4. The Biological approach to explaining OCD

define OCD

an anxiety disorder where anxiety arises from both obsessions (persistent thoughts) and compulsions (behaviours that are repeated over and over again to reduce anxiety as response to obsessions)

list emotional characteristics of OCD

anxiety and distress

feelings of embarrassment/shame as the person is aware that their behaviour is excessive

feelings of disgust (towards the obsession)

list behavioural characteristics of OCD

obsessions = intrusive thoughts that are perceived as inappropriate

list behavioural characteristics of OCD

repetitive compulsive behaviours performed to reduce anxiety created by obsessions

avoiding certain objects

state 3 genetic explanations for OCD

1) COMT gene

2) SERT gene

3) Diathesis-stress

describe the COMT gene

involved in the production of COMT

COMT regulates the production of the neurotransmitter dopamine

one form of the COMT gene has been found to be more common in OCD patients

Tukel et al (2013) says that this variation of the COMT gene produces lower activity of the COMT gene which results in higher levels of dopamine

describe the SERT gene

affects the transport of serotonin, creating lower levels of serotonin = implicated in OCD

Ozaki et al (2003) found a mutation in this gene in two unrelated families where 6/7 members had OCD

describe the diathesis-stress model in explaining OCD

suggests that people gain a vulnerability towards OCD through genes, but an environmental stressor is required to trigger OCD

the mutation of one gene would unlikely be solely responsible for the onset of OCD = mutation of the SERT gene is also implicated in other disorders such as depression

means that some people could have the COMT or SERT gene but not gave OCD

state 2 neural explanations for OCD

1) abnormal levels of neurotransmitters

2) abnormal neuroanatomy

describe the effect of abnormal levels of neurotransmitters on OCD

higher levels of dopamine are found in people with OCD = based on animal studies = Szechtman et al (1998) found that high doses of drugs that enhance dopamine induce movements resembling compulsive behaviours found in OCD patients

lower levels of serotonin are associated with OCD = Pigott et al (1992) found that antidepressant drugs that increase serotonin activity have been seen to reduce OCD symptoms

describe the effect of neuroanatomy on OCD

the caudate nucleus (located in basal ganglia) normally supresses signals from the orbitofrontal cortex (OFC)

the OFC sends ‘worry‘ signals to the thalamus about potential hazards

in OCD, the caudate nucleus is thought to be damaged so it cannot supress these ‘worry’ signals so the thalamus is alerted, which in turn sends signals to the OFC (acting as a worry circuit)

supported by PET scans of patients with OCD while their symptoms are active = shows heightened activity in the OFC

1) Comer (1998) reports that serotonin plays a key role in the operation of the OFC and the caudate nuclei, so abnormal serotonin levels may cause these areas to malfunction

2) Sukel (2007) found that high levels of dopamine leads to overactivity of the basal ganglia

one strength of genetic explanations of OCD is support from family and twin studies

Nestadt et al (2000) identified 80 patients with OCD and their first-degree relatives and compared them with 73 control patients (without mental illnesses) and their relatives. found that people with a first-degree relative with OCD had a 5x greater risk of having OCD compared to the general population

Billett et al (1998) did a meta-analysis and found that MZ twins were 2x as likely to develop OCD if their twin had OCD compared to DZ twins

supports idea that there is a genetic basis for OCD

however, concordance rates are not 100%, meaning environmental factors must play a role too (diathesis-stress model)

one limitation of genetic explanations for OCD is that it is incomplete

Cromer (2007) found that over half of the OCD patients in their sample had a traumatic event in the past, and that OCD was more severe in those with more than one trauma

suggests that individuals may gain a vulnerability towards OCD through genes that is then triggered by an emotional stressor (support for diathesis-stress approach)

means that it may be more productive focus on environmental causes = seems that the cause of OCD is not entirely genetic

one strength of neural explanations for OCD is research support for the effect of neurotransmitters

Szechtman et al (1998) conducted animal studies and found that high doses of drugs that enhance dopamine induce movements resembling compulsive behaviours found in OCD patients

Pigott et al (1992) found that antidepressant drugs that increase serotonin activity have been seen to reduce OCD symptoms

increases validity of neural explanations for OCD = research is more valuable

one strength of neural explanations of OCD is research into neuroanatomy there are real world applications

Pigott et al (1992) found that antidepressant drugs that increase serotonin activity have been seen to reduce OCD symptoms

whereas, antidepressants that have less effect on serotonin do not reduce OCD symptoms (Jenicke (1992))

increases validity of neural explanations for OCD = allows medication to be developed to help those with OCD

however, drug therapies are not effective for all patients (many harmful side effects)

also, just because administering SSRIs decreases OCD symptoms, does not mean low serotonin was the cause of OCD in the first place (cannot establish cause and effect)

one strength of neural explanations for OCD is there is scientific evidence for the effect of neuroanatomy on OCD

