Biological approach + OCD Flashcards
Behavioural characteristics of OCD
Compulsions- repetitive + unconcealed behaviour such as hand washing, individuals feel the need to perform these actions otherwise something bad might happen–> anxiety.
Avoidance- avoid certain situations in an attempt to reduce their anxiety.
Cognitive characteristics of OCD
Obsessive thoughts- obsessions are recurrent, intrusive or impulses that are perceived as inappropriate.
Insight- person recognises these obsessional thoughts/impulses are a product of their own mind but they find them uncontrollable + overwhelming which creates anxiety. For a diagnosis of OCD the person must be able to recognise their obsessions + compulsions aren’t rational.
Emotional characteristics of OCD
Anxiety + distress- OCD= unpleasant emotional experience due to the anxiety that accompanies obsessions + compulsions: engaging in compulsive behaviour brings temporary relief from anxiety.
Guilt + disgust- guilt may be experienced over minor moral issues or disgust directed externally.
biological approach in explaining OCD
Lewis (1936):
Observed that 37% of his OCD patients had parents with OCD + 21% had siblings with it too.
-Suggests OCD runs in families although what passes on is probably a genetic vulnerability to develop the condition.
-Diathesis stress model- explains that certain genes leave some people more likely to suffer a mental disorder, BUT an environmental stressor is necessary to trigger the condition.
-Genes thought to create a vulnerability are called candidate genes e.g. SERT gene (lower levels of serotonin) affects the transport of serotonin across synapses OR lack of COMT gene (which regulates production of dopamine) results in higher levels of dopamine.
-OCD= polygenic, caused by not one single gene but a combination of genes.
AO3 of biological approach strength
P-supporting evidence for the genetic basis of OCD comes from studies of firsts degree relatives + twin studies.
Ev- Nestadt et al (2000) found 80 patients with OCD + 343 of their first degree relatives and compared them to 73 control patients (no OCD) + 300 of their relatives. Found that patients with a first degree relative with OCD had a risk 5 times higher than those without one.
Ex- Also reviewed twin studies + found that 68% of monozygotic twins shared OCD opposed to 31% of dizygotic twins.
L- This data strongly suggests genetic influence on OCD
AO3 of biological approach limitation
P- However, the concordance rates reported in family + twin studies are never 100% which means that environmental factors play a role too- diathesis stress model.
Ev- Comer et al (2007) found that over half the OCD patients in their sample had a traumatic event in their past + that OCD was more severe in those who suffered more than one trauma.
Ex- In many cases, it’s the occurrence of OCD that runs in families rather than specific symptoms e.g. specific obsessions, shows there is an environmental contribution to OCD in terms of these symptoms.
L- Suggests that OCD cannot be entirely genetic in origin + may be more productive to focus on the environmental causes as we’re able to do something about them.
Neural explanations for OCD
-Serotonin- involved with the regulation of mood, if a person has low levels of serotonin then normal transmission of mood related info doesn’t take place and mood is affected.
-Dopamine levels are thought to be high in people with OCD, belief stems from animal studies where when given a high dosage of drugs which elevate dopamine levels the animals displayed movements resembling compulsive behaviours.
Neural explanations for OCD: Brain structures
Orbitofrontal cortex- relays info about things which are worrying/risky to the thalamus, normally these are suppressed by the caudate nucleus
-If the caudate nucleus is damaged, the thalamus is alert + confirms the worry and sends the signal back to the orbitofrontal cortex: worry circuit.
-Serotonin has been associated in playing a role in the operation of the orbitofrontal cortex + caudate nucleus, abnormal levels of serotonin may cause these areas to malfunction.
-Dopamine is linked to this system as it’s the main neurotransmitter of the basal ganglia, high levels of dopamine= overactivity of that region
AO3 strength of neural explanations
P- research supports the role of neurotransmitters + brain structures in OCD.
Ev- E.G. low serotonin levels have been associated with OCD as when patients are given antidepressants wthat increase serotonin levels, OCD symptoms=reduced.
Ex- Furthermore, PET scans of patients w/ OCD taken while their symptoms are active e.g. when a person w/ a germ obsession is told to hold a dirty cloth, have recorded high levels of activity in the orbitofrontal cortex.
L- However, evidence suggests neurotransmitters + brain structures do function differently in sufferers, this isn’t the same as saying that this causes OCD, these biological abnormalities could be the result of OCD not the cause.
AO3 limitation of neural explanations
P- There is quite strong competition from psychological explanations for OCD.
Ev- The two process model can explain phobias + OCD, a neutral stimulus is associated w/ anxiety, the anxiety provoking stimulus is avoided= forms obsession and then a link is learned with compulsive behaviour.
Ex- this explanation is supported by the success of exposure + response prevention (ERP). This treatment involves patients experiencing their feared stimulus but being prevented from performing their compulsive behaviour.
L- Studies of ERP have reported improvement rates of between 60-90% of adults with OCD.
Drug therapies : SSRIs
-Aim of SSRIs is to increase the serotonin levels in our brain.
-They block the re-uptake of serotonin that has been released from the presynaptic cell into the synaptic cleft= serotonin remains in the synaptic cleft longer.
-This increases the likelihood of the postsynaptic cell being stimulated + producing an action potential.
Drug therapies: tricyclics
-Where an SSRI isn’t effective after 3-4 months, the dosage can be increased or an alternative drug may be trialled.
-They are an anti-depressant used for OCD.
-Work in the same way as SSRIs but block both serotonin + noradrenaline from being reabsorbed back into the pre-synaptic cell after being fired.
-As a result, more neurotransmitters left in the synaptic cleft=prolonging activity + increasing likelihood of post-synaptic cleft firing.
AO3 drug therapies limitation
All drugs have side effects, some more severe than others
For example, nausea, headache + insomnia are common side effects of SSRIs, which may be enough for a patient to stop the treatment all together.
Tricyclics tend to have more side effects than SSRIs with patients reporting experiencing hallucinations + irregular heartbeats.
This means tricyclics are only used when SSRIs have been ineffective in treating OCD
AO3 drug therapies strength
Drug therapies may be preferred to other forms of treatment.
SSRIs/tricyclics take less time and effort than CBT where the patient has to tend regular meetings + put in thought into tackling their obsessions + compulsions.
However, review of treatments sponsored by the American Psychological Society suggested that although drug therapies are more common, psychotherapies such as CBT should be tried first.
The findings that patients often relapse a few weeks after stopping medication suggests that drugs don’t provide a long lasting cure for OCD
