Schizophrenia - Explanations for Schizophrenia

Question 1

What is the genetic basis of schizophrenia?

Answer 1

• schizophrenia runs in families

- schizophrenia is polygentic and aetiologically heterogenous

Question 2

How does schizophrenia run in families?

Answer 2

Strong relationship between genetic similarity of family members and likelihood of both developing schizophrenia.

Gottesman’s (1991) family study found MZ twins have a 48% shared risk of schizophrenia. DZ twins have a 17% shared risk and siblings (about 50% genes shared) have a 9% shared risk. This compares to 1% of the general population.

Question 3

How is schizophrenia polygenetic and aetiologically heterogeneous?

Answer 3

Existence of different candidate genes indicates the following:

• Each individual gene confers a small increased risk of schizophrenia (i.e. schizophrenia is polygenetic).
• Different combinations can lead to schizophrenia (i.e. schizophrenia is aetiologically heterogeneous).

Ripke et al. (2014) studied 37,000 patients and found 108 separate genetic variations associated with increased risk; many coded for the dopamine neurotransmitter.

Question 4

What is the dopamine hypothesis?

Answer 4

• role of dopamine
• hyperdopaminergia: linked to the subcortex
• hypodopaminergia: linked to the prefrontal cortex

Question 5

What is the role of dopamine?

Answer 5

Dopamine is widely believed to be involved in schizophrenia because it is featured in the functioning of brain systems related to the symptoms of schizophrenia.

Question 6

How does hyperdopaminergia in the subcortex explain schizophrenia?

Answer 6

High dopamine activity in subcortex (central areas of the brain) associated with hallucinations and poverty of speech (e.g. excess of dopamine receptors in Broca’s area).

Question 7

How does hypodopaminergia in the prefrontal cortex explain schizophrenia?

Answer 7

More recent versions of the hypothesis have focused on low levels of dopamine in the prefrontal cortex (responsible for thinking and decision-making).

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

Question 8

What are neural correlates?

Answer 8

Neural correlates are measurements of the structure or function of the brain that correlate with the positive or negative symptoms of schizophrenia.

The best-known neural correlate of schizophrenia is dopamine, important in the functioning of several brain systems related to the symptoms of schizophrenia.

Question 9

What is the link between avolition and the ventral striatum?

Answer 9

Ventral striatum is involved in anticipation of reward (related to motivation). Loss of motivation (avolition) in schizophrenia may be explained by low activity levels here.

Juckel et al. (2006) found a negative correlation between ventral striatum activity and overall negative symtoms.

Question 10

What is the link between hallucinations and the superior temporal gyrus?

Answer 10

Allen et al. (2007) found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus.

A task was given for participants to identify pre-recorded speech as theirs or others. Where there were lower activation levels, more errors were made.

Question 11

What are the strengths of the biological explanations for schizophrenia?

Answer 11

• strong evidence for genetic vulnerability to schizophrenia
• the role of mutation supports the genetic explanation
• there is support for dopamine in the symptoms of schizophrenia (amphetamines which increase dopamine mimic symptoms, and antipsychotic drugs which decrease dopamine reduce the intensity of symptoms)

Question 12

What are the weaknesses of the biological explanations for schizophrenia?

Answer 12

• there is mixed support for the dopamine hypothesis
• correlation-causation
• it is clear that the environment is also involved

Question 13

What evidence is there for genetic vulnerability to schizophrenia?

Answer 13

The Gottesman (1991) family study clearly shows how genetic similarity and shared risk of schizophrenia are closely related.

Adoption studies (Tienari et al. 2004) show children of people with schizophrenia are still at heightened risk of schizophrenia if adopted into families without a history of schizophrenia.

So schizophrenia may not be entirely genetic, but there is overwhelming evidence that genetic factors make some people more vulnerable.

Question 14

How does the role of mutation support the genetic explanation?

Answer 14

Schizophrenia can take place in the absence of family history of the disorder (e.g. through mutation of paternal DNA in sperm cells caused by radiation, poison or viral infection).

Brown et al. (2002) found a link between paternal age (associated with increased risks of mutation) and risk of schizophrenia, increasing from 0.7% in fathers under 25 to 2% in fathers over 50.

This evidence supports the importance of genetic factors in the development of schizophrenia.

Question 15

How is there mixed support for the dopamine hypothesis?

Answer 15

Dopamine agonists (e.g. amphetamines) that increase dopamine can induce schizoprenic-like symptoms in people without schizophrenia. Antipsychotic drugs that lower dopamine can be effective in reducing symptoms.

However, some of the candidate genes identified code for the production of other neurotransmitters such as glutamate.

This suggests that dopamine cannot provide a complete explanation for schizophrenia and that it is just one important factor.

Question 16

What is the correlation-causation problem in biological explanations of schizophrenia?

Answer 16

The question that remains is whether unusual activity in the brain causes the symptoms or whether there are other possible explanations for the correlation.

A negative correlation may suggest that low activity in the ventral striatum causes avolition. But it could be that avolition means that less information passes through the striatum resulting in the low activity.

Therefore, although neural correlates exist, they tell us relatively little about the causes of schizophrenia.

Question 17

How is the environment involved in the development of schizophrenia?

Answer 17

After all, the probablity of developing schizophrenia even if your identical twin has it is less than 50%.

