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Summary Schizophrenia model answers
- Module
- Schizophrenia
- Institution
- AQA
A* student notes on model answers for AQA exam-style questions in note format, very helpful for a level revision!
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Explain how family dysfunction might be involved in schizophrenia. Refer to one or more types offamily dysfunction in your answer. (4 marks)
The schizophrenogenic mother is a family dysfunction that can cause the onset of schizophrenia. This
is when the mother is cold and dominant, overprotective but rejecting. Therefore, individuals brought
up with this mothering style develop schizophrenia symptoms such as paranoia and high levels of
stress as they are confused by their mothers overprotective but rejecting nature. This can lead them
to not have an accurate grip on reality and develop delusions over situations.
Another family dysfunction is the double-bind. This is where communication in the family is
contradictory between the tone of voice and the content, for example, showing affection through
anger. The child’s ability to respond to this sort of communication is undermined through the
contradictions in the message and this can consequently cause paranoia. Prolonged exposure to such
interactions prevents the development of an internally coherent construction of reality; in the long
run, this shows itself as typically schizophrenic symptoms such as flattening affect, delusions and
hallucinations, incoherent thinking and speaking, and in some cases paranoia.
Outline one or more biological explanation(s) for schizophrenia. Compare biological explanation(s)
for schizophrenia with the family dysfunction explanation for schizophrenia. (16 marks) 2020
Discuss one or more biological explanation(s) explanation for schizophrenia. (16 marks) 2018
One biological explanation for schizophrenia is that it is passed on through the genes. Gottesman
reports that while the rate of schizophrenia in the general population is 1%, if one parent has
schizophrenia there is a 12% likelihood their child will develop it and if both parents have
schizophrenia, it increases to 40%. Schizophrenia seems to be polygenic, as several genes have been
implicated. It also seems to be aetiologically heterogeneous as different studies have identified
different candidate genes. For example, Ripke et al. found 108 separate genetic variations were
associated with increased risk of schizophrenia. Therefore, there is suggested evidence of a genetic
component, but the exact genetic picture is complex.
Evidence to support the genetic explanation comes from Gottesman and Shields, who found a
concordance rate of 42% for MZ and 9% for DZ. MZ twins share 100% of their genes, compared to DZ
twins who only share 50% of their genes, so this suggests that genes must have some influence on
the development of schizophrenia. However, the concordance rate for MZ twins is not 100% which
suggests that other factors must also be involved. (Good opportunity to bring in a counter
argument… family dysfunction explanation to show how environmental factors may also be
implicated in the disorder? Or a Diathesis-stress model to show how it is likely that environmental
trauma may interact with the genetic element?) It is also important to note that two-thirds of people
with schizophrenia have no relative with a similar diagnosis and therefore have no one to inherit it
from.
The dopamine hypothesis is another biological explanation for schizophrenia. The original version
suggested it was due to high levels or activity of dopamine in the subcortex (hyperdopaminergia). For
example, an excess of dopamine receptors in Broca’s area might be responsible for poverty of speech
and auditory hallucinations. More recent versions have included hypodopaminergia, where low levels
of dopamine in the prefrontal cortex are believed to be responsible for some of the negative
symptoms of schizophrenia, Such as speech poverty, avolition and anhedonia.
Research evidence from autopsies has shown that schizophrenia sufferers have more dopamine
receptors, an increased amount in the amygdala and increased dopamine in the caudate nucleus,
, which may lead to more neural firing and therefore an over production of messages. Further support
comes from Tenn et al, who induced schizophrenic-like symptoms in rats using amphetamines and
then relived those symptoms using drugs that reduced dopamine. This concluded with dopamine
being the neurotransmitter that implicated schizophrenia, allowing her to establish a cause and
effect. However, trials on other drugs such as apomorphine, that also act as dopamine antagonists do
not cause schizophrenic like symptoms. Alongside this, the newer antipsychotic drugs which have
been developed to treat schizophrenics affect other neurotransmitters such as serotonin and
glutamate as well as dopamine. Therefore it appears that several neurotransmitters may be involved
in the development of schizophrenia, meaning the dopamine hypothesis is too simplistic to explain all
the origins of schizophrenia.
Biological explanations for schizophrenia can be criticised for being biologically reductionist. By
reducing schizophrenia down into terms of genes and neurotransmitters, the social context within
which it develops has not been considered. In order to explain schizophrenia effectively it would be
better to take an interactionist approach, such as the diathesis stress model. This suggests that
biological factors predispose someone to schizophrenia, but this has to be ‘triggered’ by some sort of
experience or stressor. Evidence to support this view comes from the prospective adoption study by
Tienari et al. Although this study showed that children with a biological parent were still at greater
risk even if they had been adopted into families with no history of schizophrenia, all reported cases of
schizophrenia occurred in families rated as ‘disturbed’. When the families were rated as ‘healthy’, the
likelihood of developing schizophrenia for those with a biological mother with schizophrenia fell to
below 1%. However, biological factors must have had a role to play as none of the adoptees with no
family history of schizophrenia from ‘disturbed’ families developed schizophrenia
Evaluate one psychological explanation for schizophrenia. (8 marks) 2021
The dysfunctional family explanation for schizophrenia involving the schizophrenogenic mother and
double bind can have very negative implications for the family of the schizophrenic. This explanation
places the blame on the parents for their child’s condition. Literally calling the mother the
‘schizophrenia causing mother’ can be very harsh and doesn’t acknowledge the struggle the mother
would have been through, trying to care for a child with schizophrenia, it could additionally make
things harder for the individual with schizophrenia if those around them are also suffering with
negative mental health as a result. This could have implications on the parents mental wellbeing and
the level of care received by the child with schizophrenia if the mother believes her presence entirely
is negative. It is important to recognise the socially sensitive aspect of this explanation when
publishing research in this area to make sure it is communicated in an appropriate way. Although
family dysfunction may be a main cause of someone’s schizophrenia there are also many other
factors that could have led to the condition also so it is important to make the family aware of this
too.
One strength of family dysfunction theories as an explanation or schizophrenia is that there is
research evidence to support the link between childhood experiences and schizophrenia. For example,
there is research evidence which links insecure attachment type to schizophrenia. Read et al. (2005)
found that adults with schizophrenia were more likely to have an insecure attachment type and that
69% of women and 59% of men with schizophrenia had a history of physical/sexual abuse. This is
important because it suggests that there is a correlation between experiencing schizophrenia and
experiences of trauma or inconsistent parenting during childhood. This therefore provides support for
the idea that family processes may act as a risk factor in the development of schizophrenia.
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