Biological Explanations Flashcards

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1
Q

What are biological explanations?

A

They 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

What are the biological explanations?

A

Genetic factors
The dopamine hypothesis
Neural correlates

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3
Q

What are the parts of genetic factors?

A

Family studies
Twin studies
Adoption studies

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4
Q

What are genetics?

A

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

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5
Q

What are family studies?

A

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

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6
Q

What’s an example of family studies?

A

Gottesman (1991)
Children with two schizophrenic parents had a concordance rate of 46%, children with one schizophrenic parent a rate of 13% and siblings (where brother or sister had schizophrenia) a concordance rate of 9%.

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7
Q

What are twin studies?

A

If monozygotic (MZ) twins are more concordant than dizygotic (DZ) twins, then this suggests that the greater similarity due to genetic factors.

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8
Q

What’s an example of twin studies?

A

Joseph (2004) calculated that the pooled data for all schizophrenia 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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9
Q

What are adoption studies?

A

Because of the difficulties of disentangling genetic and environmental influences for individuals who share genes and environment, studies of genetically related individuals who have been reared apart are used.

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10
Q

What’s an example of adoption studies?

A

Tienari (2000) in Finland.

Of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnoses, compared to just 4 (2%) of the 197 control adoptees (those born to non-schizophrenic mothers).

The investigators concluded that these findings showed that the genetic liability to schizophrenia had been ‘decisively confirmed’.

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11
Q

What are the evaluative points for genetic factors?

A

MZ twins encounter more similar environments

Adoptees may be selectively placed.

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12
Q

What is meant by MZ twins encounter more similar environments?

A

A crucial assumption underlying all twin studies is that the environments of MZ and DZ twins are equivalent.

However, as Joseph (2004) points out, MZ twins are treated more similarly, encounter more similar environments and experience more ‘identity confusion’ (frequently being treated as the twins rather than as two distinct individuals) than DZ twins.

This suggests that differences in concordance rates between MZ and DZ twins reflect nothing more than environmental differences that distinguish the two type of twin.

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13
Q

What is meant by adoptees may be selectively placed?

A

An assumption of adoption studies is that adoptees are not ‘selectively placed’.

One of the largest adoption studies of schizophrenia took place in Oregon (Heston, 1966), where it was assumed that procreation by any person admitted to a mental hospital would produce offspring with an inherited tendency to ‘feeble-mindedness, insanity and degeneracy’.

It is extremely unlikely that the children born to women with schizophrenia would have been placed into the same type of adoptive families as children without such a background (Joseph, 2004).

This, coupled with other problems with twin and adoption studies, suggests we cannot accept their conclusions about the role of genetics in schizophrenia.

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14
Q

What does selectively placed mean?

A

Adoptive parents who adopt children with a schizophrenic biological parent are no different to adoptive parents who adopt children whose background is normal.

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15
Q

What is the dopamine hypothesis?

A

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

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16
Q

What are schizophrenics thought to have high numbers of? (Dopamine hypothesis)

A

Abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.

17
Q

What sources of evidence highlight the key role played by dopamine?

A

Drugs that increase dopaminergic activity

Drugs that decrease dopaminergic activity

18
Q

What is meant by drugs that increase dopaminergic activity?

A

Amphetamine is a dopamine agonist.
‘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.

19
Q

What’s a dopamine agonist?

A

It stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter.

20
Q

What is meant by drugs that decrease dopaminergic activity?

A

Although there are many different types of antipsychotic drug, they all have one thing in common, i.e. they block the activity of dopamine as the neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions.

The fact that these drugs (known as dopamine agonists because they block its action) alleviated many of the symptoms of schizophrenia strengthened the case for the important role of dopamine in this disorder.

21
Q

What is the revised dopamine hypothesis?

A

Davis and Kahn (1991) proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway.

The negative and cognitive symptoms are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway).

22
Q

What’s an example of the revised dopamine hypothesis study?

A

Patel (2010), using PET scans to assess dopamine levels in schizophrenic and normal individuals, found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls.

23
Q

What are the evaluative points for the dopamine hypothesis?

A

Evidence from treatment

Challenges to the dopamine hypothesis

24
Q

What is meant by evidence from treatment?

A

Much of the evidence supporting rather dopamine hypothesis comes from the success of drug treatments that attempt to change levels of dopamine activity in the brain.

