Neural Explanations for OCD

Question 1

What is abnormal levels of neurotransmitters?

Answer 1

• Seratonin regulates mood by facilitating synaptic transmission from one neuron to another
• People with OCD have seratonin removed too quickly so it has no chance to pass on signals
• This low level of seratonin leads to mood issues associated with OCD
• Also, abnormally high dopamine levels is linked with the anxiety associated with OCD

Question 2

What is abnormal brain circuits?

Answer 2

• Several areas in the brain’s frontal lobe are abnormal in people with OCD
• Orbitofrontal cortext (OFC) sends worry signals to the thalamus
• This is mediated by the caudate nucleus in the basal ganglia which surpresses minor signals from OFC and lets through major ones
• This prevents us from acting on every little worry
• The thalamus is alerted of major worry signals and initiates reaction
• People with OCD have a hypersensitive caudate nucleus so all major and minor signals from OFC go to the thalamus
• The thalamus then confirms and receives minor signals too creating a worry circuit leading to the person acting on worries though compulsive/repetitive actions

Question 3

How is practical applications a strength?

Answer 3

• A strength of the neural explanation is that it has practical applications in the use of SSRIs
• Knowing that low levels of seratonin causes OCD has led SSRIs being used to treat OCD as they block reuptake of seratonin into the pre-synaptic neuron which prolongs its influence on the post-synaptic neuron
• Soomro et al found that SSRIs were effective in 70% of cases
• As SSRIs are an effective treatment the underlying assumptions its based on must also be valid
• This increases the validity and utility of the neural explanation

Question 4

How is correlational evidence a weakness?

Answer 4

• A weakness of the neural explanation is that its supporting evidence is correlational
• This means evidence can’t be used to establish a cause and effect relationship between seratonin levels and OCD
• It could be that low seratonin causes OCD or that OCD causes seratonin to be low
• If the latter is true, the cause of OCD may be beyond the biological approach’s explanatory scope - e.g. OCD could be learnt through observation and immitation of compulsive behaviour
• Thus the neural explanation of OCD may be incomplete and so reduces in validity