OCD

behavioural characteristics of OCD

compulsive behaviour: 2 elements - repetition (typically feel compelled to repeat a behaviour) and anxiety reduction. compulsions reduce anxiety: around 10% of sufferers of OCD show compulsive behaviour alone - they have no obsessions, just a general sense of irrational anxiety. but, for the vast majority compulsive behaviours are performed in an attempt to manage the anxiety produced by obsessions. e.g. compulsive handwashing is carried out as a response to an obsessive fear of germs.

avoidance:
- attempt to reduce anxiety by keeping away from the situations that trigger it.
- e.g. people who wash compulsively may avoid coming into contact with germs. but, this avoidance can lead people to avoid very ordinary situations, such as emptying their rubbish bins, this can interfere with leading a regular life.

emotional characteristics of OCD

anxiety and distress:
- OCD is regarded as a particularly unpleasant emotional experience cuz of the powerful anxiety that accompanies both obsessions and compulsions
- obsessive thoughts are unpleasant and frightening, and the anxiety that comes with these can be overwhelming
- the urge to repeat a behaviour (a compulsion) creates anxiety

accompanying depression:
- anxiety can be accompanied by low mood and lack of enjoyment in activities
- compulsive behaviour tends to bring some relief from anxiety but this is temporary

guilt and disgust:
- irrational guilt, e.g. over minor moral issues
- disgust may be directed at something external like dirt, or at the self

cognitive characteristics of OCD

obsessive thoughts:
- for around 90% of people with OCD the major cognitive feature of their condition is obsessive thoughts, i.e. thoughts that recur over and over again
- these vary considerably from person to person but are always unpleasant
- e.g. worries of being contaminated by germs

cognitive coping strategies:
- e.g. a religious person tormented by obsessive guilt may respond by praying or meditating
- this may help manage anxiety but may make the person appear abnormal to others and can distract them from everyday tasks

insight into excessive anxiety:
- aware that their obsessions and compulsions are not rational (this is necessary for a diagnosis of OCD)
- in spite of this insight, people with OCD experience catastrophic thoughts about the worst case scenarios that might occur if their anxieties were justified
- tend to be hypervigilant, i.e. they maintain a constant alertness and keep attention focused on potential hazards

the genetic explanation

focuses on whether individuals inherit a genetic pre-disposition to developing OCD.

This would mean that individuals inherited specific genes from their parents that are related to the onset of OCD. OCD is likely to involve many genes so it is a polygenic disorder. Taylor (2013) found evidence that up to 230 different genes may be involved in OCD.

different types of OCD:
One group of genes may cause OCD in one person but a different set of genes may cause the disorder in another person - known as aetiologically heterogenous (more than one cause).

family and twin studies

family studies have shown that relatives of OCD are more vulnerable to developing OCD. e.g. Nestadt et al (2000) → first-degree relatives (i.e. parents, siblings) of OCD sufferers had an 11.7% chance of developing the disorder compared to a 2.7% risk in first-degree relatives of control patients without OCD.

Twin studies have also been used to investigate the role genetics play in developing OCD. They involve a comparison between MZ and DZ twins. MZ share 100% of their genes and DZ share only 50% so if genes do play a role in developing OCD we’d expect to find a higher concordance rate for MZ than DZ. e.g. Carey and Gottesman (1981) found MZ had a concordance rate of 87% for obsessive symptoms and features compared to 47% in DZ.

candidate genes

genes that give a person a vulnerability to OCD.

the COMT gene:
- regulates the production of the neurotransmitter dopamine that has been implicated in OCD. All genes come in different forms and one form of the COMT gene has been found to be more common in OCD patients than with people without the disorder.
- Tukel et al (2013) → this form of the COMT gene produces higher levels of dopamine. This in turn can lead to over activity in the basal ganglia (the worry circuit in the brain).

the SERT gene:
Also called the 5-HTT, the SERT gene is thought to affect the transport of serotonin creating lower levels of the neurotransmitter. These changed levels of serotonin are also implicated in OCD.

candidate genes - the diathesis-stress model

genotype & phenotype: biology, specifically genetics, aren’t the sole reason why an individual can develop OCD. an individual may have a genetic vulnerability to develop OCD (i.e. they have SERT or COMPT gene) but, this gene alone doesn’t cause OCD, the interaction with our environmental triggers and the gene combined causes OCD.

