Biological Explanations of Schizophrenia

Question 1

What are the biological explanation assumptions from the medical model?

Answer 1

All mental disorders have a physical cause - (genetics, biochemistry, neuroanatomy).

Mental illnesses can be described in terms of clusters of symptoms.

Symptoms can be identified, leading to a diagnosis of an illness.

Diagnosis leads to appropriate physical treatments.

Question 2

There are three biological explanations of schizophrenia. What are they?

Answer 2

Genetics - (twin studies, family studies, adoption studies, and gene mapping).

Biochemicals.

Neural correlates.

Question 3

The HGP has estimated that humans have how many genes?

Answer 3

20,000 and 25,000 genes.

Question 4

How does the genetic explanation see schizophrenia?

Answer 4

As transmitted through hereditary means.

It is not believed that one single gene is involved, instead a polygenic approach is taken.

Question 5

Researchers use what to study schizophrenic polygenetics?

Answer 5

Traditionally, family, twin, and adoption studies were used to assess concordance, but more recent research focuses on gene-mapping.

Question 6

From gene-mapping, a number of genes have been identified as exerting an influence on one’s vulnerability to developing schizophrenia. How many increase vulnerability? What does this mean for the diagnosis?

Answer 6

128 genes have been identified in increase vulnerability to schizophrenia.

Schizophrenia is thus aetiologically heterogenous.

Question 7

Outline Gottesman’s study from 1991.

(Supports the idea that schizophrenia is inherited through genes)
(Twin studies)

Answer 7

Supports the idea that schizophrenia is inherited through genes.

This is because they conducted a meta-analysis of 40 twin studies; finding the concordance rate for MZ twins to be 48% and 17% for DZ twins.

This suggests that although concordance is relatively high, for a more significant genetic explanation it should be 100% (MZ twins share 100% of genes).

This highlights how other factors and explanations also influence schizophrenia vulnerability.

Question 8

Outline Torrey’s study from 1994.

(Supports the idea that schizophrenia is inherited through genes)
(Twin studies)

Answer 8

Supports the idea that schizophrenia is inherited through genes.

This is because they showed if one twin develops with schizophrenia, there is a 28% chance the other will too.

This suggests that the condition can be passed on hereditarily.

Question 9

Outline Gottesman’s study.

(Supports the idea that schizophrenia is inherited through genes)
(Family studies)

Answer 9

Supports the idea that schizophrenia is inherited through genes.

Concluded that if both your parents suffer from schizophrenia then you have a 46% chance if developing it yourself (compared to a 1% chance of someone selected at random will suffer).

This suggests that the more genetically similar relatives are, the more concordance is found.

Question 10

Who is most likely to get schizophrenia?

Answer 10

People of colour.

Question 11

Outline Tienari’s study from 2000.

(Supports the idea that schizophrenia is inherited through genes)
(Adoption studies)

Answer 11

Supports the idea that schizophrenia is inherited through genes.

155 adopted children whose biological mothers had schizophrenia - they had a 10% likelihood of developing schizophrenia compared to 1% in adopted children in families with no history of schizophrenia.

This is very strong evidence that genetics are a risk factor for schizophrenia but also means that.

Question 12

Gene mapping offers the opportunity to develop tests to identify high risk individuals. How is this socially sensitive?

Answer 12

It could provide long-term effect for the patients.

E.g. if they haven’t shown symptoms before gene mapping and are diagnosed with a high risk, then they are more prone to the stress of when an episode may occur; when without diagnosis they would not be free of this anxiety.

Question 13

Outline Gurling’s study from 2006.

(Supports gene-mapping)

Answer 13

Supports gene mapping.

This is because they found evidence from family studies that indicate that the PCM1 gene has been implicated in susceptibility to schizophrenia.

This suggests that gene mapping can be used to explain schizophrenia vulnerability.

However, this is a very reductionist and simplistic approach, only looking at a single biological explanation; it takes a heavily naturistic approach, and should consider environmental factors in order to provide a complete explanation.

Question 14

Outline the schizophrenia working group of psychiatric genomics consortium: Ripke et al’s study from 2014.

(Supports biological causation, especially between immune systems and schizophrenia)

Answer 14

Supports biological causation, especially between immune systems and schizophrenia.

Analysed the DNA of 36,989 schizophrenia sufferers and 113,000 non-schizophrenic individuals to identify 128 genetic variations at 108 locations on the human chromosomes that contribute most to schizophrenia.

Findings showed that associations were higher in genes expressed in the brain and in tissues associated with important immunity roles.

This suggests that differing immune system may cause schizophrenia.

Question 15

What does dopamine do?

(The Dopamine Hypothesis)
(Biochemicals)

Answer 15

Dopamine acts to increase the rate of firing of neurones during synaptic transmission.

