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Biological Explanations and Treatments of OCD

Biological Explanations and Treatments of OCD. PSYA4: Psychopathology. Biological theories of atypical behaviour. The basic view of the biological approach is that things go wrong with thinking, emotion and behaviour because things have gone wrong with the brain:

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Biological Explanations and Treatments of OCD

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  1. Biological Explanations and Treatments of OCD PSYA4: Psychopathology

  2. Biological theories of atypical behaviour • The basic view of the biological approach is that things go wrong with thinking, emotion and behaviour because things have gone wrong with the brain: • One or more parts is abnormally structured • One or more parts is functioning abnormally (i.e. too active or not active enough)

  3. Biological theory of OCD Orbito-frontal cortex Thalamus

  4. Brain activity in OCD patients Orbito-frontal cortex

  5. Genetics • How can genetic links be researched? • Family studies • Twin studies • Adoption studies

  6. Genetics • Family studies – relatives of OCD sufferers have a higher prevalence of OCD than the general population (Nestadt et al, 2000) • Twin studies – a review of 14 published twin studies into OCD found 54/80 concordance for MZ twins and 9/29 DZ twins.

  7. AO2 (However…) • We can’t completely eliminate the influence of the environment in twin and family studies.

  8. AO2 (However…) • Gene therapy is very new. • Anthropomorphism!

  9. An “OCD gene”? • Sapap3 – a gene expressed in the striatum, which controls processes such as planning and action has been implicated in OCD. Feng et al (2007) found mice lacking the gene showed high levels of anxiety and pulled out their own fur. When given the sapap3 protein however, the symptoms disappeared.

  10. Biochemical Research • Pigott et al (1998) found drugs which increase serotonin reduce OCD symptoms (eg SSRIs used for treating depression) • In comparison, antidepressants which do not affect serotonin do not reduce OCD symptoms (Jenicke, 1992) • Comer (1998) suggests that serotonin plays a key role in the functioning of the OFC, therefore low serotonin = poor functioning. • Animal studies have found that high levels of dopamine could link to OCD, where enhancing dopamine levels resulted in OCD-like behaviour (Szetchman et al, 1998)

  11. AO2 (However…) • The link is not straightforward, particularly is serotonin is an effect of OCD and not a cause. • Insel (1991) found that drugs only partially relieve the symptoms. • Other research does support the link however. For example Kim et al (2007) found SSRIs which raise serotonin, reduce dopamine and this reduction was positively correlated with a reduction in Y-BOCS scores.

  12. Neuroanatomical factors • Genetic factors may affect the brains’ structure. • Research suggests the following areas are implicated in OCD:- basal ganglia- orbito-frontal cortex (OFC)- the caudate nucleus- the thalamus • Read through pages 379-80 and note down a piece of evidence to support or an example to explain their involvement. • Include notes on the Menzieset al (2007) study.

  13. AO2 (However) • Not entirely sure what the causal factor is in these cases (i.e. genetic or abnormalities). • Doesn’t necessarily help with treatments.

  14. Evolutionary approach • OCD could be seen as adaptive:- Grooming behaviour (OCD patients often wash and groom)- Concern for others (OCD patients are often concerned with harming or embarrassing others)- Hoarding (OCD Patients might hoard collections) • How might these things be seen as adaptive?

  15. Evolutionary Approach • Abed and de Pauw (1998) suggest a mental module for OCD, which has evolved over time. • They call it the Involuntary Risk Scenario Generating System (IRSGS), where individuals are able to evaluate risk before engaging in behaviour. • They suggest OCD sufferers may have an overactive IRSGS.

  16. AO2 (However) • The mental module idea creates some testable hypotheses according to Abed and de Pauw (1998), which has been supported by others. For example, OCD patients should be less prone to risk taking because the IRSGS alerts them to the dangers. • Other evidence comes from research into increased OCD symptoms during times of increased risk (e.g. during pregnancy). Buttolph et al (1998) found this to be the case where OCD was higher during pregnancy.

  17. Past paper question • Discuss two or more biological explanations of OCD (8 marks + 16 marks) • Using the research covered so far, work out a plan in response to this question. • Try and make the links between ideas and statements clear in your plan.

  18. Biological Treatments • Biological responses to OCD mainly focus on:- Drugs (chemotherapy)- Psychosurgery

  19. Drug treatments • As discussed, there is evidence to suggest that drugs which raise levels of serotonin can help with OCD.

  20. Anti-anxiety drugs • Benzodiazepines (BZs) are commonly used to reduce anxiety (e.g. Valium, Xanox and Diazepam). They slow down the nervous system by increasing GABA, a NT which quietens the neurons in the brain, by reducing stimulation.

  21. AO2 • There is lots of evidence to support the use of SSRIs in treating OCD (see previous notes) • Side effects – using a tricyclic antidepressant like clomipramine leaves greater side effects, but there is some evidence to show it is a helpful in treating OCD. • Treatment aetiology fallacy – just because the symptoms disappear, doesn’t mean the cause has been treated. There is a higher relapse rate in OCD patients who start a drug treatment compared to psychological treatments.

  22. Psychosurgery • This refers to surgical intervention to relieve symptoms of OCD. It may involve removal or disconnection of brain regions responsible. In this case the capsule and cingulum are implicated (part of the limbic system).

  23. Psychosurgery • Using p384 in the blue textbook, note down what transcranial magnetic stimulation involves as a method of psychosurgery.

  24. AO2 • Dougherty et al (2002) found that up to 45% of patients studied who had been unsuccessfully treated with drugs showed improvement after cingulotomy. • Jung et al (2006) supports this with no adverse side effects. • However, Koran et al (2007) suggests the results may be biased as patients know they are being treated (i.e. placebo effect). • Greenberg et al (1997) used TMS for 20 mins on frontal sites to treat patients and found a reduction in compulsive behaviour which lasted for 8 hours. • However,Rodriguez-Martin et al (2003) found that an experimental TMS group compared to a placebo TMS group showed no significant reduction in OCD symptoms.

  25. Past paper question • Discuss two or more biological therapies for OCD (9 + 16 marks) • Write a detailed plan OR have a go!

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