OCD Flashcards
- Biological explanation of OCD
What are the 2 biological explainatioms for OCD
-genetic explanations: some people are predisposed to develop the disorder as a result of inherited familial influence.
-neural explanations (neurotransmitters/biochemical and brain structures/physiological)
—> Biochemical explanation - low levels of serotonin associated with anxiety; high levels of dopamine linked to compulsive behaviour / stereotypical movements.
—> Physiological explanation - basal ganglia in the brain responsible for psychomotor functions, hypersensitivity of the basal ganglia may result in repetitive movements; linked to abnormality I excessive activity in the orbital frontal cortex.
- Biological explanation of OCD
Genetics: How do alleles relate to disease vulnerability?
variations in the sequence of nucleotides within a gene.
The diversity in alleles eg: mutations, contributes to variation in humans affecting how genes function.
Depending on the role of the gene, these effects may have no effect, or can be beneficial. But sometimes they cause harmful biological changes, which can lead to various diseases
This is the genetic basis of psychopathological disorders
- Biological explaination of OCD
Genetics: In what way do monozygotic and dizygotic twins differ?
Fraternal (dizygotic, DZ)
eggs released during menstruation and both eggs are fertilised zygotes (fertilised eggs), they share 50% of their DNA
• Identical (monozygotic)
1 egg released during menstruation. Fertilised then splits into two eggs.
Now 2 zygotes, but came from 1 zygote, they share 100% of their DNA
- Biological explanation of OCD
Neurotransmitters: how do neurons communicate
1) Electrical: action potential passes down the body of the neuron to reach the axon terminal to the synaptic gap / synapse
2) Chemical: as the electrical signal arrives at the end of the axon terminal of the pre-synaptic neuron, it causes a neurotransmitter to be released across the synapse Receptors on the post-synaptic neuron on the other side of the synapse The neurotransmitter eg; dopamine binds to the complementry neurotransmitter.
This activation of thr receptors determines whether the post-synaptic neuron will generate a electrical signal
- Biological explanation of OCD
Neurotransmitters:
How might changes in neurotransmitters causes brain disorders?
Changes in communication between neurons can disrupt brain function and lead to psychopathological disorders
- Biological explanation of OCD
Genetic explaination:
What evidence is there from family studies that OCD has a genetic component?
Nestadt eg al. Found first-degree relatives (parents, siblings and children) of OCD sufferers had a higher chance of developing the disorder.
12% chance for those with first degree relatives diagnosed with OCD
3% risk for control group ppts
Marini & Stebnick found people with a family member with OCD is approx 4 times as likely to develop it as someone without
Family members are more closely genetically related so supports genetic vulnerability
- Biological explanation of OCD
Genetic explanation:
Which 3 candidate genes that create vulnerability to OCD?
1) COMT gene
2) SERT gene
3) 5-HT1D
These genes produce changes in neurotransmitters in the brain
- Biological explanation of OCD
Genetic explanation: how does the COMT gene cause changes relevant to OCD?
And who’s research supported this?
Mutation of COMT gene causes low levels of COMT enzyme
This enzyme metabolises neurotransmitters
Low levels of COMT enzyme means less dopamine is metabolised so there’s high levels of dopamine
Supported by: Turkel et al. (2013) found that the low-activity version of the COMT gene was more common in patients with OCD compared to controls.
- Biological explanation of OCD
Genetic explanation: how does the SERT gene cause changes relevant to OCD?
And who’s research supported this?
SERT gene creates/codes for the serotonin transporter protein
Transporters detect the amount of neurotransmitter in the synapse, and remove from the synapse after it’s released.
Mutations of SERT gene can create too much seratonin transporter so serotonin levels go down as the transporter is removing serotonin from the synapse
Supported by: Ozaki et al. found two families with the high- activity version of the gene (which made too much of the protein): 6/7 people in these two families had
OCD.
- Biological explanation of OCD
Genetic explaination: how does the 5HT-1D gene cause changes relevant to OCD? And evidence to support
Chemical name for serotonin is 5HT
Receptor sub types respond differntly to neurotransmitters (1D in 5-HT1D)
5-HT1D gene codes for a pre-synaptic receptor, 5-HT1D
This is a pre-synaptic receptor involved in monitoring the level of serotonin released in the synapse.
