to remember about the dopamine hypothesis?

A

It was originally just hyper and hen adapted to include hypo

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10
Q

What is the theory of the Dopamine Hypothesis?

A

This theory claims that excessive amounts of dopamine or an oversensitivity of the brain dopamine is the cause of schizophrenia.
So messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic symptoms of schizophrenia.

However, it was adapted to include the effects of lower levels of dopamine

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11
Q

What is the general overview of the dopamine hypothesis?

A

An excess of the neurotransmitter dopamine has been implicated in the symptoms of schizophrenia
Hyperdopaminergia in the subcortex
Hypodopaminergia in the cortex

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12
Q

What is the ending of that long word?

A

Dopamine rgia

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13
Q

Where may hyperdopaminegia occur?

A

The sub cortex

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14
Q

Where may hypodopaminegia occur

A

Cortex

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15
Q

Explain hyperdopaminegia in the subcortex?

A

Higher levels of dopamine in the subcortex
So there is excess levels of dopamine receptors in Brocca’s area. This may be the cause of the disorganised speech (as brocca’s area is overexcited)
Furthermore, as there is excess dopamine in the subcortex his could explain the experience of auditory hallucinations

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16
Q

Explain hypodopaminegia in the cortex?

A

Lower levels of dopamine in the brain’s cortex
Goldman and Rakic et al (2004) identified that low levels of dopamine in the prefrontal cortex
It will increase the negative symptoms of schizophrenia as it effects thinking and decision making

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17
Q

Explain in great detail how the dopamine hypothesis and schizophrenia interact?

A

• People with schizophrenia are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing

18
Q

What 3 things can be used as evidence for the dopamine hypothesis?

A

Amphetamines
Cocaine
Antipsychotic drugs

19
Q

Explain the evidence of the DH: Amphetamines

A

➢ Amphetamines; this is a dopamine agonist, this stimulates nerve cells containing dopamine causing the synapse to be ‘flooded’ – large doses of the drug can cause hallucinations and delusions of a schizophrenic episode.

20
Q

Explain the evidence of the DH: Cocaine

A

➢ Cocaine also increases the levels of dopamine in the brain and can cause the positive symptoms of schizophrenia and exaggerate them in people who already have the disorder.

21
Q

Explain the evidence of the DH:

A

➢ Antipsychotic drugs (dopamine antagonists) which block the activity of dopamine in the brain, by reducing the stimulation of the dopamine system, eliminates hallucinations and delusions. By alleviating many of the symptoms of schizophrenia, antipsychotic drugs strengthen the case for dopamine being a significant contributory factor.

22
Q

What is an agonist?

A

An agonist is a chemical that binds to a receptor of a cell and triggers a response by that cell.

23
Q

What is a antagonist

A

An antagonist blocks or reduces the effect of a neurotransmitter

24
Q

What drug can be used to treat Parkinson’s

A

L Dopa

25
Q

Why may Parkinson’s be confused with schizophrenia?

A

The disease increases dopamine

26
Q

Explain post mortem evidence for the dopamine hypothesis?

A

• Post mortems of schizophrenics, show an increase of dopamine in parts of the brain. (Seeman 1987)

27
Q

What are Neural Correlates?

A

• Neural correlates are measurements of the structure or function of the brain that occur in conjunction with an experience

28
Q

What is a newer approach to Schizophrenia?
How?

A

• There is growing evidence that schizophrenia is down to structural abnormalities in the brain
• Brain scanning techniques have made it possible to investigate living brain images
People with schizophrenia have abnormally large ventricles in the brain. Ventricles are fluid filled cavities. This means that the brains of people with schizophrenia are lighter than normal.

29
Q

What section of the brain is linked with Neural Correlates of Schizophrenia Negative Symptoms?

A

Ventral Striatum

30
Q

Explain Neural Correlates of Schizophrenia negative symptoms

A

Activity in the ventral striatum has been linked to the development of avolition (loss of motivation)
The ventral striatum are believed to be particularly involved in the anticipation of a reward for certain (2006) found lower levels compared to control
Negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms

31
Q

What section of the brain is linked with Neural Correlates of Schizophrenia Positive Symptoms?

A

Reduced activity in the superior temporal gyrus and anterior cingulate grus

32
Q

Explain Neural Correlates of Schizophrenia positive symptoms

A

Reduced activity in the superior temporal gyrus and anterior cingulate grus have been linked to the development of auditory hallucinations
Studies show that patients experiencing auditory hallucinations showed lower activations levels in these areas than controls

33
Q

What studies can be used as supporting evidence for a genetic basis?

A

• Genetic links - Gottesman (1991)
• Adoption studies- Tienari et al. (2004)
• Genetic variation- Ripke et al. (2014)

34
Q

Explain the evaluations of twin studies?

A

• Twin studies demonstrate that there may be a predisposition to develop schizophrenia, however, the fact that both twins do not always develop schizophrenia means that environmental factors must also play a part
Sample sizes are small so they can’t be generalised

The higher concordance rates between MZ twins could be explained by environmental similarities not genetics
MZ twins elicit more similar treatment than DZ twins
There isn’t yet one gene which haas been found to be causing schizophrenia
Many studies in this areas lack temporal validity (Using DSM III etc)

35
Q

Explain the evaluations of Adoption Studies

A

Tienari conducted his study within Finland, therefore we are not able to generalise this study to the rest of the world

36
Q

What are the general evaluations?

A

Ignorance of psychological explanation

37
Q

Explain the evaluation for the dopamine hypothesis?

A

Mixed Evidence for the dopamine hypothesis
• Curran et al. (2004) found that dopamine agonists increase the levels of dopamine and can make the symptoms of schizophrenia worse.
• Tauscher et al. (2014) found that antipsychotic drugs reduce the levels of dopamine.

• Lindstoroem et al. (1999) found that the chemicals needed to produce dopamine are taken up faster in the brains of people with schizophrenia – suggesting they produce more dopamine.
• Moghaddam and Javitt (2012) have found evidence for the role of a neurotransmitter called glutamate which indicates more signalling to other cells which could induce symptoms of schizophrenia

38
Q

What are the evaluations for Neural Correlates?

A

Correlation or Causation
General

39
Q

Explain the negative evaluation of general bio/neural explanations…

A

Ignorance of the psychological explanation
• It is a reductionist approach
• Family functioning during childhood may play a role or another “diathesis stress” relationship
• In terms of inheritance – less than 50% chance of developing schizophrenia if your identical twin has schizophrenia

40
Q

Explain the evaluation of Neural Correlates: Correlation or Causation

A

• Neural correlations tell us very little about causes of schizophrenia
• The correlation between the ventral striatum and negative symptoms could suggest that there is something wrong in the ventral striatum which is causing negative symptoms or that the negative symptoms mean less information passes through the striatum.

41
Q

Explain the evaluations of Neural Correlates: General

A

• Findings are inconsistent and therefore inconclusive

• MRIs have made it possible to investigate living brain images which is an
advance on merely having to rely on post mortems

42
Q

Explain the evaluation for a genetic basis: Mutations

A

• There is evidence of mutations in parental sperm.
• Caused by radiation, poison or viral infection
• Brown et al. (2002) – positive correlation between paternal age
and risk of schizophrenia
• Increasing from around 0.7% fathers under 25 and 2% in fathers over 50