Example Answers for Psychopathology: A Level Psychology, Paper 1, June 2019 (AQA)

Here are some example answers to the written Paper 1 questions on Psychopathology in the 2019 AQA exams.

Question 12

One behavioural characteristic is a change in activity levels where you might have a lack of energy, withdraw from activities that were once enjoyed or begin to neglect personal hygiene. A second behavioural characteristic is disruption to sleep with some people suffering from insomnia (lack of ability to sleep) or hypersomnia (sleeping all the time).

Question 13

Statistical infrequency defines abnormality as any behaviour which is mathematically rare in a population - for example Agoraphobia “affects less than 1% of adults”. Whereas Failure to Function Adequately defines abnormality as anything which interferes with everyday life often causing personal distress or observer discomfort – for example Agoraphobia is described as “very stressful for the individual and their family” and “may prevent suffers from living a normal life”. Finally Deviation from Ideal Mental Health defines abnormality as behaviour which fails to meet the criteria for psychological wellbeing. This includes having an accurate perception of reality, being resistant to stress and being able to self-actualise - for example Agoraphobics are described as “perceiving threats everywhere” it is “very stressful” and “prevents sufferers…achieving their potential”

Question 14

The two-process model is flawed due to its assumption that all phobias arise from a traumatic experience which cannot account for why some phobias are more common than others. The learning theory misses the possible evolutionary nature of some phobias such as the dark, spiders and heights which are more common in the population as they would have proposed a real threat to our ancestors and phobic behaviour would have provided an evolutionary advantage.

Question 15

Questionnaires are well suited to large samples and allow the collection of large amounts of data from many individuals at one time. However this research is aiming to gain a greater understanding of Agoraphobia from studying one patient – Patient X. Therefore it is more important to be able to gain a rich a detailed understanding. Case studies are able to utilise many forms of data collection and therefore the researcher can use some self-report techniques but may also be able to conduct observations of the patient as well and gather both qualitative and quantitative data which can act as triangulation for checking the reliability and validity of the data. In addition, case studies can be conducted longitudinally and can therefore create a more detailed understanding of the patient which questionnaire as a “snapshot” of an individual would not be able to provide.

Question 16

Neural explanations focus on abnormality in brain structures. In OCD patients the orbitofrontal cortex is found to be overactive which increases the amount of ‘worry signals’ being sent by the brain. This is combination with the caudate nucleus which should suppress any minor worries but in patients with OCD is found to be broken, and therefore more worries are allowed through to the thalamus. Abnormal levels of neurotransmitters are implicated in the malfunction of these areas which OCD patients having lowered levels of the mood stabiliser Serotonin which is linked to the obsessions part of the disorder and higher levels of the action rewarding neurotransmitter Dopamine which is linked to the compulsions.

Evidence to support the role of serotonin in OCD comes from the prescription of SSRIs to OCD patients. It has been found that by giving these drugs, which effectively increase the levels of serotonin available in the synapse patients report reduced symptoms of the disorder. This suggests that a lowered level of serotonin may be involved in the development of OCD. However, whilst this is true in a lot of cases not all patients are responsive to SSRIs which casts doubt on this being the only causal factor in OCD and may demonstrate that for some patients the cause lay outside of neural malfunction.

In addition the neural explanations suffer from a research flaw in that we are able to tell that a patient with OCD has got altered levels of neurotransmitters or abnormal brain structures but due to only studying them once they have developed the disorder it is impossible to tell if this is the cause of the OCD or in fact a symptom of it. Possibly the over worrying causes the damage to the OFC and Caudate Nucleus rather than the other way around.