Pre-synaptic receptors uptake serotonin back into the presynaptic neuron
Zohar et al. found that while some studies have found associations between certain genetic markers in serotonin receptor genes and OCD, others have not replicated these findings
- Biological explanation of OCD
Genetic explaination: What evidence is there that OCD may be polygenic?
And who supported this?
means OCD is caused by more than one genetic variation that together cause significantly increased vulnerability
Supported by: Taylor found evidence of up to 230 candidate genes - OCD is likely to be polygenic
These are often associated with the functioning of neurotransmitters, such as dopamine and serotonin, both associated with regulating mood.
- Biological explanation of OCD
Genetic explanation:
What does it mean to say that OCD is aetiologically heterogenous?
meaning different combinations of genes cause different types of OCD in different people.
- Biological explanation of OCD
Genetic explanation:
1.4 What is the diathesis-stress model in relation to OCD?
certain genes leave some people more likely to suffer a mental disorder but it is not certain as some environmental stress is necessary to trigger the condition.
Diathesis = genetic vulnerability Stress = environment
suggests that some have a genetic vulnerability towards developing depression. For example, Lewis et al. found that of his OCD patients, 37% had parents with OCD and 21% had siblings with OCD.
Genetic predisposition and childhood trauma can lead to vulnerability to mental disorders. This can either lead to:
1) minimal stressful circumstances resulting in lower probability of mental disorder
Or
2) inability to cope with excessive stressful circumstances resulting in a higher probability of mental disorder
- Biological explanation of OCD
Genetic explaination:
A strength of the genetic explaination
P: the increased concordance between monozygotic compared to dizygotic twins.
Eg: Nestadt (2010) shows that there is a higher concordance rate for OCD in MZ twins (68%) compared to DZ twins (31 %)
Ex: supports the role of genetics in OCD, since MZ and DZ twins grow up sharing similar environments like food, upbringing and education, and life events like bereavement or parental divorce, so non-genetic factors can be controlled for when comparing MZ and DZ twins.
Cou: However, increased concordance rates does not necessarily indicate a role of genetics: monozygotic twins may be treated more similarly because they look alike, compared to dizygotic, non-identical twins. Also, since the concordance rate was 68% and not 100%, there must also be an environmental component to OCD
L: suggests that the additional shared DNA in MZ twins may be responsible for the increased concordance rate, but that this evidence should be treated cautiously, and may be best understood as a diathesis stress model, whereby a genetic vulnerability is inherited and triggered by an environmental stressor
- Biological explanation of OCD
Genetic explanation:
2 limitations of the genetic explanation
1) environmental factors
2) alternative explainatioms
P• there are also environmental factors.
Eg: Cromer et al. ) found that over half of the OCD patients in their sample had experienced a traumatic life event, and that OCD was more severe in those, suggesting a diathesis-stress model, one or more traumas.
Ex: supports the idea that OCD is not entirely genetic in origin, and that environmental factors can also trigger, or increase the risk, of developing OCD.
L: This means that genetic vulnerability only provides a partial explanation for OCD, and may therefore be too reductionist, which limits the validity of this explanation.
P: there are credible alternative explanations for the development of OCD, such as the two-process model proposed by behaviourists, that suggest that learning plays a crucial role.
Eg: Eg: Albucher eg al. found in the success of behavioural treatments for OCD where symptoms of patients are improved for 60-90% of adults
Eg: Initial learning of the feared stimulus could occur through classical conditioning’s associative process where, for example, dirt is paired with anxiety. This behaviour pattern would be maintained through operant conditioning and negative reinforcement whereby the stimulus is avoided so the anxiety is removed. This could result in an obsession forming which is linked to the develooment of a combulsion e.g. washing of hands, which serves to reduce the anxiety felt.
L: This suggests that the genetic model may only provide a partial explanation for
OCD
- Biological explanation of OCD
Neural explanations: how are neurotransmitters important?