Diathesis-stress model: genetic mutations in the COMT or SERT genes may lead to a vulnerability to OCD, other factors (stressors) need to be present for the condition to manifest itself. Diathesis - biological predisposition or tendency towards. Stress - environmental trigger e.g. childhood experiences.

neural explanations

include biochemical causes (e.g. the role of neurotransmitters) and neurophysiological causes (certain areas of the brain e.g. the orbitofrontal cortex)

biochemical causes

neurotransmitters, in particular serotonin and dopamine, have been found to play a role in OCD.

Serotonin: If a person has low levels of serotonin then normal transmission of mood-relevant info doesn’t take place which means mood, and sometimes other mental processes, are affected. e.g. when low serotonin levels are experienced by someone with OCD, it can make them edgier and more hyperaware of their environments than usual, resulting in increased OCD-related behaviours such as obsessive hand-washing, counting or organising. Piggott et al. (1990) → drugs which increase the level of serotonin in the synaptic gap are effective in treating patients with OCD, suggesting that serotonin is a contributory factor.

Dopamine: High levels of dopamine have been linked to OCD. This may be cuz dopamine is thought to influence concentration which could explain why OCD individuals experience an inability to stop focussing on obsessive thoughts and repetitive behaviours.

neurophysiological causes

research has found sufferers of OCD have elevated levels of activity in the orbitofrontal cortex and the caudate nucleus (located in the basal ganglia).

PET scans of patients with OCD have shown higher levels of activity in the OFC. The orbitofrontal cortex is part of a brain circuit; one of the functions of this circuit appears to be turning sensory info into thoughts and actions. Primitive impulses, e.g. to check and clean, arise from the orbitofrontal cortex in response to sensory inputs.

how does the circuit relate to OCD?

the orbital frontal cortex sends a message of panic to the caudate nucleus. A normal brain would decide whether or not this issue is important and if it is, it would get passed on to the thalamus to take action. If the message isn't important or has already been dealt with it will filter out ending the circuit. but, in a brain of an OCD sufferer, the caudate nucleus doesn’t work correctly and sends the potentially faulty message of panic to the thalamus which then sends strong signals back to the OFC which carries out the action e.g. washing hands. This will keep repeating on a loop which is why someone with OCD performs compulsions which are repetitive rituals.

e.g. a non-suffer of OCD may have an impulse to wash dirt from their hands; once this is done the impulse to perform the activity stops and so does the behaviour. It may be that the brains of those with OCD have difficulty switching off these impulses so that they turn into obsessions, resulting in compulsive behaviour.

AO3 - evaluations of genetic explanation

strength: evidence from twin studies
Nestadt et al. (2010) reviewed twin studies and found that 68% of MZ shared OCD as opposed to 31% of DZ twins.

strength: evidence from family studies
research has found that a person with a family member diagnosed with OCD is around 4x as likely to develop it as someone without (Marini and Stebnicki 2012).

limitation: there are environmental risk factors
OCD doesn’t appear to be entirely genetic in origin and it seems that environmental risk factors can also trigger or increase the risk of developing OCD. Cromer et al. (2007) → over half the OCD clients in their sample had experienced a traumatic event in their past. OCD was also more severe in those with one or more traumas. This means that genetic vulnerability only provides a partial explanation for OCD.

AO3 - evaluations of neural explanation

strength: supporting evidence
Antidepressants that work purely on serotonin are effective in reducing OCD symptoms and this suggests that serotonin may be involved in OCD. Also, OCD symptoms form part of conditions that are known to be biological in origin, such as the degenerative brain disorder Parkinson's disease, which causes muscle tremors and paralysis (Nestadt et al. 2010). If a biological disorder produces OCD symptoms, then we may assume the biological processes underlie OCD.

limitation: the serotonin-OCD link may not be unique to OCD
Many people with OCD also experience clinical depression. Having two disorders together is called co-morbidity. This depression probably involves (though isn’t necessarily caused by) disruption to the action of serotonin. This leaves us with a logical problem when it comes to serotonin as a possible basis for OCD. It could simply be that serotonin activity is disrupted in many people with OCD cuz they’re depressed as well. This means that serotonin may not be relevant to OCD symptoms.

biological therapies (drugs) for treating OCD

aim to increase or decrease levels of neurotransmitters in the brain. Low levels of serotonin are associated with OCD, thus drugs work in various ways to increase the level of serotonin in the brain.

1 - Anti-depressants (e.g. SSRI's such as Prozad)
2 - anti-anxiety drugs (e.g. Benzodiazepines)

anti-depressants (e.g. SSRI's such as Prozad)

anti-depressants work by raising levels of serotonin in the brain (as low levels of serotonin have been linked with an increased likelihood of OCD).

