Psychopathology

OCD:

• Obsessions

• Compulsions

• Obsessions

What people think about, which lead to extreme feelings of extreme anxiety (cognitions).

• Compulsions

What people do as a result of the obsessions (the behaviour). They comprise intense, uncontrollable urges to repetitively perform tasks and behaviours.

Different types of OCD

• Hygiene and contamination e.g. washing hands and clothes.

• Counting and numbers e.g. multiples.

• Hoarding and collecting.

• Fear of harming others e.g. children.

Different types of behaviours within OCD

• Behavioural

• Emotional

• Cognitive

Behavioural

• Compulsive behaviour - repeating a behaviour to help reduce anxiety.

• Avoidance - keeping away from situations that trigger it.

Emotional

• Anxiety and distress - obsessive thoughts → unpleasant / frightening → anxiety → urge to repeat compulsion → anxiety.

• Accompanying depression - anxiety is often accompanied by low mood and lack of enjoyment in activities. It can also involve irrational guilt or disgust (directed at the self or something external).

Cognitive

• Obsessive thoughts - major cognitive feature.

• Hyper-vigilant - i.e. maintain constant alertness and attentions focused on potential hazards.

Genetic explanations

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

• OCD is polygenic - meaning it can not be caused by one single gene, but several genes are involved. Taylor (2003) suggested that as many as 230 genes may be involved - different variations of genes are likely to contribute to different types of OCD.

• The COMT gene - regulates the neurotransmitter dopamine, has a variation which results in higher levels of dopamine (found to be common in people with OCD).

• The SERT gene - linked to neurotransmitter serotonin and affects the transport of the serotonin, causing lower levels of serotonin (also associated with OCD).

Family studies and Twin studies

Family studies:

• Relatives of OCD are more vulnerable to developing OCD. Nestadt et al (2000) found lifetime prevalence of OCD was 11.7% in people who had first- degree relatives (e.g. parents, siblings) with OCD

• In comparison to 2.7% in the control group who had no first-degree relatives with OCD.

Twin studies: (comparing MZ, identical twins, and DZ, non-identical twins)

• MZ twins share 100% of their genes where as DZ share only 50% of their genes

• If genes do play a role in developing OCD there would be a higher concordance rate for MZ than DZ.

• For example, Carey and Gottesman (1981) found MZ twins had a concordance rate of 87% and DZ twins had a 47% concordance rate (for obsessive symptoms and features).

Evaluation of genetic explanations

• R - supporting evidence

• I - research on twin studies

• A - diathesis stress model

Supporting evidence:

• Consistent evidence from twin and family studies suggests that genetic factors are important in developing OCD.

• Nestadt et al (2010) reviewed previous twin studies and found that 68% of identical twins shared OCD as opposed to 31% of non- identical twins. This study supports the link between genetics and OCD as MZ twins share 100% of their genes whereas DZ twins only share 50%.

• Therefore as the concordance rates and percentages are higher for MZ twins this shows that genetics must play a role in developing OCD.

Research on twin studies:

• Research supporting twin studies suggests there may be a genetic influence, however it is not the only cause of the disorder. If OCD was entirely caused by genetics we would expect the concordance rates for identical twins to be 100% (as they share 100% of their genes) which they are not.

• Suggesting there are other factors that play a role in OCD. For example, cognition or the small differences in the environments of twins.

Diathesis stress model:

• Evidence suggests some are more susceptible to OCD however it does not suggest that genes are the sole cause of OCD. It seems that environmental factors also trigger or increase the risk of developing OCD.

• For example, Cromer et al (2007) found over half the OCD sufferers in their sample had a traumatic event in their past, and that OCD was more severe in those with more than one trauma.

• Suggesting the genetic explanation alone is not a sufficient to explain OCD and the diathesis-stress model would be a more suitable explanation.

Neural explanations

The neural explanations for OCD include both the role of neurotransmitters and abnormal brain functions.

Neurotransmitters

• Low levels of serotonin

• High levels of dopamine

Low levels of Serotonin → obsessions / anxiety

• Serotonin may be removed too quickly before it transmits its signal, resulting in abnormal transmission of mood-related information. Suggested to be linked to obsessive thoughts and anxiety that people with OCD experience.

• Pigott (1990) found that anti-depressant drugs (+ serotonin) have been shown to reduce OCD symptoms.

High levels of dopamine → compulsions

• High levels of dopamine have been linked to OCD symptoms, especially compulsive behaviours.

• Abnormalities in dopamine levels may contribute to the reward-seeking aspect of compulsions. Individuals with OCD often experience relief + gratification after performing their rituals (could involve dopamine pathways).

• Kim et al (2007) gave OCD sufferers drugs that affected their dopamine levels and found this was correlated with less compulsive behaviours.

Neural explanations evaluation

• R - supporting evidence

• I - causation

• A - drug therapies

Research - supporting evidence

• Hu (2006) compared serotonin activity in 169 OCD sufferers and 253 non-sufferers, finding serotonin levels to be lower in the OCD group.

