Psychopathology - 05 The Biological Approach To Explaining and Treating OCD Flashcards
What two factors of the biological approach can be used to explain the causes of OCD?
1)genetic explanations
2)neural explanations
What do genetic explanations suggest about the cause of OCD?
suggests that individuals inherit specific genes from their parents that are related to the onset of OCD
What evidence did Lewis (1936) have which suggested that OCD is inherited?
-37% of his patients with OCD had a parent with OCD
-21% had siblings with OCD
-suggesting that genes play a role
What evidence did Nestadt et al (2010) have to suggest that OCD has genetic links?
-concordance rate of 68% for monozygotic twins and 31% for dizygotic twins
-suggests strong genetic component
What are the two genes which have been identified as having a link to OCD?
1)COMT gene
2)SERT gene
How does the COMT gene link to OCD?
-regulates the production of dopamine
-COMT gene has mutated causing high levels of dopamine
What did Tukle et al (2013) find about the COMT gene and OCD?
-compared 101 OCD sufferers with 100 healthy controls
-found lower activity of COMT gene resulting in higher levels of dopamine
How does the SERT gene link to OCD?
-affects the transport of serotonin
-SERT gene has mutated causing low levels of serotonin
What did Ozaki et al find about the SERT gene and OCD?
-found mutated SERT gene in two different families
-6/7 family members had OCD
What does polygenic mean?
something is not caused by a single gene but that many genes are involved
How many genes did Taylor say may be involved in OCD?
230 genes
weakness of genetic explanations of OCD (not the sole cause of OCD)
-Lewis only 37% had OCD parent and Nestadt concordance rate 68% in MZ twins
-suggests must be another reason for OCD
-if genes was sole reason concordance rate would be 100% and all patients would have OCD parent too
weakness of genetic explanations of OCD (deterministic)
-suggests no free will or control as it is determined through genes
-problem as patients may become passive and do nothing to help
weakness of genetic explanations of OCD (environmental factors ignored)
-environment can trigger/increase risk of OCD
-Cromer et al (2007) 1/2 OCD patients had traumatic events in past and OCD was more severe with more than 1 trauma
-so cannot be entirely genetic
weakness of genetic explanations of OCD (need for interactionist approach)
-needs diathesis-stress model
-individual may have a genetic vulnerability to develop OCD
-BUT it is the interaction between genes and environment that causes OCD
What are the two neural explanations of OCD?
1)neurotransmitters
2)abnormal brain circuits
What are the 2 neurotransmitters which are thought to link to OCD?
1)dopamine
2)serotonin
How does abnormal levels of dopamine link to OCD?
-dopamine levels are high in people with OCD
What evidence is there to suggest that high levels of dopamine cause OCD?
-animal studies
-high dosages of drugs which enhance levels of dopamine induce stereotyped movements resembling the compulsive behaviour of OCD
How does abnormal levels of serotonin link to OCD?
-lower levels of serotonin are associated with OCD
What evidence is there to suggest that low levels of serotonin cause OCD?
-antidepressant drugs that increase serotonin activity have been shown to reduce OCD symptoms
What symptom of OCD is serotonin thought to cause?
obsessive thoughts
What is low levels of serotonin likely due to?
serotonin being removed too quickly from the synapse (reuptake) before it is able to transmit its signal
What abnormal brain circuit is linked to people with OCD?
the worry circuit
What happens at the first stage of the worry circuit?
the Orbital frontal cortex (OFC) notices when something is wrong and it sends a worry signal to the Thalamus
What happens at the second stage of the worry circuit?
Caudate nucleus usually supresses the worry signal and stops it from reaching the Thalamus BUT in OCD patients it is damaged
What happens in the third stage of the worry circuit?
Caudate nucleus fails to supress the worry signal and so the Thalamus is alerted
What happens in the forth stage of the worry circuit?
Thalamus sends a signal back to the OFC which responds by increasing compulsive behaviours and anxiety
What did Cormer say about the role of serotonin in the worry circuit?
-serotonin plays a key role in the operation of the worry circuit and the caudate nucleus
-so abnormal serotonin levels might cause these areas to malfunction
Supporting evidence for the role of neural mechanisms in OCD + counterargument
-antidepressants like SSRIs work on the serotonin system, increasing the levels
-they are effective in reducing symptoms suggesting that serotonin systems are involved in OCD
-BUT not all sufferers respond to antidepressants suggesting that it is not the neural network causing OCD in these patients
weakness of of neural explanations (cause of effect?)
-neural mechanisms may not cause OCD
-could be a result of OCD rather than the cause itself
-problem as if neural mechanisms are not the cause then we need to find out what is
-also if neural mechanisms do not cause OCD, no point using antidepressants to treat it
What do biological treatments for OCD aim to do?
restore chemical imbalances in the brain since this is assumed to be the main cause of the disorder
What are the two types of drugs used to treat OCD?
1)antidepressants
2)anti-anxiety drugs
What re the three types of antidepressant drugs used to treat OCD?
1)SSRIs (selective serotonin reuptake inhibitors)
2)TCAs (tricyclics)
3)SNRIs (serotonin-noradrenaline reuptake inhibitors)
Which antidepressant is the most common used to treat OCD?
SSRIs
How do SSRIs work?
-increase serotonin available in synapse by preventing reabsorption
-this increases serotonin in synapse which improves serotonin concentration at receptor sites on post-synaptic neuron
-this increases stimulation on receiving nerve
How do TCAs work?
-block transporter mechanism that reabsorbs serotonin and noradrenaline in pre-synaptic cell after firing
-so more is left in synapse, prolonging activity
-only used when SSRIs are ineffective
How do SNRIs work?
-increase serotonin and noradrenaline
-only used when SSRIs are ineffective
What anti-anxiety drug is used to treat OCD?
benzodiazepines (BZs)
What are two example of BZ drugs?
Valium and diazepam
What do BZ drugs aim to do?
reduce anxiety which will reduce compulsions
How do BZs work?
-enhance action of GABA (gamma-aminobutyric acid)
-GABA tells neurons in brain to slow-down and stop firing
-around 40% of neurons respond
-means the drugs have quietening influence on brain reducing anxiety, experienced as a result of obsessive thoughts
Effectiveness of drug treatment for OCD
-Soomro et al (2008) reviewed 17 studies of SSRIs found them to be more effective than placebos in reducing symptoms for up to 3 months
-BUT most studies only last 3 months so little long term data exists
Suitability of drug treatment for OCD
do not work in all OCD patients so not suitable for all patients
Conflicting evidence of drug treatment for OCD
-unreliable evidence, some psychologists believe evidence favouring drug therapy is biased as it is sponsored by drug companies
-only publish studies which show their drug as being effective (publication bias)
-Simpson, 45% cases relapsed in 12 weeks , compare to only 12% who had CBT
Alternative treatments of drug treatment for OCD
-drugs criticised for treating symptoms not the cause
-plus once a patient stops taking drugs they are prone to relapse
-so CBT may be more effective long-term solution to provide a lasting treatment and a potential cure
Practical issues of drug treatment for OCD
-cost effective, beneficial to health providers plus CBT needs patients to be motivated to engage whereas drugs are non-disruptive
-side effects BZs only recommended for up to 4 weeks also diminishes effectiveness as patients will often stop taking it if they experience negative side effects
ethical issues of drug treatment for OCD
-side effects e.g. nausea, headaches and insomnia & BZs also highly addictive
-valid consent, people often in vulnerable state and so may not fully understand things e.g. side effects & fact it is short term solution
-so patient may not be making full decision
