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Summary AQA Psychology A level essays for schizophrenia.

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AQA Psychology A level essays for schizophrenia. All grade A essays for 16 markers including issues and debates. 10 essays including: issues with reliability and/or validity of classification and diagnosis, biological explanations for schizophrenia, psychological explanations for schizophrenia, biological therapies (typical and atypical drugs), psychological therapies (CBT, family therapy and token therapy) and the interactionist approach. Designed for AQA specification using text books, teacher resources and further research. Not perfect but useful for students to help structure their essays and reach the top marks without the essays being too complex or complicated.

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Schizophrenia
Subido en
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Essay 1 – issues with the classification system
One issue with the classification and diagnosis of schizophrenia is its reliability. The inter-rater
reliability is low as different psychiatrists use different diagnostic tools. America uses the DSM which
requires 2 symptoms to be present for at least 6 months and Europe uses the ICD which requires 1
symptom for 1 month. This therefore creates issues with consistency in diagnosis.

Support for low inter rater reliability comes from Cheniaux et al who had two psychiatrists
independently diagnose 100 patients using the DSM and ICD. One psychiatrists diagnosed 26
patients using the DSM and 44 using the ICD. Therefore, more people were diagnosed with
schizophrenia using the ICD showing issues with consistency in diagnosis.

Another issue affecting reliability is the difficulty differentiating between delusions and bizarre
delusions. For Schizophrenia, if a person has bizarre delusions, they only need one other symptom
to be diagnosed, however if they have non bizarre delusions, they need two or more.
Mojitabi and Nicholson support this issue when they found a correlation of only 0.4 between
psychiatrists distinguishing between bizarre delusions and non-bizarre delusions. This means that
some patients may be diagnosed with Schizophrenia while others are not. Thus, giving support for
fact that the diagnostic system has low reliability.
Further support comes from Copeland et al when he showed a video of a patient describing their
symptoms to US and UK psychiatrists. 69% of the US psychiatrists diagnosed schizophrenia, whereas
only 2% of the UK psychiatrists diagnosed schizophrenia, with UK patients being mainly diagnosed
with depression. This highlights a massive variation between Western countries and questions the
reliability of the classification system.

A further issue with validity is Comorbidity. This is where Schizophrenia coexists along-side another
disorder. Buckley et al found schizophrenia had a 50% comorbidity with depression and 47% with
substance abuse. This contributes to the difficulties with predictive validity and treating people with
schizophrenia. Often the co-morbid disorder is untreated therefore causing the patient difficulties.
Support for this was found in a meta-analysis study of over 6 million American patients. Weber et al
discovered that over 45% of people diagnosed with schizophrenia were co-morbid with both
psychotic and non-psychotic disorders. He then went on to discover that many of the non-psychotic
diagnosis were undertreated thus affecting the recovery of patients whose main diagnosis is

, Essay 2 – biological explanation – dopamine hypothesis

The dopamine hypothesis suggests the brain is overactive. Too many neurons release
dopamine flooding the synaptic gap with dopamine causing symptoms of schizophrenia.
Schizophrenics are thought to have abnormally high levels of D2 receptors on receiving
neurons resulting in more dopamine binding and thus more neurons firing. Dopamine plays
a key role in guiding attention so disturbances in this process may well lead to the problems
related to attention, perception and thought found in people with Schizophrenia.

High levels of dopamine in the Mesolimbic dopamine system are associated with positive
symptoms of schizophrenia while low amounts in the Mesocortical system are associated
with negative symptoms. The over production of dopamine receptors in one area may
reduce the production of dopamine in another area.

Amphetamine are dopamine agonists which stimulate the nerve cells causing the synapse to
be flooded with dopamine. Large amounts of Amphetamines can cause the characteristic
symptoms of Schizophrenia such as Hallucinations and delusions.
Grilly proposed that when individuals who suffered from Parkinson’s disease, were given the
drug L-dopa to increase the level of dopamine, they began to show schizophrenic
symptoms.

Support for this explanation comes from research using PET scans, so can be considered
objective and scientific. Lindstrom et al studied the effects of dopamine using PET scans
and the drug L dopa and found that schizophrenics had a higher rate of uptake than the
control group; which could be due to their increased number of D2 receptors in the brain.
This shows real world application increasing the validity of the dopamine hypothesis.

On the other hand, If the dopamine hypothesis was correct, we would expect the treatment
to correlate with the reduction of the symptoms. Noll claims that blocking the D2 receptors
has little effect on reducing schizophrenic symptoms in many individuals as they still
experience hallucinations and delusions even when their dopamine levels are normal. This
suggests that although dopamine may be involved there are other factors contributing to
the cause of the disorder. Therefore, it can be argued that the dopamine hypothesis is too
reductionist.

It is also argued that the dopamine hypothesis may be too focused on nature and underplay
the importance of nurture. The environmental breeder theory believes that the increased
rates of schizophrenia in the working class is due to their lack of time and money which
results in developmental issues for their children. This shows environmental influences on
schizophrenia should also be considered in addition to biological factors.
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