Psychological explanation of schizophrenia summary and plan
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Course
Psychopathology Schizophrenia
Institution
Queen Mary, University Of London (QMUL)
This is a detailed summary and can be used as a plan for psychological explanations of schizophrenia essay. Includes relevant research and evaluation on cognitive factors, family communication, social causation and multi-dimensional approach - the diathesis stress model.
PLAN - Outline and evaluate psychological explanations of
schizophrenia
Cognitive factors
According to this approach, the cognitive impairments expressed by
schizophrenia sufferers e.g. poor attentional control, language deficits,
disorganised thinking lead to the development and maintenance of
schizophrenia.
Recent research suggests that schizophrenic symptoms may be due to a
lack of self-monitoring, and consequently thoughts and ideas are
attributed to external sources such as hallucinations, or result in delusions
because the individual does not realise that they are self-generated. This
explains symptoms such as disorganised speech, delusions, and
hallucinations.
Hemsley suggests there is a substantial breakdown in the relationship
between memory and perception in schizophrenics. As a result, people
with schizophrenia are often unable to predict what will happen next, their
concentration is poor, and they attend to unimportant or irrelevant
aspects of the environment. Their poor integration of memory and
perception leads to disorganised thinking and behaviour.
McGuigan found that the larynx of patients with schizophrenia was
often active during the time they claimed to be experiencing auditory
hallucinations. This suggests that they mistook their own inner speech
for that of someone else.
McGuire et al found schizophrenics to have reduced activity in those
parts of the brain involved in monitoring inner speech.
PET scans show under-activity in the frontal lobe of the brain, which
is linked to self-monitoring and so provides biological support for this
explanation.
The research into brain structural abnormality did not identify such
dysfunctions and so there is a need for further research to link together
the cognitive and biological explanations.
The cognitive explanation provides a reasonable account for positive
symptoms of schizophrenia but not the negative symptoms, therefore
there are issues with generalisability.
Research on self-monitoring employs the experimental method and so
has high internal validity. However it lacks mundane realism and
so may lack generalisability to the schizophrenic symptoms because
of the artificiality of the research conducted.
It is not clear whether the cognitive dysfunction is a cause or effect of
the disorder. Therefore longitudinal research with children at risk of
developing schizophrenia is necessary to establish the direction of the
effect.
, Despite many brain-damaged patients having cognitive deficits
problems, they fail to develop schizophrenic symptoms this
undermines the cognitive explanation to a certain extent.
Other factors have been found to have a greater influence in the
development of schizophrenia. Such as genetic factors, stressful life
events, and various social factors inter-link with cognitive factors.
Life events
Brown and Birley who suggested that stressful life events may
trigger schizophrenia they found that 50% of patients with
schizophrenia had experienced at least one major life event in the 3
weeks beforehand, only 12% had experienced a life event in the
preceding 9 weeks, very few healthy controls reported any life events over
the same 12-week period.
Hirsch et al carried out a prospective study on life events experienced in
a year period. They used the Life Events and Difficulties Scale and found a
23% risk of patients having a relapse during the 1-year period due to life
events. 41% for patients who had twice the average number of life events.
The findings contradict Brown and Birley 1968 as they did not find that the
life events needed to immediately precede the schizophrenic episode.
Myin-Germeys et al. 2003 found patients with schizophrenia showed more
intense negative emotional reactions to daily hassles. This suggests that
these emotional reactions make patients with recent major life events
more vulnerable to relapse.
Life events are not a prerequisite of schizophrenia; some develop
schizophrenia without any recent life events. Not all
schizophrenics experience an episode after a life event therefore we
need to consider the impact of individual vulnerability factors and
differences. However we need to consider that some are more likely
to trigger an episode than others.
Life events are more strongly linked to relapse than onset.
Patients’ recall of life events is retrospective and so may be biased.
The data is correlational and so we cannot conclude a causation but
rather a relationship.
Brown and Birley’s research didn’t distinguish between whether the life
events preceded the schizophrenia or whether they were a result of the
disorder therefore need a better understanding of the direction of
effect.
The wider context of the life event needs to be considered as some
may cope with marital separation if they have a new partner and a
good network of friends.
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