Psychopathology

Definitions of abnormality, including deviation from social norms, failure to function adequately, statistical infrequency and deviation from ideal mental health.

• The Statistical infrequency definition of abnormality states that abnormal behaviour is behaviour that is very rare.

• Statistics are how we measure how common behaviours or traits are when measured in comparison to the rest of the population. The most uncommon ones are defined a abnormal.

• For example low IQ is when someone’s intelligence is two standard deviations from the average. Just 2.28% of the population have low IQ. It is an objective measure of individuals needing support.

Evaluation

• Not all statistically infrequent traits are negative. This definition would include high IQ, but whilst this is statistically rare it is also highly desirable.

• Where the cut-off point falls results in some people receiving treatment and some not, so deciding where to put the cut-off is subjective.

• Some psychopathologies such as depression and anxiety are quite common. Around 1 in 6 adults (17%) surveyed in England by the NHS met the criteria for a common mental health disorder (CMD) in 2014. The statistical infrequency definition does not match with the high incidence of mental health disorders within society.

Failure to function adequately

• Failure to function adequately is inability to cope with daily life (interacting with the world and people around us).

• Rosenhan and Seligman (1989) suggested the following features of failure to function adequately:

1. Maladaptive behaviour- this is when individuals behave in ways that are against their long-term interests (i.e: self-harm or unhealthy eating patterns).

2. Personal anguish- suffering from anxiety and distress because of their inability to cope.

3. Observer discomfort- The person’s behaviour causes distress to the people around them (i.e: poor personal hygiene or not respecting personal space).

4. Irrationality and unpredictability- behaviour that is hard to understand and/or seems uncontrolled

5. Unconventionality- behaviours go against normal expectations.

Marbled pigs often irritate uncle

Evaluation

• Deciding whether an individual is coping or not is a subjective judgement that is affected by the opinions of the observer, so two observers may not rate a person in the same way (potential low inter-rater reliability).

• Some abnormal behaviour is not linked to an inability to cope or intense distress. It is thought that there are many psychopaths that may be more able to function in certain roles in society, which may be at the detriment of people other than themselves.

• Not all maladaptive behaviour is an indication of mental illness. For example, smoking and poor diet are seen as against a person’s long-term interests in their personal health, but neither of these behaviours are assumed to constitute mental illness.

• However failure to function does respect and recognises the patient’s own lived experiences and perspective, which statistical infrequency and deviation from social norms cannot really address.

Deviation from social norms

• Social norms are unwritten social expectations of behaviour that may differ from one culture to the next. They often change over time and vary depending on the context.

• Therefore according to this definition, those who deviate from the society's’ expectations will be seen as abnormal ‘social deviants’.

• An issue with this explanation of mental illness is that, as norms are a group judgement on what is acceptable, certain behaviours in one culture that are considered acceptable may be considered deviant in another culture (i.e: homosexuality, face/hair covering, queuing, chopsticks, public displays of emotions).

Evaluation

• It respects cultural differences by not imposing a set definition of abnormality (avoids western ethnocentrism that would cause other cultures to be viewed as abnormal).

• It is a clear definition of what is and is not abnormal whilst also taking context into consideration.

• Different social classes within the same society may have different social norms. This could, for example, result in an overdiagnosis of mental health problems in those of working class backgrounds if most of the psychiatrists are from middle or upper class backgrounds.

• Can create problems for people living in a culture that is different from their culture of origin. For example Cochrane (see the schizophrenia topic) suggests that the there is 7x higher diagnosis rate of schizophrenia for people from Afro-caribbean heritage living in the UK compared to those native to the UK living in the UK or those native to the Caribbean who are living there. Fernando considers this to be a “category failure” that has occurred due to western definitions of mental illness being applied onto non-western cultures, specifically how hallucinations and religious experiences are interpreted.

• This definition can result in society imposing punishments to unconventional mentally healthy people for expressing their individuality, which is unethical

Deviation from ideal mental health

• Marie Jahoda (1958) uses humanist principles in not defining abnormality but defining six features of ideal mental health, suggesting that deviation from these features would indicate an abnormality. To remember the six features we use the acronym EAR SPA.

1. Environmental mastery- competent in meeting the demands of situations. Involves flexible thinking.

2. Autonomy- able to act independently of others and rely on their own abilities.

3. Resisting stress- able to cope with the anxiety caused by the demands of life.

4. Self actualisation- maximising personal growth and development to reach their potential.

5. Positive attitude towards oneself- positive self-concept (so high self-esteem and self respect).

6. Accurate perception of reality- realistic view of the world not distorted by personal biases.

Evaluation

• A positive holistic approach to diagnosis that identifies areas for personal development.

