Evaluation of Explanations of Schizophrenia

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Evaluation of the Explanations of Schizophrenia

Explain

why the psychodynamic approach provides an interesting alternative to the

dominant biological explanations?

The psychodynamic approach provides an interesting

alternative to the dominant biological approaches, as it

brings psychologists' attention to the impact of early childhood

experiences on later mental health. Therefore, this explanation of schizophrenia

has good face validity because the belief that early childhood experiences can

have a significant impact on our later mental health is a plausible idea.

As

there is a lack of empirical evidence to support the psychodynamic explanation,

what does this suggest?

There is a significant lack of empirical evidence to

support the psychodynamic explanation of schizophrenia, this suggests that this

explanation lacks external validity, as it is difficult to apply to people who

suffer from schizophrenia.

Explain

how the findings of the Mednick et al (1984) study support the idea that a

dysfunctional family and, in particular, the mother, can cause schizophrenia.

The findings of Mednick et al's study suggest that

the mother's behaviour and living in a dysfunctional family could cause a child

to develop schizophrenia, as it was found that out of a group of 207

children who were identified as being at a high risk of developing

schizophrenia due to having a mother with a schizophrenogenic personality

(cold, domineering, over-protective, rigid, and moralistic about sex), 17 developed

schizophrenia compared to one child developing the disorder in a control group

of 107 children.

Some

critics would argue that the mother's behaviour may be the result of having to

look after a child with schizophrenia rather than causing the disorder in their

child. Explain what this would mean for this explanation is it was an effect

rather than a cause.

Some critics of this

explanation of schizophrenia argue that the mother’s “schizophrenogenic”

behaviour may be a result of having to care for a child with schizophrenia,

rather than being the cause of their child’s disorder. This viewpoint suggests

that the cause and effect of this explanation cannot be established, as the

child’s disorder may have caused their mother’s cold, domineering and over-protective

behaviour rather than the mother’s behaviour causing the child’s disorder.

Explain

the ethical issue that may arise from accepting the schizophrenogenic mother as

a valid explanation for the disorder, as we now have objective scientific

explanations and schizophrenia is clearly caused by biological factors and/or a

complex interaction of biological and psychological factors.

One ethical

issue that may arise from accepting the schizophrenogenic mother as a valid

explanation of schizophrenia is deception. The British Psychological Society

states in its ethical guidelines that an individual should not be purposely misled

without strong scientific justification. Due to the extensive research that has

been undertaken with regards to the cause of schizophrenia and the wealth of

evidence that strongly suggests that there are other factors that can

contribute to the development of schizophrenia in an individual, it would be

ethically unacceptable to tell a mother of a child with schizophrenia that she

has caused her child’s disorder.

This point also

raises another ethical issue, which is protecting people from harm. Allowing a

mother to believe that she has caused her child’s disorder could lead to her

feeling extremely guilty and could possibly affect her mental health.

How does Rosenhan’s research demonstrate how the

label “schizophrenic” can become a self-fulfilling prophecy?

Rosenhan’s research

demonstrates how the label of “schizophrenic” can become a self-fulfilling

prophecy, as even though the pseudopatients displayed no further

characteristics of schizophrenia after being admitted to the hospital, the

hospital staff interpreted their behaviour as being typical of the disorder,

spent little time interacting with them, answered questions abruptly, were very

authoritarian in manner and often acted as though the patients were invisible.

Explain why the labelling theory is a flawed

explanation for the cause of schizophrenia.

The

labelling theory is a flawed explanation of the cause of schizophrenia as it

does not consider any biological factors that could contribute to the development

of the disorder. Therefore, this explanation is extremely over-simplified and

reductionist.

Another

reason why the labelling theory is a flawed explanation of the cause of

schizophrenia is that the cause and effect cannot be established. For a person

to be labelled as “schizophrenic,” they must have been displaying

characteristics of the disorder prior to be labelled. Therefore, in theory, it

should not be surprising to see the individual displaying characteristics of

the disorder after being given a label. However, it can be argued that giving

an individual a label does not help in the recovery of the disorder and it may

encourage characteristic behaviour of the disorder as it is what is expected of

them by others.

It takes 2-3 weeks for the anti-psychotic drugs to

reduce the symptoms of schizophrenia, however they reduce an individual’s

dopamine levels almost immediately. What does this imply about the dopamine

hypothesis?