• Soomro et al (2009) found SSRIs were more effective than placebos in reducing symptoms of OCD. These studies support the link between low levels of serotonin and OCD.

Issue - causation

• Although the supporting evidence shows a link between neurotransmitter activity and OCD it does not provide any causal evidence. It is possible that low levels of serotonin or high levels of dopamine is an effect of having the disorder rather than being the cause of it.

• Not all OCD sufferers respond to SSRI treatment suggesting that other factors could play a role. Therefore, this explanation could be seen as limited as there are no firm conclusions to what actually causes OCD.

Application - drug therapies

• Understanding the role neurotransmitters play in OCD has led to the development of treatments such as drug therapies.

• SSRIs are used as a treatment for OCD and have been found to be successful in reducing the symptoms (Soomro et al, 2009). This highlights the usefulness of the neural explanations as well as providing further support for the idea that low serotonin levels are involved in OCD.

Abnormal brain functions

• ‘The worry circuit’ for a sufferer of OCD

• Research using PET scans shows that OCD sufferers have elevated levels of activity in the orbitofrontal cortex and the caudate nucleus (located in the basal ganglia).

• The OFC is part of a brain circuit also known as ‘the worry circuit’. The OFC is thought to turn sensory information into thoughts and actions.

• When the OFC detects something is wrong it sends a ‘worry’ signal to the thalamus.

• These signals are normally suppressed or filtered by the caudate nucleus, however if the caudate nucleus does not work correctly it cannot filter the worry signals leading to the thalamus becoming overactive.

• When this happens, the thalamus sends strong signals back to the OFC to carry out an action (e.g. washing hands). This leads to an overactive worry circuit (the worry message keeps repeating on a loop) which could explain why people with OCD perform compulsions which are repetitive rituals.

Evaluation of ‘the worry circuit’

• R - supporting evidence

• I - challenging evidence

• A - causation

Research - supporting evidence

• Review of brain-imaging research show elevated activity in the orbital region and the caudate nucleus has been found consistently in OCD sufferers compared to healthy controls.

• After treatment, activity in these brain areas reduces to a level comparable to that of controls as found by Saxena and Rauch (2000). This supports the neurophysiological explanation as it shows that these areas of the brain are linked to OCD.

Research - challenging evidence

• Many neural mechanisms have been identified but these are not always present in all OCD cases. Neuroimaging studies have so far failed to identify basal ganglia impairments in all OCD sufferers, and some people with brain impairments involving the basal ganglia show no signs of OCD (Ring and Serra Mestres, 2002).

• This suggests there may be other factors that are also involved in OCD. Therefore, this neural explanation does not provide a complete explanation of OCD.

Issue - causation

• Supporting evidence shows a link between abnormal brain functions and OCD, however there is no evidence. This means an overactive worry circuit can not be concluded as the cause.

• It is possible that having OCD leads to changes in the brain meaning that abnormal brain functions are an effect of having OCD rather than the cause. Therefore, this explanation could be seen as limited as no firm conclusions can be made as to what actually causes OCD.

The biological approach to treating OCD

• What drugs relating to OCD do

• An example of a drug for OCD

• In relation to OCD, drug therapy consists of drugs that increase levels of the neurotransmitter serotonin.

• SSRIs (selective serotonin reuptake inhibitor) are a type of antidepressant drug which 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.

How SSRIs work

• In relation to OCD, drug therapy consists of drugs that increase levels of the neurotransmitter serotonin.

• SSRIs (selective serotonin reuptake inhibitor) are a type of antidepressant drug which 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.

Evaluation for biological treatment

• Effectiveness

• Appropriateness

• Appropriateness

Effectiveness

• Soomro et al (2009) reviewed 17 studies comparing SSRIs to placebos in the treatment of OCD and found SSRIs were more effective than placebos in reducing symptoms of OCD, being specifically effective in reducing symptoms between 6 and 13 weeks after starting the treatment.

• This suggests that drug therapies are an effective short-term treatment.

Appropriateness

• There are numerous common side effects to using drug treatments for OCD. For example, loss of appetite, loss of sex drive, irritability, sleep pattern disturbance and headaches.

• IF severe enough, it can lead to patient ending their treatment altogether.

• In addition, it is suggested that SSRIs may increase the risk of suicidal thoughts and self-harm in people with depression and in younger people. Therefore, drug therapy might not always be an appropriate treatment for all OCD sufferers.

Appropriateness

• Drug therapies may not be an appropriate long-term treatment if the cause of OCD is not biological. Evidence from Cromer et al (2007) suggests some cases of OCD are linked to trauma.

• Therefore, although SSRIs could help reduce the symptoms in the short-term, they would not be treating the underlying cause.

• This could also explain why many people relapse once medication has been stopped. Therefore, it may be more appropriate to offer drug therapy alongside other psychological therapies such as CBT.

Types of depression

Major depressive disorder

• Severe but often short-term depression

Unipolar depression Sufferers

• Only experience depression and not manic episodes.

