OCD

What is OCD? AO1

An anxiety disorder where anxiety arises from obsessions and/or compulsions

What are obsessions? AO1

Internal components - cognitions that repeatedly enter a person’s mind & cause anxiety

What are compulsions? AO1

External components - repetitive behaviour or mental act someone feels they must carry out to relieve unpleasant feelings brought on by obsessions

What are the DSM 5 categories of disorders that involve obsessions & compulsions? AO1

• OCD

• Trichotillomania

• Hoarding disorder

• Excoriation disorder

What are the behavioural characteristics? AO1

• Repetitive compulsions eg tidying, counting & ordering items

• Compulsions reduce anxiety - carried out to manage unpleasant feelings of obsessions

• Avoidance

What are the emotional characteristics? AO1

• Anxiety & distress

• Accompanied by depression

• Guilt & disgust

What are the cognitive characteristics? AO1

• Uncontrollable obsessive thoughts

• Insight into excessive anxiety - sufferer is aware their thoughts aren’t rational, crucial for a diagnosis as it could indicate schizophrenia if not

Genetic explanations AO1

• Inheritable via genes - Lewis studied patients with OCD & found 37% had parents with OCD & 21% had siblings with OCD

• Candidate genes - create vulnerability such as SERT gene which affects transportation of serotonin & COMT gene (dopamine)

• Diathesis stress model - genetic vulnerability & environmental stressor causes OCD

• Polygenic - OCD determined by multiple genes, Taylor found 230 genes may be involved

Genetic explanations strengths AO3

• P - strong scientific evidence to support

• E - Nestadt et al twin studies found 68% of identical twins shared OCD as opposed to 31% of non-identical twins

• T - suggests there’s a very strong genetic component

  HOWEVER no twin studies have 100% concordance rate so must be environmental factors & nurture rather than nature

Genetic explanations limitations AO3

• P - research supports diathesis stress model

• E - Cromer found that over half of patients had a traumatic past event & OCD was more severe in those with 1+ traumas

• T - genetic vulnerability isn’t the sole explanation as it also needs an environmental stressor

• P - single candidate genes create OCD vulnerability eg SERT gene

• E - difficult to know if having OCD affects SERT gene or if SERT gene causes OCD

• T - difficult to establish a cause & effect relationship so could lower validity

Neural explanations AO1

• Low levels of serotonin - prevents normal transmission of mood relevant info from taking place so mood & mental processes can be affected & anxiety heightened

• Impaired decision making systems - frontal lobe is responsible for logical thinking & decision making. Damage to the lateral can affect this, especially common in hoarding disorders

• Damage to caudate nucleus (part of basil ganglia) stops suppression of worry signals from orbitofrontal cortex, creating a worry circuit

Neural explanation strengths AO3

• P - supporting evidence

• E - some antidepressants like SRRIs increase serotonin levels & are effective in reducing OCD symptoms

• T - supports involvement of serotonin systems in OCD

• P - parkinson’s disease share symptoms - evidence of involvement of dysfunction of basil ganglia in OCD

• P - research comes from brain scanning techniques eg PET scans

• E - objective & falsifiable

• T - high validity

Neural explanation limitations AO3

• P - serotonin-OCD link may be simply co-morbidity with depression (suffering from 2 disorders at once)

• E - OCD often accompanied by depression which disrupts serotonin so low levels may be because of this, not OCD

• T - partial explanation as fails to explain why chemical imbalance is in both even though they’re separate disorders

• P - difficult to establish cause & effect relationship

• E - evidence to show abnormal brain structures & neurotransmitters are abnormal. However this is not the same as saying they cause it

• T - biological abnormalities could be the effect of OCD rather than the cause so lowers validity

SSRIs AO1

• Serotonin is released from presynaptic neuron into the synapse & travels to receptor sites on post synaptic neuron

• Unabsorbed serotonin is reabsorbed into the presynaptic neuron

• SSRIs increase level of serotonin available in synapse so more can be received by post synaptic neuron & less can be reabsorbed by presynaptic neuron

• Can be used alongside CBT to reduce symptoms so patient can engage better

Alternatives to SRRIs AO1

• Tricyclics - increase serotonin levels but have more severe side effects

• BZs- increases GABA (neurotransmitter that controls hyperactivity) to quieten the brain & reduce obsessive thoughts

Drug therapy strengths AO3

• P - evidence to support effectiveness

• E - Soomro et al study compared placebos to SRRIs & found all 17 studies showed better results for SSRIs - 70% of symptoms reduced

• T - supports that serotonin plays a role as SSRIs increase levels

• P - cost effective & non-disruptive

• E - cheap compared to CBT so beneficial to public health system. Non disruptive as can be taken quickly & part of everyday life where as CBT takes multiple sessions & may require people to take time off work

• T - more accessible than CBT & more suitable for patients who lack motivation

Drug therapy limitations AO3

• P - side effects

• E - mild side effects like indigestion & blurred vision. More severe ones like hallucinations. BZs can be highly addictive & cause aggression

• T - BZs can only be taken for a short time & patients may stop taking them which reduces effectiveness

• P - not a long term fix as they mask the symptoms instead of treating underlying cause

• E - Maina found that when patients stop taking drugs their symptoms return in a few weeks

• T - not the most effective long term solution as CBT may be more effective in treating root cause