Dopamine is important in the functioning in several brain areas/ systems that may be implicated in the symptoms of schizophrenia.

Question 16

Is schizophrenia a result of too much or too little dopamine? Why was this suggested?

(The Dopamine Hypothesis)
(Biochemicals)

Answer 16

Originally, it was believed that too much dopamine lead to schizophrenia.

This was suggested because an antipsychotic drug (phenothiazine) seemed to work by decreasing dopamine activity.

In addition, L-dopa (a dopamine releasing drug) created schizophrenic symptoms in non-schizophrenics.

However, in 1991, Davis et al updated the theory, concluding that high levels of dopamine are not found in all schizophrenics.

Question 17

High levels/ activity of dopamine is referred to as what?

(The Dopamine Hypothesis)
(Biochemicals)

Answer 17

Hyperdopaminergia.

Question 18

Low levels/ activity of dopamine is referred to as what?

(The Dopamine Hypothesis)
(Biochemicals)

Answer 18

Hypodopaminergia.

Question 19

Outline hyperdopaminergia in the brain sub-cortex.

(Biochemicals)

Answer 19

An excess of dopamine receptors in Broca’s area may be associated with poverty of speech and/or the experience of auditory hallucinations (e.g. hearing voices).

Question 20

Outline hypodopaminergia in the brain sub-cortex.

(Biochemicals)

Answer 20

Goldman-Rakic et al (2004) Identified a role for low levels of dopamine in the prefrontal cortex in the negative symptoms of schizophrenia.

Question 21

It may be that both hyper and hypodopaminergia are correct explanations, but is just dependent on what?

(Biochemicals)

Answer 21

Which brain region is targeted.

Question 22

What do hallucinogenic drugs do?

(Biochemicals)

Answer 22

Produce similar effects to schizophrenia.

Question 23

What did Curran et al state in 2004?

(Biochemicals)

Answer 23

That amphetamines are dopamine agonists, and increase levels of dopamine - making schizophrenia worse or induce schizophrenic-like symptoms in non-sufferers.

Question 24

What did Tauscher et al state in 2014?

(Biochemicals)

Answer 24

That antipsychotics work by reducing dopamine activity.

Question 25

Outline Lindstroem’s study from 1999.

(Supports the idea that schizophrenia is caused by increased dopamine activity)
(Biochemicals)

Answer 25

Supports the idea that schizophrenia is caused by increased dopamine activity.

This is because they used radioactive labelling and found chemicals needed to produce dopamine are taken up faster in the brains of schizophrenics, than in controls.

This suggests that they produce more dopamine.

Question 26

Outline Randrup and Munkvard’s study from 1966.

(Supports the dopamine hypothesis)
(Biochemicals)

Answer 26

Supports the dopamine hypothesis.

This is because they created schizophrenic-like behaviour in rats by giving them amphetamines; activating dopamine production.

They then reversed the effects by giving them neuroleptic drugs, which inhibit the release of dopamine.

This suggests that the increased production of dopamine creates schizophrenic behaviour.

Question 27

What did Owens state in 1987?

(Biochemicals)

Answer 27

Stated that it is not excessive dopamine, but the fact that there are more dopamine receptors, that causes schizophrenia.

More receptors lead to more firing, and an over production of messages.

Autopsies have found that there are generally a large number of dopamine receptors and there was an increase in the amount of dopamine in the left amygdala and increased dopamine in the caudate nucleus and putamen (middle of the brain).

Question 28

Evaluate biochemicals (dopamine) as a biological explanation for schizophrenia.

(Biochemicals)

Answer 28

Some genes involved in schizophrenia, also code for the production of other neurotransmitters, suggesting that it isn’t just dopamine that is associated with schizophrenia.

Chlorpromazine, an early antipsychotic drug, does not seem to work for all schizophrenics, suggesting that dopamine works as an explanation, but not a full explanation.

Aetiology fallacy: The theory is over-simplistic and has been criticised for using the treatment to determine the cause.

Question 29

Outline Moghaddam and Javitt’s study from 2012.

(Challenges the idea that it is only dopamine involved in schizophrenia)
(Biochemicals)

Answer 29

Challenges the idea that it is only dopamine involved in schizophrenia.

They found that glutamates were also involved in schizophrenia.

This suggests that the evidence for dopamine as an explanation of schizophrenia is mixed.

Question 30

What are neural correlates? How are they measured?

(Neuroanatomy - Brain structure and neural correlates)

Answer 30

Abnormalities within specific brain areas being correlated with schizophrenia.

Both positive and negative symptoms have neural correlates.

Originally, evidence was limited to post-mortems, but the introduction of non-invasive scanning techniques gives a picture of the brain in action; meaning the functioning brain of a schizophrenic can be compared to a non-schizophrenic.