COMT AND SERT and 5-HT1D genes produced changes in neurotransmitters
Neurotransmitters are important for communication within the brain. They can either excite or inhibit neurons - either increase or decrease brain activity.
- Biological explanation of OCD
Neural explanations: how is serotonin involved in OCD? And who supports this
important for the regulation of mood. It has an overall calming effect on the brain.
Low levels of it means the brain doesn’t communicate information about mood effectively
The reduction of it functioning is linked to OCD
Low levels of serotonin have been associated with the symptoms of OCD e.g. anxiety
The reduction of serotonin can explain some cases of OCD
SUPPORTED BY: Piggot et al. reported that SSRIs, which reduce the uptake of serotonin, and so prolong its action at the synapse, are effective in treating OCD
- Biological explanation of OCD
Neural explanations: how is dopamine involved in OCD?
Dopamine: neurotransmitter which is important for maintaining interest and motivation
High levels of dopamine help to maintain a compulsive thought or behaviour, leading to some of the symptom of OCD, in particular, compulsive behaviours
Dopamine levels are thought to be abnormally high in people who suffer from OCD
Denys et al. Found that patients with OCD have increased dopamine D2 receptor availability in the striatum, which correlates with the severity of OCD symptoms
- Biological explanation of OCD
Neural explanations:
What 3 brain regions are implicated in OCD?
basal ganglia (made up of the putamen and caudate head)
orbitofrontal cortex.
parahoppocampal gyrus
- Biological explanation of OCD
Neural explanations: how is the region basil ganglia assossiated with OCD and research to support
It’s involved in multiple processes, including the coordination of movement. Patients who suffer head injuries in this region often develop OCD-like symptoms, following their recovery.
made up of the putamen and the cluster of neurons, including the caudate nucleus
Max et al. (1994) found that when the basal ganglia is disconnected from the frontal cortex during surgery, OCD-like symptoms are reduced, providing further support for the role of the basal ganglia in OCD.
- Biological explaination of OCD
Neural explanations: how is the region orbitofrontal cortex is assossiated with
OCD
Region which converts sensory information into thoughts and actions. PET scans have found higher activity in the orbitofrontal cortex in patients with OCD. it may increasethe conversion of sensory information to actions (behaviours) which results in compulsions. The increased activity also prevents patients from stopping their behaviours.
- Biological explanation of OCD
Neural explanations: explain the parahippocampal gyrus region linked to OCD
an area of cortex close to the hippocampus on the brain’s underside, is also linked to OCD. It is responsible for regulating and processing unpleasant emotions and has been seen to function abnormally in cases of OCD.
(Kwon et al., 2009)
- Biological explaination of OCD
Neural explanations: explain the ‘Worry circuit linked to OCD
1) OFC involved in converting sensory info into thoughts and actions. It sends ‘Worry’ signal to basil ganglia to report on things which should cause worry, e.g. a potential germ hazard or a door which might not be locked.
2) In normal functioning, the basal ganglia filter out minor worries coming from the OFC, but if this area is hyperactive, even small worries get to the thalamus, which is then passed back to the OFC, forming a loop (recurring obsessive thoughts)
3) Repetitive motor functions (compulsions) are an attempt to break this loop. While carrying out the compulsion may give temporary relief, the hyperactive basal ganglia will soon resume the worry circuit.