Menzies et al (2007) used MRI to produce images of brain activity in OCD patients and their immediate family members without OCD (and a group on unrelated, healthy people) = found that OCD sufferers and their close relatives had reduced grey matter in key regions of the brain (including the OFC)

supports view that anatomical differences are inherited and these may lead to OCD in some people

possible that brain scans may be used to detect OCD risk in the future

however, possible that these neural changes could be caused by OCD, but not the cause of OCD

one limitation of biological explanations for OCD is there are alternative explanations

the two-process model of phobias can also be applied to OCD

e.g. the neutral stimulus of dirt is associated with anxiety (classical conditioning). this association is maintained because the anxiety-provoking stimulus is avoided (operant conditioning) = obsession is formed, and a link is created between compulsive behaviours (e.g. handwashing) that temporarily reduce the anxiety

psychological explanations are supported by the success of a treatment for OCD called exposure and response prevention (ERP) = patients experience their feared stimulus whilst being prevented from performing their compulsive behaviour

high success rates of ERP

Albucher et al (1998) reported that between 60-90% of adults with OCD have improved significantly using ERO

suggests that OCD may have psychological causes

state 4 drug therapies used to treat OCD

1) antidepressants = SSRIs

2) antidepressants = tricyclics

3) anti-anxiety drugs

4) antibiotic = D-Cycloserine

describe SSRIs

Selective Serotonin Reuptake Inhibitors

work on increasing levels of serotonin in the brain by preventing the reabsorption of serotonin (which increases serotonin levels in the synapse) = can continue to stimulate the post-synaptic neurone

when serotonin is released from the pre-synaptic neurone into the synapse, it travels to receptors on the post-synaptic neurone = serotonin which is not absorbed in the post-synaptic neurone is reabsorbed into the pre-synaptic neurone

low levels of serotonin are implicated in the ‘worry circuit‘ (OFC, caudate nucleus, thalamus)

describe anti-psychotic drugs

lower dopamine levels (as high levels are associated with OCD)

e.g. Benzodiazepines (BZs) lower anxiety levels by slowing down activity in the CNS by enhancing GABA activity

GABA is a neurotransmitter that has a dampening effect on many neurones within the brain and work by locking onto GABA receptors = opens channel that increases the flow of Cl^- ions into the neuron = makes it harder for the neuron to be stimulated by other neurotransmitter, thus slowing down its activity = relaxing the individual

describe tricyclics

e.g. clomipramine

tricyclics block the transporter mechanism that reabsorbs both serotonin and noradrenaline into the pre-synaptic neuron after it has fired = causes more neurotransmitters to be left in the synapse, prolonging their activity

have advantage of targeting more than one neurotransmitter

however, have greater side-effects = is used as a second-line treatment where SSRIs are not effective

describe D-Cycloserine

an antibiotic used in treatment of tuberculosis, also reduces anxiety

Kushner et al (2007) found D-Cycloserines enhance the transmission of GABA, reducing anxiety

one strength of biological treatments for OCD is there is research support for the effectiveness of drug therapies

support which used randomised drug trials

Soomro et al (2008) reviewed 17 studies of the use of SSRIs with OCD patients and found them to be more effective than placebos in reducing OCD symptoms up to 3 months after treatment

symptoms typically decline for around 70% of patients

Koran et al (2007) found than an issue regarding the evaluation of treatment is that most studies are only 3-4 months in duration

suggests that while drug therapies have been shown to be effective in the short term, the lack of long-term data is a limitation

one strength of biological treatments for OCD is drug therapies are cost-effective and non-disruptive

anti-psychotic drugs are relatively cost-effective in comparison to psychological treatments, such as CBT

drug therapies are also cheaper for the NHS because they require little monitoring and cost much less than psychological treatments

drug therapies are non-disruptive to patients’ lives = easy to take, whereas engaging in CBT may be difficult

drug therapies are more appropriate for a lot of patients and are more economically beneficial for the NHS (compared to CBT)

one limitation of biological treatments for OCD is the side effects of drug therapies

Soomro et al (2008) found that nausea, headache, and insomnia are common side effects of SSRIs

BZs are renowned for being highly addictive and can also cause increased aggression and long-term memory impairments = means that BZs are only prescribed for short-term treatment

consequently, these side effects reduce the effectiveness of drug therapies as patients will often stop taking the medication if they experience these side effects

limit the usefulness of drugs as treatments for OCD