Schizophrenia - Biological Explanations For Schizophrenia Flashcards

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1
Q

What evidence suggests that schizophrenia has a genetic basis?

A

Research has found that SZ runs in families.

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2
Q

What did Gottesman (1991) found?

A

He demonstrated a positive correlation between the increasing genetic similarity of family members and their increased risk of developing schizophrenia.

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3
Q

What were the concordance rates of monozygotic twins in Gottesman’s studies?

A

48%

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4
Q

What were the concordance rates of dizygotic twins in Gottesman’s studies?

A

17%

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5
Q

What were the concordance rates of siblings in Gottesman’s studies?

A

9%

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6
Q

What were the concordance rates of parents in Gottesman’s studies?

A

6%

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7
Q

What do Gottesman’s studies suggest?

A

Strongly suggests a genetic basis and the existence of candidate genes for SZ.

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8
Q

What is important to note about concordance rates?

A

There are no 100% concordance rates , therefore demonstrating that there are environmental influences acting on the development of SZ like the schizophrenogenic mother and dysfunctional thought processing.

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9
Q

What does polygenic mean?

A

Schizophrenia is a polygenic disorder because it has multiple, contributing candidate genes - not just one.

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10
Q

Who studied candidate genes - what was their procedure?

A

Ripke et al conducted a genome-wide study of 5001 cases of Swedish nationals with SZ and compared them to 6243 healthy controls. Each candidate gene represents a genetic variation which marginally increases the risk of developing SZ.

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11
Q

What is the dopamine hypothesis?

A

Suggests that symptoms of schizophrenia are associated with too much or an imbalance of the dopamine neurotransmitter across the brain.

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12
Q

What did the revised dopamine hypothesis suggest?

A

Suggests that hypodopaminergeria (abnormally low dopamine levels) in the cortex is more likely to be responsible for SZ.

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13
Q

What is the modern understanding of the role of dopamine in SZ?

A

It is that both hyper- and hypodompaniergeria in different areas of the brain contribute to the development of SZ.

For example, an excess of dopamine in the frontal lobe, specifically in Broca’s area which may have an excess of D2 receptors, may be responsible for the positive SZ symptom of auditory areas of the brain.

It has been suggested that hypodomaniergia in the prefrontal cortex may be responsible for negative symptoms of SZ, such as speech poverty and avolition. This is because the prefrontal cortex is associated with logical thinking, so abnormally low dopamine levels in this area may impair an individual’s ability to construct grammatical sentences that are focused upon on topic (speech poverty) or the ability to make decisions about how to function in day to day living (avoilition).

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14
Q

What implications does the dopamine hypothesis have?

A

Has particularly important implications for the development of drug treatments for SZ, such as antipsychotics/ dopamine antagonists.

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15
Q

What is neural correlates?

A

Neural correlates are the variations in neural structure and bio chemistry that are correlated with an increased risk of developing schizophrenia.

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16
Q

What did Juckel et al suggest ?

A

Abnormally low levels of activation in the ventral striatum, when compared to a healthy control group, can cause avolition. The ventral striatum is associated with evaluating reward values, predictability and risks. So low levels of activation could mean that individuals can’t accurately assess the reward of having enough motivation to carry out normal day-to-day tasks, and so are unable to cope with ‘normal’ life.

17
Q

What is a strength of biological explanations for schizophrenia?

A

+ There is evidence supporting the biological and genetic basis of schizophrenia.
Brown et al (2002) found that the risk of having offspring with SZ increased by over 1.3% if the father was over 50 years old, compared to if the father was under the age of 25. This suggests that mutations in the sections of DNA containing the candidate genes, for serotonin and dopamine can cause SZ. This means that SZ is likely to have a strong heritability coefficient and biological basis. Supports the use of family studies and neural correlates as ways of studying and explaining concordance rates of SZ.

18
Q

What are the limitations of the dopamine hypothesis ?

A

The evidence for the dopamine hypothesis can be best described as ‘‘mixed’’. Support comes from researchers who found that antipsychotics, alleviated the symptoms of SZ because they reduce dopamine activity by binding to complementary receptors on the post-synaptic membrane, This suggests that dopamine has a key role in its
development.

However, some researchers such have criticised biological explanations for overemphasising the role of dopamine. The neurotransmitters Glutamate and Serotonin may also play a key role, as evidenced by the antipsychotic acting upon both of these substances being more effective than other atypical antipsychotics in reducing SZ symptoms.

19
Q

What are the limitations of neural correlates?

A

— The main issue associated with the use of neural correlates is that evidence is correlational and so does not take into account the ‘third variable problem’, a third unstudied factor could be affecting both outcomes. For example with auditory hallucinations. One explanation would be the lowered activation levels causing the hallucinations, or the hallucinations themselves causing the lowered activation levels. This demonstrates that correlational research cannot be used to reliably demonstrate a ‘cause and effect’ relationship between two variables.

20
Q

What might lead to auditory hallucinations according to the dopamine hypothesis?

A

Excessive amounts of dopamine (hyperdopaminergia) in speech centres like Broca’s area may lead to auditory hallucinations.

21
Q

What might lead to negative symptoms according to neural correlates/ dopamine hypothesis?

A

Lower levels of dopamine (hypodopaminergia) in areas like frontal cortex are thought to lead to negative symptoms like avoilition and speech poverty.

22
Q

What might lead to negative symptoms according to neural correlates/ dopamine hypothesis?

A

Lower levels of dopamine (hypodopaminergia) in areas like frontal cortex are thought to lead to negative symptoms like avoilition and speech poverty.

23
Q

What other alternate neurotransmitters are implicated?

A

Glutamate = an excitatory neurotransmitter involved in learning, attention and memory is found in low quantities in people with schizophrenia

Serotonin = suggested as a drug that acts on the serotonin system, clozapine is an effective treatment.

24
Q

Describe research support for neural correlates

A

Leueht et al, conducted a meta-analysis review of 212 studies. These studies assess the effectiveness of anti-psychotic drug treatments that work by normalising levels of dopamine. These drugs were more effective than a placebo. This suggests that the underlying biological theory of schizophrenia’s cause has validity. Otherwise drugs would not be effective.

25
Q

How are ventricles related to neural correlates?

A

Ventricles are voids filled with cerebospinal fluid deep in the brain, these are thought to provide a protective cushioning effect for the brain. Enlarged ventricles are associated with people with schizophrenia.

26
Q

Give research support for enlarged ventricles in sz patients

A

Research using CT scans by Johnstone first identified people with schizophrenia had larger than average ventricles. Suggesting this structural difference may be linked to the cause of schizophrenia.

27
Q

Limitations of biological explanation

A
  • Genetic basis to the explanations assumes that sz is inevitable, or biologically determined . Making sufferers feel disempowered when diagnosed .
  • Bio explanations take a biologically reductionist approach which fails to consider evidence for the range of psychological aspects of schizophrenia such as expressed emotion that seems to have a large influence