- Biological explanation of OCD
Neural explanations: explain the parallel cortio-striatio-thalamic-circuit in OCD
OCD is a frontal striatal disorder
The 2 out of the 5 parallel circuits assossiated with OCD is the
-‘sensorimotor’ CSTC circuit: the stimulus-response-based habitual behaviour
-‘ventral motivatiomal’ CSTC circuit: stimulus outcome based motivational behaviour
- Biological explanation of OCD
Neural explanations: 2 strengths of the neural explaination of OCD
OFC has empirical supportive evidence from structal and functional imaging studies
• empirical evidence from the effects of SSRI’s that neurotransmitters do play a role
P: OFC has empirical supportive evidence from structal and functional imaging
studies
Eg: Menzies et al. found that OCD sufferers and their family members had reduced grey matter in the key regions of the brain including the OFC. In addition, several neuroimaging studies using PET scanners have shown hyperactivity in the OFC and the caudate nucleus in people with OCD both while scanning the brain at rest and when symptoms are stimulated
Ex: This supports the involvement of the ventral motivation cortico-striato-thalamic circuit in OCD, also known as the ‘Worry circuit’
Cou: However, one problem with this evidence is that it is correlational: researchers cannot be sure if the hyperactivity in these areas is the cause of OCD or a consequence of having OCD. Maia et al. (2008) reviewed evidence from other lines which permitted stronger causal inferences, including the development of OCD following brain injury, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and neurosurgical lesions that attenuate OCD.
L: findings therefore suggest that there are multiple lines of evidence which support the
involvement of the OFC and caudate in OCD, which strengthens the involvement of the OFC and caudate in OCD, which strengthens the validity of the biological explanation
P: empirical evidence from the effects of SSRI’s that neurotransmitters do play a role Eg: A meta-analysis by Soomro et al. (2008) demonstrated SSRIs are more effective than placebos, suggesting there is serotonergic involvement in OCD
Ex: These drugs are effective at reducing OCD symptoms, and SSRIs work by increasing the levels of this neurotransmitter by blocking the serotonin reuptake process, the data therefore suggests that serotonin does play a role in OCD.
Cou: However despite altering levels of serotonin in the synapse within hours, these drugs take weeks to reduce symptoms, and 40% to 60% of patients show no or just partial symptom improvement
L: findings suggest low levels of serotonin have a role to play in OCD but are not the sole cause of OCD
- Biological treatment of OCD
What does SSRI stand for?
Give 1 example of an SSRI
Selective serotonin reuptake inhibitors
Common Brand names include: prozac (flouxitine) and sertraline
- Biological treatment of OCD
What levels of serotonin are associated with OCD and how does this link to SSRI’s
Low levels of serotonin neurotransmitters
SSRI increase levels of serotonin in the brain to regulate mood and anxiety
Remember: high levels of serotonin transporter = low levels of serotonin bc the
transporter is removing serotonin from the synapse
- Biological treatment of OCD
How do SSRI’s work
Neurotransmitters are stored in pre-synaptic vesicles
-when an action potential stimulates it, the vesicle is pushed to the end of the axon terminal and fuses with the presynaptic neurons membrane to release the neurotransmitters stored inside it across the synapse from the pre-synaptic neuron to the post-synaptic neuron
-the neurotransmitter bind to the post-synaptic receptors which increase or decrease the likelihood of the post-synaptic neuron firing (excites it over the threshold charge so more likely and inhibits lower than the threshold charge so less likely) -the neurotransmitter is cleared from the synapse by reuptake mechanisms
-serotonin is a neurotransmitter
-OCD is thought to involve a lack of serotonin at the synapse
-SSRI’s block the reuptake of serotonin, so increase its presence at the synapse
-this reduces symptoms of OCD as the serotonin transporter is removing less serotonin from the synapse so there’s an increase in serotonin levels
SSRI’s interfere with step between 3 and 4:
-when serotonin is released into the synapse (step 3), it either binds to the postsynatic receptors (step 4) or it’s removed from the synapse by reuptake mechanisms
- SSRI’S block this reuptake, so more serotonin is present in the synapse so it can bind to post-synaptic receptors
- Biological treatment of OCD
What are the 3 alternatives to SSRI’s
Tricyclic antidepressants
-SNRI’s (serotonin and noradrenaline reuptake inhibitors)
-benzodiazepines
- Biological treatment of OCD
What does SNRI’s stand for and give 2 examples
serotonin and noradrenaline reuptake inhibitors
Venlafaxime and duloxetine
- Biological treatment of OCD
How do SNRI’s work (mechanism)?
SNRI’s (more selective than tricyclics) block the transporter mechanism that re-absorbs serotonin and noradrenaline
-there’s a lot of evidence supporting the idea that noradrenaline is involved in OCD.