Prozac works by reducing the rate of re-absorption enabling the serotonin to remain active at the synapse, where it continues to stimulate the post-synaptic neuron. If Serotonin levels don't drop and the patient's mood can remain constant they’re less likely to suffer from obsessive thoughts and compulsions.

Since low serotonin levels are implicated in the brains' ‘worry circuit’, increasing serotonin may have the effect of normalising this circuit. Prozac is usually taken over the course of weeks, months or even yrs.

anti-anxiety drugs

anti-anxiety drugs, e.g. Librium, slow down the activity of the CNS. They do this by enhancing the activity of GABA (gamma-aminobutyric acid) this has a generalised quietening effect on the neurones in the brain. Basically, shutting down the 'worry circuit'.

often also referred to as minor tranquillisers, Benzodiazepines (BZs) include Librium, Valium and Diazepam. are used to treat a range of anxiety disorders but they’re also a key method used to treat the symptoms of OCD. They enhance the activity of GABA which has a general quietening effect on many brain neurones.

GABA is a neurotransmitter that is the body's natural form of anxiety relief. Sufferers of OCD often experience lots of anxiety due to their obsessions and compulsions. when GABA locks into these receptor sites in the brain it opens a channel that increases the flow of chloride ions into the neurone. Chloride ions make it harder for the neurone to be stimulated by other neurotransmitters, thus slowing down activity and making a person feel more relaxed (has a calming effect).

BZ's work by enhancing the activity of GABA which reduces levels of anxiety, (persistent and inappropriate or forbidden ideas create excessively high levels of anxiety in people who have OCD so anti-anxieties aim to reduce this tension and nervousness). BZs react with GABA receptors on the receiving neurone. The neurone's activity is slowed down and induces feelings of relaxation. BZs are sedatives and they also act to decrease heart and respiration rate and thus reduce feelings of anxiety.

Drugs are often used alongside CBT. The drugs reduce a patient's emotional symptoms, such as feeling anxious or depressed. This means that patients can engage more effectively with CBT.

SSRIs (selective serotonin reuptake inhibitor)

prevent the re-absorption and breakdown of serotonin. This results in more serotonin being made available in the synapse. Increasing levels of serotonin can result in improved symptoms for the sufferer.

when serotonin is released from the pre-synaptic neurone into the synapse, it travels, and binds, to the receptors on the post-synaptic neurone. Serotonin which isn’t absorbed into the post-synaptic neurone is reabsorbed into the pre-synaptic neurone. SSRIs increase the level of serotonin available in the synapse by preventing it from being reabsorbed into the pre-synaptic neurone cell. this results in more serotonin being received by the post-synaptic neurone.

One type of SSRI is Fluoxetine. If SSRIs prove ineffective then the dose can be increased or it can be combined with other drugs. Sometimes alternative drugs are given as patients can respond differently to different drugs. Two other examples of drug treatments are; Tricyclics, which have the same effect as SSRI's (but these are generally only used when patients don’t respond to SSRIs as the side effects are more severe) and SNRIs, which are newly developed anti-depressants that increase the level of serotonin and noradrenaline.

As a treatment for OCD, it’s common for drugs to be used alongside other treatments, such as CBT.

AO3 - evaluations of biological treatments of OCD

strength: effective
Soomro et al. (2009) reviewed studies comparing SSRIs to placebos in the treatment of OCD and concluded that all 17 studies reviewed showed significantly better results for SSRIs than for placebo conditions. suggests that altering serotonin levels in OCD patients often helps to reduce the symptoms and that despite drug treatments not always being completely effective, they should still be considered as a possible treatment option for people who suffer from OCD.

limitation: not always appropriate
Patients can experience a number of side effects with drug treatments. e.g. loss of appetite, loss of sex drive, irritability, etc. This could mean that it may not always be an appropriate treatment for all OCD sufferers plus if the side effects are severe enough, it could lead to the patient stopping the treatment all together.

strength: less disruptive
drug therapies require little input form the patient in terms of time and effort. Also, drugs are cost effective and non-disruptive. Drugs are less disruptive to patients' lives than psychological therapies. CBT requires the patient to attend regular meetings and put considerable thought into tackling their problems, as well as requiring the therapists time. drug therapies more economical for the health service than psychological therapies.
COUNTER: Drug therapy isn’t always appropriate. evidence suggests that OCD is not always biological in origin and could be caused by a response to traumatic life events. thus psychological therapies may be more appropriate to treat these cases of OCD.