Biological Approach to explaining and treating OCD Flashcards
Nestadt (2010)
Aim was to see if OCD was down to environmental or biological factors.
- He reviewed evidence from twin studies that saw concordance rate of OCD for identical (MZ) twins was 68%, and the concordance rate of OCD for non-identical twins was 31%.
Conclusion: OCD must have a genetic explanation, but also an environmental because identical twins don’t have a 100% concordance rate.
Koran et al (2000)
Aimed to investigate whether adding olanzapine to SSRI medication (fluoxetine) is effective in treating OCD.
-10 patients with OCD who hadn’t responded to fluoxetine took part. OCD symptoms were assessed using Y-BOCS with a max score of 40. Mean score was 29.
Results: one dropped out, mean Y-BOCS dropped to 24. One patient showed a 68% improvement maintained over 6 months.
Polak et al (2012)
Aim: Investigated a case of compulsions following damage to basal ganglia.
- man had a heart attack resulting in damage to basal ganglia which resulted in him having obsessive and compulsive whistling behaviour of the same carnival song for nearly 16 years for 5-8 hours everyday.
- his behaviour would be reduced with a drug which increased the neurotransmitter, serotonin.
Conclusion: symptoms of OCD can be reduced by altering the activity between the basal ganglia and the orbito-frontal cortex.
What are the assumptions of OCD
That they’re due to NAGI
- nural abnormalities
- genes
- illness
Key symptoms of OCD
Obsessions- persistent and intrusive thoughts about something that seems revolting
Compulsions- urges to perform a particular behaviour.
What neural abnormalities cause OCD
Malfunctioning brain circuits that are involved in detecting and responding to potential danger between the basal ganglia and the orbito-frontal cortex that causes the obsessions and compulsions.
What has shown to reduce symptoms of OCD
Deep brain stimulation
- 50 patients treated
- improvements in up to 60% of patients symptoms
- 40% have no significant improvements
Evaluation of neural abnormalities effect on OCD
👎🏿we can’t be sure as to the cause and effect, does the abnormalities cause OCD or the other way around.
👍🏿 positive results of DBS suggests the problem lies between the basal ganglia and orbito-frontal cortex.
👎🏿scanning studies haven’t found problems in all patients.
What is a theory for abnormalities in neurotransmitters
That there is a deficiency in levels of serotonin (an inhibitory neurotransmitter to decrease electrical activity of neurons)
Evidence for abnormalities in neurotransmitters causing OCD
- Mutations in a gene that’s linked to serotonin activity have been found in some gene mapping studies comparing patients with OCD and without.
- drugs that increase serotonin levels have been effective in reducing OCD symptoms
Evaluation of abnormalities with neurotransmitters theory of OCD
👎🏿the over activity of neurotransmitters have also been see to cause OCD?
👎🏿the drug that increases serotonin may be treating the symptoms but not the cause (too little serotonin)
👎🏿Baxter et al (1992)
Baxter et al (1992)
Aim- looking at changes in activity in the brain following SSRI treatments or behavioural therapy for OCD.
Results- changes in brain activity occurred from both methods
Conclusion- the fact that psychological treatment decreased brain activity suggests that the brain abnormality may be a consequence rather than a cause of OCD symptoms.
OCD is likely to be polygenic. What does this mean?
Meaning that it’s related many genes, not just one
What provides evidence for genes causing OCD?
Nestadt (2010)
What is the most common implication of drugs to reduce symptoms of OCD?
SSRI’s (specific serotonin re-uptake inhibitors)
- they reduce the re-uptake of serotonin back to the presynapse, so that serotonin stays in the synaptic Gap for longer to reduce activity.
