ocd

behavioural characteristics of ocd

• repetitive and time consuming compulsions

• compulsions are performed to reduce anxiety

• avoidance of situations that may trigger obsessive thoughts and compulsive behaviours

emotional characteristics of OCD

• extreme anxiety

• guilt

• disgust directed towards themselves or the outside world

• depression due to feeling trapped by their disorder

comorbidity definition

having more than one mental illness at the same time

cognitive characteristics of ocd

• obsessive thoughts

• using mental coping mechanisms to deal with obsessive thoughts

• awareness that their anxiety and fear are irrational

• catastrophising around their OCD

genetic explanation of ocd (biological approach)

• genetic explanation assumes that mental illnesses are heritable

• risk of developing OCD is higher for first degree relatives (siblings or children)

• OCD is polygenic

  • relevant genes include those involved in serotonergic and dopaminergic pathways

• researchers suggest a variation of the COMT gene is linked to OCD

  • COMT plays an important role in de-activating dopamine

  • irregular dopamine levels are implicated in OCD

  • COMT gene helps to balance dopamine levels

• the SERT gene has also been linked to OCD, as it affects the transport of serotonin

  • lower levels of serotonin activity are implicated in OCD

  • serotonin plays a role in balancing mood, which may help to regulate obsessive thoughts

strengths of the genetic explanation of OCD

• there is some strong research support for a genetic explanation of OCD

  • Nestadt et al (2010) found that 68% of MZ twins both had OCD compared to 31% of DZ twins

  • this increases the validity of the explanation

weaknesses of the genetic explanation of OCD

• ignoring the role that the environment plays in the development of a mental illness means that a genetic explanation is prone to biological reductionism

  • this means the theory lacks full explanatory power

• Pato et al (2001) noted that although there does seem to be a genetic explanation for OCD, there is insufficient understanding of the actual genetic mechanisms surrounding OCD

  • this means that this explanation by itself lacks validity

biological reductionism definition

attempts to explain complex human behaviour by reducing it to a physiological level

neural explanation of OCD (biological approach) - SEROTONIN

• serotonin plays a role in regulating mood - low or disrupted levels have been implicated in mood disorders (e.g. depression)

• low mood may also be accompanied by cognitive disturbances, such as FIP

• FIP can be located to the frontal cortex of the brain

  • the frontal cortex is linked to executive functioning

  • if serotonin levels are low/irregular, it is likely someone will experience difficulty in applying logic, reason and rationality to their thoughts and behaviours

  • obsessive thoughts are thus more likely if serotonin levels in the frontal cortex are irregular/low

executive functioning in the brain definition

• set of skills and behaviours which means that people are able to manage their time, pay attentions, plan, organise and multitask

neural explanation of OCD (biological approach) - DOPAMINE

• dopamine activity in the dorsomedial striatum (DSM) has been linked to the development of compulsive behaviours

• neural circuits connecting the cerebral cortex to the dorsomedial striatum are thought to control movement and reward-seeking behaviours

  • high levels of dopamine in the DSM increase compulsive reward-seeking

  • this reward-seeking may explain OCD as compulsive behaviours are performed to decrease obsessive thoughts and reduce anxiety

  • thus dopamine reinforces the compulsive behaviours, which are necessary to reduce obsessive thoughts

strengths of the neural explanation of OCD

• antidepressants such as Selective Serotonin Reuptake Inhibitors (SSRIs), which are used to regulate serotonin levels, have also been effective in reducing OCD symptoms

  • this supports the neural theory that irregular levels of OCD are linked to serotonin, making the theory valid

• research into the neural explanation tends to use objective, clinical methods such as fMRI scanning, which increases the reliability

weaknesses of the neural explanation of OCD

• not all OCD sufferers respond positively to SSRIs, which reduces the external validity of the theory as this means the explanation cannot be solely neural

• although sophisticated apparatus (such as fMRIs) are used to measure brain activity in OCD patients, this in itself is not 100% evidence of neurotransmission

  • it is not yet possible to track and measure live neurotransmission

  • thus it is not possible to claim that OCD has neurological correlates; there is no absolute proof of the neural explanation

how SSRIs work

• re-uptake occurs when molecules of serotonin do not cross the synaptic cleft (they have not been transmitted to the postsynaptic neurone)

  • the ‘spare’ molecules of serotonin are then take back up into the presynaptic neurone

• SSRIs work by inhibiting the re-uptake of serotonin in the synaptic cleft back into the presynaptic neurone

  • prevention of re-uptake makes serotonin more accessible in the brain

  • more serotonin is then available to improve the transmission of messages between neurones

• SSRIs are SELECTIVE as the mainly affect serotonin, not other neurotransmitters

name for anti-anxiety drugs

benzodiazepines (BZs)

how BZs work

• BZs are anti-anxiety drugs designed to induce a feeling of calm

• BZs encourage the transmission of gamma-aminobutyric acid (GABA)

  • GABA is a neurotransmitter which works to control neurone hyperacitivity (associated with fear, anxiety and stress)

  • BZs thus help to quieten the brain by reducing neurotransmission - this has been linked to the reduction of obsessive thoughts in OCD patients

strengths of drug therapy for OCD

• drug therapy is cost-effective and widely available

• there is good research support for the efficacy of drug therapy

  • Greist et al (1995) conducted a meta-analysis where they reviewed placebo-controlled trials

  • they found that drugs in each study were significantly more effective than the placebo at reducing symptoms of OCD

weaknesses of drug therapy for OCD

• drug therapies can come with potentially serious side effects, which limits the usefulness of the drugs

  • SSRIs - blurred vision, loss of libido, irritability, indigestion, sleep disturbances

  • BZs - drowsiness, light-headedness, confusion, dizziness, slurred speech

• research supporting drug therapy may be prone to publication bias, as positive results are more likely to be published

  • this is unethical and impairs validity

connection of the orbitofrontal cortex (OFC - worry circuit) to OCD

• OFC contains brain areas which seem to play a crucial role in how humans evaluate information and assign emotional significance to it

• OFC sends ‘worry’ signals to the thalamus in the basal ganglia

• these signals are normally screened by the caudate nucleus (part of the striatum, also in the basal ganglia) and unimportant/irrelevant impulses are filtered out

• in OCD, the caudate nucleus is thought to be damaged so it cannot suppress the signals which becomes increasingly excited, causing obsessive anxious thoughts

evidence for the OFC’s implication in OCD

• Rauch et al (1994) found that PET scans of patients with OCD, taken while their symptoms are active show increased activity in the OFC

  • but Aylward (1996) found that evidence for structural differences in the caudate nucleus is somewhat inconclusive

• Kant et al (1996) found that head injuries (that cause damage) to the basal ganglia can result in OCD-like symptoms

• Max et al (1994) found that surgical disconnection (intentional lesions) of basal ganglia from frontal cortex relives OCD symptoms in SOME patients