There is evidence that environmental factors (e.g. family functioning during childhood) can also play a role in the development of schizophrenia.

This suggests that schizophrenia may be the result of a combination of biological and psychological approaches (as acknowledged by the interactionist approach).

Question 18

What are the key features of family dysfunction in schizophrenia?

Answer 18

• schizophrenogenic mothers: rejecting and controlling
• double-bind theory: conflicting family communication
• expressed emotion: criticism and hostility lead to relapse in patients

Question 19

Who are schizophrenogenic mothers?

Answer 19

Fromm-Reichmann’s (1948) psychodynamic explanation based on patients’ early experiences of ‘schizophrenogenic mothers’ (mothers who cause schizophrenia).

These mothers are cold, rejecting and controlling, and create a family climate of tension and secrecy. This leads to distrust and paranoid delusions and schizophrenia.

Question 20

What is the double-bind theory?

Answer 20

Bateson et al. (1972) described how a child may be regularly trapped in situations where they fear doing the wrong thing, but receive conflicting messages from family about what counts as wrong. They cannot express their feelings about the unfairness of the situation.

When they ‘get it wrong’ (often) the child is punished by withdrawal of love - they learn the world is confusing and dangerous, leading to disorganised thinking and delusions.

Question 21

What is expressed emotion?

Answer 21

Expressed emotion is the level of emotion (mainly negative) expressed towards the schizophrenic patient and includes:

• verbal criticism of the patient
• hostility towards them
• emotional over-involvement in their life

High levels of expressed emotion cause stress in the patient, a primary explanation for relapse in patients with schizophrenia.

Question 22

What are the key features of cognitive explanations in schizophrenia?

Answer 22

• dysfunctional thought processing
• metarepresentation leads to hallucinations
• dysfunction of central control leads to speech poverty

Question 23

What is dysfunctional thought processing?

Answer 23

Lower levels of information processing in some areas of the brain suggest cognition is impaired.

For example, reduced processing in the ventral striatum is associated with negative symptoms.

Question 24

What is metarepresentation?

Answer 24

Metarepresentation is the cognitive ability to reflect on thoughts and behaviour (Frith et al. 1992).

This dysfunction disrupts our ability to recognise our thoughts as our own - could lead to the sensation of hearing voices (hallucination) and having thoughts placed in the mind by others (delusions)

Question 25

What does dysfunction of the central control lead to?

Answer 25

Frith et al. (1992) also identified dysfunction of central control as a way to explain speech poverty - central control being the cognitive ability to suppress automatic responses while performing deliberate actions.

People with schizophrenia experience derailment of thoughts and spoken sentences because each word triggers automatic associations that cannot suppress.

Question 26

What are the strengths of the psychological explanations for schizophrenia?

Answer 26

• there is support for different information processing

Question 27

What are the weaknesses of the psychological explanations for schizophrenia?

Answer 27

• evidence for family relationships is often retrospective
• evidence for family-based explanations is weak
• biological factors are sometimes overlooked
• cognitive explanations have no direction of causality

Question 28

What support is there for different information processing?

Answer 28

Stirling et al. (2006) compared 30 patients with schizophrenia with 18 non-patients (control group) on cognitive tasks (e.g. in the Stroop Test participants had to name the ink colour of colour words).

Patients took over twice as long as the control group to suppress the impulse to read the word and to name the ink colour instead. This supports Frith’s theory of central control dysfunction. Other evidence also shows that processing differs in schizophrenic patients.

However, it is not clear whether these faulty cognitions are merely the proximal cause (i.e. cause of the symptoms) or the underlying distal cause (i.e. the origins of the disorder).

Question 29

How is evidence for family relationships often retrospective?

Answer 29

Read et al. (2005) reviewed 42 studies and concluded that 69% of all adult female inpatients with schizophrenia (59% of men) had a history of physical and/or sexual abuse in childhood.

But most of this evidence is based on information about childhood experiences gathered after the diagnosis. The symptoms may have distorted the patients’ recall of their childhood experiences.

This creates a problem with the validity of the evidence.

Question 30

Why is evidence for family-based explanations weak?

Answer 30

Poor childhood experiences may be associated with schizophrenia, but there is little evidence to support the importance of schizophrenogenic mothers, expressed emotion or double-bind.

These theories are mainly based on clinical observation of patients (open to interpretation). They have also historically led to blaming of parents already suffering over their child’s symptoms.

These issues undermine the appropriateness and credibility of the family-based explanation.

Question 31

How are biological factors sometimes overlooked?

Answer 31

Psychological explanations can be hard to reconcile with biological ones (e.g. genetics). If the biological explanations are valid, how do they fit with psychological ones?

Perhaps both biological and psychological factors can separately produce the same symptoms - this raises the question of whether both outcomes are really schizphrenia.

Alternatively, we can view this in terms of the diathesis-stress model where the diathesis may be biological or psychological.

Question 32

Why does the cognitive explanation have no direction of causality?

Answer 32

It remains unclear whether cognitive factors are a cause or a result of the neural correlated and abnormal neurotransmitter levels in schizophrenia.

For example, does dysfunctional metarepresentation reduce levels of dopamine in the superior temporal gyrus? Or is the direction of causality the reverse?

This questions the validity of the cognitive approach in explaining the underlying origins of the condition.