Leucht (2013) carried out a meta-analysis of 212 studies. They concluded that all the antipsychotics drugs tested in these studies were significantly more effective than placebo in the treatment of positive and negative symptoms, achieved by reducing the effects of dopamine.

These findings also challenge the classification of antipsychotics into typical and atypical groupings because differences in their effectiveness were only small.

25
Q

What is meant by challenges to the dopamine hypothesis?

A

Noll (2009) claims there is strong evidence against both the original dopamine hypothesis and the revised.

He argues that antipsychotic drugs do not alleviate hallucinations and delusions in about 1/3 of people experiencing these symptoms.
Noll also points out that, in some people, hallucinations and delusions are present despite levels of dopamine being normal.

This suggests that, rather than dopamine being the sole cause of positive symptoms, other neurotransmitter systems, acting independently of the dopaminergic system, may also produce the positive symptoms associated with schizophrenia.

26
Q

What are neural correlates?

A

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

27
Q

What are the specific brain areas?

A

The prefrontal cortex

The hippocampus

28
Q

What is the prefrontal cortex?

A

The prefrontal cortex (PFC) is the main area of the brain involved in executive control (i.e. planning, reasoning, and judgment), and research has shown that this is impaired in schizophrenia patients (Weinberger and Gallhofer, 1977).
It has been hypothesised that the cognitive symptoms of schizophrenia results from deficits within the PFC and its connections with other areas of the brain, particularly the hippocampus.

29
Q

What is the hippocampus?

A

The hippocampus is an area of the brain in the temporal lobe.

Several studies have reported anatomical changes in the hippocampus in schizophrenia patients (Conrad, 1991).

Deficits in the nerve connections between the hippocampus and the prefrontal cortex have been founds to correlate with the degree of working memory impairments, a central cognitive impairment in schizophrenia (Mukai, 2015).

Goto and Grace (2008) suggest that hippocampal dysfunction might also influence levels of dopamine release in the basal ganglia, indirectly affecting the processing of information in the prefrontal cortex.

30
Q

What is white matter?

A

It’s found in the brain and spinal cord and is made up of nerve fibres covered in myelin.

Myelin creates an insulting sheath around nerve fibres and helps to conduct information quickly through the central nervous system, enabling efficient information processing.

31
Q

What’s a study involving white matter?

A

Research (Du, 2013) has 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.

32
Q

What is grey matter?

A

mostly cell bodies and unmyelinated axons

33
Q

What have researchers discovered about grey matter and schizophrenia?

A

Individuals with schizophrenia have a reduced volume of grey matter in their brains, especially in the temporal and frontal lobes.
Researchers have also found that many people with schizophrenia, particularly those displaying negative symptoms, have enlarged ventricles (brain cavities filled with cerebrospinal fluid) (Hartberg, 2011).

Enlarged vertices are thought to be a consequence of nearby parts of the brain not developing properly or being damaged.
Cannon (2014) found that individuals at high clinical risk who develop schizophrenia showed a steeper rate of grey matter loss and a greater rate of expansion of brain ventricles compared to those whose didn’t develop schizophrenia.

34
Q

What are the evaluative points for neural correlates?

A

Support for the influence of grey matter deficits

Implications for treatment

35
Q

What is meant by support for the influence of grey matter deficits?

A

Support for the significance of grey matter deficits in schizophrenia comes from a meta-analysis by Vita (2012).

They analysed the results of 19 studies. Patients with schizophrenia, compared to healthy controls, showed a higher reduction in cortical grey matter volume over time.
This pattern of grey matter reduction was specific to discrete cortical areas in frontal, temporal and parietal lobes.

This loss of grey matter was especially active in the first stages of the disease, consistent with the relatively early onset of schizophrenia (late teens/early 20s).

36
Q

What is meant by implications for treatment?

A

The importance of neural correlates for schizophrenia is that early intervention might prevent development of the later stages of this disorder.

This concept of ‘treatment as prevention’ is seen in the North American Prodrome Longitudinal Study (Addington, 2015), which uses a number of different assessments, including neuroimaging, to predict who will develop psychoses such as schizophrenia.

With a better understanding of how schizophrenia develops, researchers can detect loss of brain tissue early and treat at-risk patients before psychosis develops.