The fact

that it takes two to three weeks for anti-psychotic drugs to reduce the

symptoms of schizophrenia even though the level of dopamine in an individual’s

brain is reduced almost immediately greatly discredits the validity of the

dopamine hypothesis. If the dopamine hypothesis was completely correct, then

the symptoms of schizophrenia would be reduced as soon as the levels of

dopamine were reduced, due to the dopamine hypothesis believing that too much

or too little dopamine in the brain causes schizophrenia. Therefore, there must

be other factors that cause schizophrenic symptoms, such as a complex combination

of neurotransmitters. This suggests that the dopamine hypothesis is far too oversimplified

and extremely reductionist.

How does the effects of the Parkinson’s drug L-Dopa

provide supporting evidence for the dopamine hypothesis?

The

dopamine hypothesis is the theory that too much or too little of the

neurotransmitter dopamine in the brain can cause schizophrenia.

L-Dopa is a

drug given to people who have Parkinson’s disease which increases the level of

dopamine in the brain. An overdose of L-Dopa in a person with Parkinson’s

disease can produce symptoms similar to those of schizophrenia, such as

hallucinations and delusions. Giving L-Dopa to a person suffering from

schizophrenia can worsen their symptoms. These findings support the dopamine

hypothesis, as increasing the amount of dopamine in the brain of a person who

does not suffer from schizophrenia can produce schizophrenic symptoms, which

suggests that high levels of dopamine can cause schizophrenia.

It has been suggested that there is a problem with

cause and effect with the dopamine hypothesis. What does this mean?

This means that it cannot

be confirmed whether an imbalance of the neurotransmitter dopamine in the brain

causes symptoms of schizophrenia, or whether the symptoms of schizophrenia

cause an imbalance of dopamine in the brain.

What

percentage of DNA do identical (MZ) twins share?

Monozygotic twins share

100% of their DNA.

What

concordance rate would you therefore expect to see if schizophrenia did have a

genetic basis?

If schizophrenia did have

a genetic basis, it would be expected that there would be a 100% concordance

rate of having schizophrenia for monozygotic twins, due to the fact that they

share 100% of their DNA.

Can

you think of any alternative reasons as to why the concordance rates may be

higher in twins?

The concordance rates for

schizophrenia may be higher in twins, as twins are often brought up in the same

environment and share the same experiences. This supports the behavioural

approach which believes that every person is born as a blank slate and that all

behaviours are learned.

Research

by Tienari (1991) found that in a study of 155 adopted children whose

biological mothers had schizophrenia and compared these with 185 adopted

children whose biological mother had no mental disorder, 10.3% of children with

schizophrenic mothers had developed schizophrenia by adulthood compared to 1.1%

of the control group. What does this suggest?

These findings suggest

that schizophrenia does have a genetic basis, as even though the children whose

mothers had schizophrenia were adopted and raised away from them, 10.3% of the

children had developed schizophrenia by adulthood compared to only 1.1% of the

control group. This eliminates any extraneous variables such as being brought

up in environment with a mother who has schizophrenia, which gives the study

good external validity.

What

would be a reasonable conclusion to draw regarding the genetic basis for

schizophrenia?

A reasonable conclusion

regarding the genetic basis for schizophrenia could be that the absolute

genetic theory, which believes that only genes can cause schizophrenia, is

incorrect. This is due to findings from Tienari’s study which show that only

10.3% of children who had mothers with schizophrenia developed the disorder. If

the absolute genetic theory was correct, then 100% of the children would have

developed the disorder. Twin studies also show that the conconrdance rate of

schizophrenia in monozygotic twins who share 100% of their DNA is only 40-50%.

It would be expected that the concordance rate would be 100% if the absolute

genetic theory was correct.

The genetic predisposition

theory, which believes that maladaptive genes can be inherited which raise the

likelihood of the individual developing schizophrenia, but that the disorder

will only develop if other factors are present, is much more plausible. The

findings from Tienari’s study support this theory, as the children whose

mothers had schizophrenia may have inherited the maladaptive gene which

increases the likelihood of the individual developing the disorder, and as only

10.3% of these children developed schizophrenia, these children may have experienced

other factors that could have contributed to the development of the disorder

that the other 89.7% of the group did not experience.

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