OCD and the biological approach

• OCD is an anxiety disorder characterised by obsessions and compulsions which are time-consuming and cause distress.
• A cognitive characteristic of OCD is obsessions. This is disturbing, persistent thoughts which create feelings of guilt and anxiety.
• An emotional characteristic of OCD is feelings of guilt and anxiety. Sufferers will experience overwhelming anxiety and guilt that accompany obsessions and compulsions.
• A behavioural characteristic of OCD is compulsions. This is repetitive actions that people feel urged to do to reduce feelings of guilt and anxiety.
• To be diagnosed with OCD, a person has to display all three symptoms: feelings of guilt and anxiety, obsessions and compulsions.
• The neural explanation of OCD suggests OCD is caused by abnormalities in the brain which is a consequence of abnormal levels of neurotransmitters.
• The orbitofrontal cortex detects worrying stimuli in our environment and is involved in deciding how to deal with worrying stimuli. It is the part of the brain responsible for logical thinking and decision making.
• The orbitofrontal cortex decides an action to deal with a worrying stimulus and then sends signals to the motor cortex to carry out this action.
• The basal ganglia monitors the outcome of actions and when a worrying stimulus has been dealt with, the basal ganglia sends inhibitory signals back to the orbitofrontal cortex to shut down the signals relating to the worrying stimulus.
• The neural explanation suggests those with OCD have impaired communication between the basal ganglia and orbitofrontal cortex. As a result, the signals sent from the basal ganglia to the orbitofrontal cortex are much weaker and the neural activity in the orbitofrontal cortex is less inhibited than it should be and becomes hyperactive which generates the symptoms of OCD.
• Serotonin is an inhibitory neurotransmitter, which is released from the pre-synaptic terminal during synaptic transmission. Serotonin causes inhibitory post-synaptic potentials to occur in post-synaptic neurons.
• For people with OCD, when the basal ganglia sends signals to the orbitofrontal cortex, less serotonin is released than usual. As a result, the neurons in the orbitofrontal cortex are not as inhibited meaning the neurons in the orbitofrontal cortex become hyperactive. If neurons in the orbitofrontal cortex become hyperactive, signals in response to the worrying stimuli persist.
• The neural explanation of OCD says that people with OCD have less serotonin release than normal.
• The neural explanation says that people with OCD have impaired communication between the orbitofrontal cortex and basal ganglia. Normally, when the basal ganglia sends signals to the orbitofrontal cortex, serotonin is released in the orbitofrontal cortex. However, for people with OCD, as the signals between the two structures are weaker, less serotonin is released in the orbitofrontal cortex. Because serotonin is an inhibitory neurotransmitter, and there is less of it than usual, this results in a hyperactive orbitofrontal cortex.
• Supporting evidence for neural explanation of OCD. Max et al 1995 conducted a case study on a girl who developed OCD after experiencing brain damage and found she had structural damage to the basal ganglia. This is positive as the study supports the idea that damage to the basal ganglia causes OCD.
• Supporting evidence for neural explanation of OCD. Saxena and Rauch 2000 reviewed brain imaging studies that compared the brain activity of adults who have OCD with the brain activity of adults without OCD and found increased brain activity in the orbitofrontal cortex of adults with OCD compared to the control group. This is positive as it suggests hyperactivity in the orbitofrontal cortex may cause the symptoms of OCD.
• Inconsistent results for neural explanation of OCD from brain imaging studies. Aylward et al 1996 found no differences between the basal ganglias of people with OCD and healthy controls which contradicts Max et al 1995 findings. This is problematic as the results of studies haven't always replicated
• The genetic explanation of OCD suggests OCD is a genetically inherited disorder.
• Specific gene alleles can increase a person’s risk of developing OCD. If a person has more of these gene alleles, their chances of having OCD are increased.
• The SERT gene has been associated with OCD. SERT genes produce re-uptake proteins. The more re-uptake proteins that are produced, the less serotonin is available in the synapse.
• People who carry the long allele of the SERT gene will have a decrease in serotonin at the synapse. This means that they will have less inhibition of neural activity in the brain region where a lot serotonin is released, including the orbitofrontal cortex
• The long allele of the SERT gene produces more re-uptake proteins whereas the short allele of the SERT gene produces less re-uptake proteins.
• The SERT gene controls serotonin levels at the synapse by controlling re-uptake of serotonin.
• Supporting evidence for genetic explanation from twin studies. Billet et al 1998 reviewed twin studies comparing the concordance rate of MZ and DZ twins with OCD and found a concordance rate of 68% for MZ twins having OCD whereas concordance for DZ twins was 31%. This is positive as it supports the genetic explanation that OCD is partially genetically inherited.
• Supporting evidence for genetic explanation from family studies. Nestadt et al 2000 conducted a family study on a control group and experimental group of OCD patients and concluded when a person has OCD, it is more likely their relatives will also have OCD. This is positive as it supports the idea that OCD is likely to be partially inherited.
• Supporting evidence for the long SERT allele and OCD. Hu et al 2006 conducted a gene study analysed the DNA of people with OCD, comparing them to a control group and concluded that carrying the long allele of the SERT gene led to an increased chance of developing OCD. This is positive as it supports the genetic explanation of OCD.
• However, a limitation of twin studies is that they assume monozygotic twins and dizygotic twins both have a similar amount of shared environment and the impact of the environment on phenotype is similar for both sets of twins, however, MZ twins are more likely to be treated the same because they look more similar. This is problematic as differences in concordance rates might be due to a mix of differences in shared environment and shared genetics.
• SSRI drugs block serotonin reuptake, resulting in more serotonin being available at the synapse. SSRIs increase inhibition of neural activity in the orbitofrontal cortex and reduce hyperactivity
• SSRIs block re-uptake of serotonin into the pre-synaptic terminal, which then increases the amount of serotonin available at the synapse. Serotonin acts as an inhibitory neurotransmitter, so, after binding to post-synaptic receptors, serotonin creates a negative charge that inhibits the post-synaptic neuron, making a nerve impulse less likely to occur. This leads to a decrease in neural activity in the orbitofrontal cortex. This means that the orbitofrontal cortex no longer remains hyperactive in people with OCD.
• Supporting evidence for effectiveness of SSRI's. Soomro et al 2008 conducted a review of 17 studies investigating the effectiveness of SSRIs as a treatment for OCD and found SSRIs are more effective than placebo sugar pills as 70% of patients treated with SSRIs experienced an improvement in symptoms. This is positive as the effectiveness of SSRIs are supported by studies.
• Biological treatments can cause side effects. Soomro et al 2008 found that when patients took SSRIs they experienced nausea, difficulty sleeping and headaches. This is problematic as drugs don’t just affect the areas of the brain that are targeted for treatment and can cause unwanted side effects.
• Reductionist. Biological treatments do not consider cognitive factors of OCD. O'Conner et al 1999 found that combining both types of treatment, using SSRIs and CBT led to the biggest reduction in symptoms of OCD. This is problematic as biological treatments may need to be used alongside cognitive treatments to be most effective.