In low levels: person is unable to focus their attention which can result in anxiety and compulsions
-although low noradrenaline may not cause OCD, preventing reuptake of this neurotransmitter (increasing it) has been assossiated to relief symptoms and anxiety
- Biological treatment of OCD
How are SNRI’s used clinically
-2nd line of treatment for those non-responsive to SSRI’s
-they habe an advantage of targeting more than one neurotransmitter.
-BUT they have greater side effects so only used as a 2nd line treatment if SSRI’s aren’t effective
- Biological treatment of OCD
Give an example of tricyclic antidepressants
Clomipramine - 1st medication approved for OCD
- Biological treatment of OCD
How do tricyclic antidepressants work
increase serotonin and noradrenaline by blocking their reuptake, causing increase
I’m levels of these transmitters at the synapse.
-they act at various other receptors (makes them less selective) so can contribute to clinical efficiency and also side effect
- Biological treatment of OCD
How are tricyclic antidepressants used clinically
Has more servere side effects that SSRI’s, so used only for those who don’t respond to SSRI’s and SNRI’s
- Biological treatment of OCD
Give an example of benzodiazepines
Valium and diazepam
- Biological treatment of OCD
How do benzodiazepines work
increase activity of neurotransmitter GABA (gamma-aminobutyric) which is an inhibitory neurotransmitter, which calms and reduces activity of neurons
-when GABA docks at the receptor site of a neuron, it makes it less likely to fire an action potential
- Biological treatment of OCD
How are benzodiazepines used clinically
commonly used to reduce anxiety
- Biological treatment of OCD
Give 2 strengths of drug therapy/treatment of treating OCD
P: drug therapy is more cost effective and less disruptive on patients life compared to talking therapies
Eg: As SSRIs are cheaper than talking therapies it has economic implications for the
UK. It is better for the NHS as it could reduce the financial pressure on an already struggling public service
Ex: Drug therapies are also less disruptive on a patients life. The patient just needs to take one tablet a day compared to attending weekly sessions and completing homework for CBT
Cou: However, a systematic review by Skapinakis et al. (2016) found that cognitive and behavioural (exposure) therapies were more effective than SSRIs for OCD L: For these reasons drug therapies can be the preferred treatment for many patients, however, increased efficacy of SSRIs may be a better long term solution
P: drug treatment has considerable supporting evidence
Eg: Eg: Soomro 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
Ex: This supports 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.
Cou: 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.
L: suggests that randomized, 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
- Biological treatment of OCD
Give 2 limitations of the biological approach to treating OCD
P: drug therapy often has unpleasant side effects
Eg: Even first line treatments such as SSRIs can cause indigestion, blurred vision and a loss of sex drive. Clomipramine can also cause more serious problems: more than 1 in 10 experience erectile dysfunction and weight gain; 1 in 100 become aggressive and experience heart-related problems.
Ex: Ashton (1997) recommends that drugs for OCD are used for no longer than 4 weeks due to the side effects.
L: It could therefore be argued that drug therapies are therefore not an effective long- term treatment for OCD.
P: drug treatments are critisized for treating the symptoms of the disorder and not
the cause
Eg: Koran et al. (2007) suggest that psychological treatments such as CBT may be a more effective long-term solution to provide a lasting treatment and a potential cure
Ex: because although SSRIs work by increasing the levels of serotonin 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 are
prone to relapse
L: suggests that the biological issues that drug treatments are intended to target may
not be fundamental to the disease, so only have symptomatic effects. This means
that the use of drug therapy is only a temporary treatment for OCD, and that the
biological causes of the disease may be unknown.
Describe one drug therapy that has been used to treat obsessive-compulsive disorder
(OCD). Identify one limitation of drug therapy.
use of SSRIs eg fluoxetine
acts to inhibit the re-uptake or re-absorption of serotonin in the brain
enabling the serotonin to remain active at the synapse
where it continues to stimulate the post-synaptic neuron
Define genetic Variation
as a result of allelic variation, individuals have different physical manifestations; these manifestations can affect psychological functioning, where the proteins involved impact brain function