• Clinical symptoms usually occur in cycles.

Bipolar depression

• Sufferers experience mixed episodes of mania and depression.

Characteristics of depression

• Behavioural

• Emotional

• Cognitive

Behavioural

• Change in activity levels – for example, increased lethargy (lack of energy) and withdrawal from activities that were once enjoyed.

• Neglecting personal hygiene – e.g. bathing, wearing clean clothes etc.

• Sleep disruption – decreased sleep, insomnia (inability to fall asleep or stay asleep) or increased sleep, hypersomnia (oversleeping).

Emotional

• Low mood - A key characteristic is the ever present and overwhelming feelings of sadness/negativity, sometimes described as feelings of ‘emptiness’.

• Worthlessness - Those suffering from depression often have constant feelings of low self-worth and/or inappropriate feelings of guilt. In extreme cases, it could involve a feeling of self-loathing (hating themselves).

Cognitive

• Poor concentration - There can be difficulty in paying attention/maintaining attention and/or slowed- down thinking and indecisiveness. This is likely to interfere with an individual’s work or everyday functioning.

• Negative schemas – People with depression tend to possess negative self-schemas which are a set of beliefs and expectations about themselves that are essentially negative and pessimistic.

The cognitive approach to explaining depression

• Becks Negative Triad

• Ellis’s ABC Model

Ellis’s ABC model

As an explanation of depression, the ABC model suggests that a particular situation or event will trigger irrational beliefs which will then lead to unhealthy emotional consequences e.g. low mood, feelings of low self-worth.

Suggested these irrational beliefs stem from mustabatory thinking, which is believing that certain ideas or things must be true in order to be happy and to live.

(A) Activating event → Friend doesn’t smile back in the hallway.

(B) Irrational Beliefs →”My friend doesn’t like me anymore”.

(C) Consequence → Low mood and feeling upset.

Beck’s Negative Triad

• He believed depression is caused by an individual with a thinking bias towards negative interpretations of the situations involving the self, the world and the future.

The Self → Feelings of hopelessness, worthlessness, feeling self conscious, e.g. “I’m a failure.”.

The World → Pessimistic view of the world, e.g. “The world is horrid.”.

The future 0> A negative outlook into the future, e.g. “I could never be good at anything.”.

• The negative triad is maintained through negative schema and cognitive biases/distautions.

• A schema is a mental framework for interpretations of information. The schemas are developed through experience e.g. saving money to buy something but you are worried it will sell out before you buy it.

Cognitive approach to treating depression

• CBT

• CBT (Cognitive Behavioural Therapy) is the most common treatment for depression and has many different variations, based on the research of cognitive explanations of ABC model.

• Its most effective as it challenges the irrational thoughts themselves.

• It also encourages the service user to engage in positive behaviour patterns and making conscious decisions to improve their depressive symptoms.This is behavioural activation.

One form of CBT is Ellis’s Rational Emotional Behavioural Therapy

REBT extends from the ABC model to an ABCDE model.

The aims is for the individual with depression to identify and challenge their negative thoughts and beliefs by reinterpreting them in a positive way, preventing further negative thinking and emotions such as low mood.

The D stands for dispute, which is challenging the irrational thoughts.

The E stands for effect, which is irrational beliefs are replaced with rational beliefs.

• The individual will first identify the activating agent, which may have resulted in the negative and irrational beliefs.

• The therapist then uses rational confrontation to reduce the negative cognitive and emotional symptoms of depression.

• One way they are disputed is through empirical dispute, this involves asking the individual for proof that they are true e.g. what evidence is there that no one likes them.

• Another way is logical dispute, which involves asking if the negative belief is logical or based on common sense.

Evaluation of CBT

• Appropriateness

• Effectiveness

• Appropraiteness

Appropriateness

• CBT requires commitment and motivation which may be problematic for individuals with depression due to loss of motivation as a symptom of depression. They may be unable to engage with the CBT or attend the sessions.

• Therefore it may be more appropriate to treat them with anti depressant drugs, which don’t require the same level of commitment.

• Once the symptoms have lessened, they can attend the treatment.

• CBT may be more appropriate to use as a part of a combination treatment for cases of severe depression.

Effectiveness

• March looked at 327 adolescents with depression with 3 conditions.

• One was the CBT treatment, another was drug therapy and the other was a combination of both.

• After 36 weeks, 81% of the CBT treatment and drug therapy conditions had improvements in their symptoms. Which shows they are both equally effective. The third condition showed 86% had improved.

• This shows drug therapy and CBT work best together and it is better than CBT or drug therapy alone.

Appropriateness

• CBT could be criticised for minimising the importance of the individuals social situation, CBT is about challenging rational thoughts. The individual may be experiencing very real world problems, e.g. abuse.

• This not address any wider problems which could contribute to the person’s depression. Therefore, CBT treatment may be inappropriate until their circumstances change.

• Maslows hierarchy of needs shows that self actualisation can not be reached without first meeting their physiological and safety needs and love and belonging.