Psychopthology : Biological Approach to OCD (treating) Flashcards
Whats SSRI?
Selective serotonin re-uptake inhibitors (common brands are Prozac and Sertraline) → the 1st line treatment for OCD
Why do SSRIs work?
Low levels of serotonin are associated with OCD aswell as depression. SSRIs increase levels of serotonin in the brain- regulating mood and anxiety.
How do SSRIs work?
• neurones are stored in pre-synaptic vesicles
• when stimulated by action potential, the vesicles release the neurotransmitters across the synapse, from the pre-synaptic neurone to the post-synaptic neurone
• the neurotransmitter binds at the post-synaptic receptor, which increases/ decreases the likelihood of the post-synaptic neurone tiring
• the neurotransmitter is then cleared from the synapse by re-uptake mechanisms
• SSRIs block the re-uptake of serotonin, increasing it’s presence and reducing OCD symptoms
What are SNRIs?
Serotonin and noradrenaline re-uptake inhibitors, eg: venlafaxine, duloxetine → 2nd line treatment for those non-responsive to SSRIs
How do SNRIs work?
• SNRIs (more selectively vs tricyclics) block the transporter mechanism that re-absorbs both serotonin and noradrenaline
• not much evidence that noradrenaline is involved in OCD but when levels are low, a person is unable to focus their attention which may result in anxiety and compulsions
• although it’s not the cause, increasing it has been associated with relief of symptoms and anxiety
What are tricyclic antidepressants?
an older type of antidepressant, first medication approved for OCD, eg: clomipramine → has more severe side-effects than SSRIs, so only used for those who don’t respond to SSRIs or SNRIs
How do tricyclic antidepressants work?
• increase serotonin and noradrenaline by blocking their re-uptake
• also act as various other receptors (less selective), which may not contribute to both the clinical efficacy and side effect
What are benzodiazepines?
BZs, eg: Valium and Diazepam → commony used to reduce anxiety
How do benzodiazepines work?
• increasing activity in the neurotransmitter GABA (gamma-aminobutyric acid) → an inhibitory neurotransmitter which calms and reduces the activity of neurones.
• when GABA docks at the receptor site of a neurone, it makes it less likely to fire an electrical signal (action potential)
Advs of SSRIs to treat OCD
• more cost effective + less disruptive on patients lives us talking therapies → SSRIs are cheaper than talking therapies (reduces financial pressure on the struggling public service). Drug therapies are also less disruptive on a patients life as they only need to take a set amount of tablets a day (based on diagnosis) compared to weekly sessions and completing HW for CBT. However, a systematic review by Skapinakis et al (2016) found that cognitive + behavioural (exposure) therapies were more effective than SSRIs for OCD
• considerable supporting evidence → Soomo et al (2009) reviewed studies comparing SSRIs to placebos in the treatment of OCD and concluded that all 17 studies (meta-analysis) showed significantly better results for the SSRI groups in the short term, supporting the argument that biological treatments are effective as on average 70% of OCD patients had improved symptoms with drug therapy, also suggesting serotonin has a role in the development of the disorder. However, a limitation of the studies is that they were typically 3-4 months long and therefore there is little data on the long-term effects of drug therapy. This suggests that randomised, double-blind clinical trials of SSRIs of 12 months or longer to establish whether efficacy observed in shorter trials is maintained, and whether additional side effects emerge.
Disadvs of SSRIs to treat OCD
• drug treatments are critisised for treating the symptoms of the disorder and not the cause → Koran et al (2007) suggests that psychological treatments such as CBT may be a more effective long-term solution to provide a lasting treatment and a potential cure as although SSRIs work by increasing serotonin levels in the brain, which reduces anxiety and alleviates the symptoms of OCD, but it does not treat the underlying cause of OCD. Furthermore, once a patient stops taking the drug, they’re prone to relapse, suggesting the biological issues that drug treatments are intended to target may not be fundamental to the disease, so any have symptomatic effects.
• publication bias → Turner (2008) claims there’s evidence to show a ‘favourable outcome’ publication bias that more studies are published in peer review journal that show the treatment to be effective. This could be critically explained by the fact that drug companies often sponsor the research into the effectiveness and therefore have a strong interest in continuing success. Currently, many drug companies don’t publish all results and could be suppressing evidence.