Question 31

Outline brain structures of schizophrenics.

(Neuroanatomy - Brain structure and neural correlates)

Answer 31

People with schizophrenia have abnormally large ventricles in the brain.

Ventricles are fluid filled cavities.

Question 32

What did Johnstone stated in 1976.

(Neuroanatomy - Brain structure and neural correlates)

Answer 32

Stated that the brains of schizophrenics are lighter than non-schizophrenics.

However, this is only correlational; have enlarged ventricles caused the schizophrenia, or are they a result of schizophrenia.

Question 33

Outline Suddath et al’s study from 1990.

(Provides empirical support for brain structures causing schizophrenia)
(Neuroanatomy - Brain structure and neural correlates)

Answer 33

Provides empirical support for brain structures causing schizophrenia.

This is because they used MRI to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic; finding that the schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus.

The differences were so large the schizophrenic twins could be easily identified from the brain images in 12 out of 15 pairs.
This suggests that there is wider academic credibility for enlarged ventricles determining the likelihood of schizophrenia developing.

Question 34

Outline Lyon’s study.

(Challenges brain structure as a neuroanatomical explanation of schizophrenia)
(Neuroanatomy - Brain structure and neural correlates)

Answer 34

Challenges brain structure as a neuroanatomical explanation of schizophrenia.

This is because they found as the dose of medication increased, the density of brain tissue decreased, leading to larger ventricles.

This suggests that schizophrenia may not cause the observed brain differences.

Question 35

What should be considered about all brain structure research?

(Neuroanatomy - Brain structure and neural correlates)

Answer 35

All correctional, as it only shows the relationships between brain structure and schizophrenia, not that one causes the other.

Question 36

How is avolition thought to be involved in brain structure?

(Neural correlates of negative symptoms)
(Neuroanatomy - Brain structure and neural correlates)

Answer 36

Ventral striatum is believed to be involved with anticipation.

Therefore abnormalities here may be involved with avolition.

Question 37

Outline Juckel’s study from 2006.

(Support abnormal ventral striatums to be involved in avolition)
(Neural correlates of negative symptoms)
(Neuroanatomy - Brain structure and neural correlates)

Answer 37

Support abnormal ventral striatums to be involved in avolition.

This is because they measured levels of activity in the ventral striatum in schizophrenics, finding levels of activity were lower than in controls.

This suggests that the lower activity experienced has caused the low motivation.

Question 38

How are hallucinations thought to be involved in brain structure?

(Neural correlates of positive symptoms)
(Neuroanatomy - Brain structure and neural correlates)

Answer 38

Abnormalities with the superior temporal gyrus and anterior cingulate gyrus are thought to be involved with auditory hallucinations.

Question 39

Outline Allen et al’s study from 2007.

(Supports the idea that certain brain areas are neural correlates of auditory hallucinations)
(Neural correlates of positive symptoms)
(Neuroanatomy - Brain structure and neural correlates)

Answer 39

Supports the idea that certain brain areas are neural correlates of auditory hallucinations.

They scanned the brains of schizophrenic patients experiencing auditory hallucinations, and compared them to a control groups.

During the scan they had to identify pre-recorded speech as theirs or others.

They found lower activity levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group, (they also made more errors than the control).

This suggests that reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

Question 40

State 3 evaluative points about the neural correlate biological explanation.

Answer 40

High reliability, as there is a lot of research that supports dopamine’s involvement in schizophrenia; e.g. autopsies showing the increased number of dopamine receptors in schizophrenics.

Biologically deterministic, as it assumes that schizophrenia is a direct result of a person’s genetic makeup - not considering other factors and the role of the environment; this could be overcome through the use of a diathesis stress explanation.

Difficult to establish cause and effect. E.g. It could be that there are abnormalities in the ventral striatum which causes the avolition, or, it could be that less messages are getting to the ventral striatum resulting in reduced activity. Also as many participants have suffered from schizophrenia for a while and have been undergoing treatment.

Aetiology fallacy, the false belief that antipsychotics and the reduction of dopamine is such an effective treatment that it can be used to determine the cause.

There could be a confounding variable, and this is hard to remove as the isolation of human biological factors is very difficult.

While assessing the role that brain abnormalities play in the development of schizophrenia, consideration must also be given to environmental factors, such as substance abuse and stress, which may also have a damaging influence upon brain tissue.

Question 41

What may be necessary to fully explain the causes of schizophrenia? Why?

Answer 41

An interactionalist approach.

It considers genetics, biochemicals, brain structures - as well as psychological factors.

Question 42

Biology does account for schizophrenia. However…

Answer 42

However, the fact that there is no conclusive explanation that accounts for all schizophrenics - meaning that psychological explanations need to be considered in addition.