• Criteria are culturally biased to reflect an ethnocentric western viewpoint on what ideal mental health is. This could be an example of a culturally specific (emic) viewpoint being applied to all people as a universal (etic) construct. For example, many cultures place less value on the autonomy and personal freedom found in western cultures, seeing playing a social role as more important.

• It is very difficult to achieve all of these criteria at the same time, so most people would be judged as failing to achieve ideal mental health, and would therefore be classed as abnormal.

The behavioural, emotional and cognitive characteristics of phobias, depression, and obsessive compulsive disorder (OCD)

• Phobias are extreme irrational fears of certain objects or situations. Examples of phobias are arachnophobia (fear of spiders) and claustrophobia (a fear of enclosed spaces).

• Three key behavioural characteristics of phobias are avoidance (behavioural adaptations made to prevent encountering the phobic object or situation), panic (an uncontrollable physical response such as screaming, escaping, or hyperventilating), and failure to function (inability to conduct normal necessary behaviours due to excessive thoughts of the phobia and/or avoidance).

• Two key emotional characteristics are anxiety (an uncomfortable high arousal state that inhibits relaxation and pleasurable emotions. Thought is focused on a future encounter with the phobic object or situation) and fear (an intense emotional state of panic linked to physiological fight or flight response when presented with the phobic object or situation).

• Two key cognitive characteristics of phobias are irrational beliefs (sufferers overstate the potential danger of the phobic object or importance of the social situation) and reduced cognitive capacity (sufferers focus their attention on the phobic object to the extent that it interferes with other tasks).

• The three subtypes of phobias are simple/specific phobias (fears of objects), social phobias (fear of social interactions that could cause rejection or embarrassment) and agoraphobia (fear of leaving a safe environment).

• Obsessive compulsive disorder (OCD) is an anxiety disorder defined by obsessions (constant intrusive thoughts, usually concerning contamination or safety) and compulsions (behavioural responses to the obsessions).

• Three key behavioural traits of OCD are compulsions (these often involve checking behaviour such as repeatedly testing the lights and checking that the door is locked, and ritual behaviour such as constant hand washing, and hoarding), avoidance (sufferers avoid behaviour that may lead to obsessive thoughts so may stop using public toilets for fear of germs), and social impairment (unable to take part in normal relationships due to excessive anxiety).

• Two key emotional traits of OCD are extreme anxiety (caused by the constant presence of the persistent obsessive thoughts and the fear associated with them. Also attempting to resist the urge to carry out compulsions can cause anxiety) and distress/depression (low mood due to not being able to engage in enjoyable activities and a feeling of not being in control of own behaviour).

• Two key cognitive traits of OCD are recurrent thoughts (intrusive unpleasant thoughts that are anxiety-producing. Often of the worst case scenario or something else that distresses the person) and understanding the irrationality (sufferers know that the worst case scenarios imagined by their catastrophic thinking are unlikely, but are still unable to control them).

• Depression is a category of mood disorders, which is often divided into two main types: unipolar and bipolar depression, otherwise known as manic-depression.

• Four behavioural traits of depression are weight loss or gain (appetite is reduced or increases), low energy (lack of desire to participate in normally enjoyable activities such as sex, exercise, and socialising), self harm (this may be injuring such as cutting or, in extreme situations, suicide), and poor personal hygiene (low motivation to keep themselves or their environments clean and tidy).

• Two emotional characteristics of depression are sadness (persistent intense lowered mood is the defining feature of depression) and reduced self worth (feelings of guilt, helplessness, or low self esteem).

• Two cognitive features of depression are poor concentration (difficulty in keeping attention on tasks and indecisiveness) and persistent concern (thoughts biased towards a negative perspective of events and outcomes).

• Unipolar/major depression effects 25% of women and 12% of men during their lifetimes, and includes only depressive episodes

• Bipolar/manic depression affects 2% of people. They also have manic episodes where they have high energy and high moods, engage in risk-taking behaviour, and potentially have delusions.

The behavioural approach to explaining and treating phobias: the two-process model, including classical and operant conditioning; systematic desensitisation, including relaxation and use of hierarchy; flooding

• Explaining Phobias- A behaviourist model for explaining phobias is the two-process model. Behaviourists see all behaviour (including phobias) as learnt via experience. In the two-process model Mower (1960) suggests that phobias are first acquired (learned) via association (classical conditioning), and then maintained via reinforcement (operant conditioning).

• In acquisition (classical conditioning- learning by association) the phobic object(s) are at first neutral stimulus, not producing the phobic response. However, if the phobic object is presented with an unconditioned stimulus that produces an unconditioned negative response, then the neutral stimulus will then be associated with the unconditioned stimulus and thus the unconditioned response, and so the fear (the phobia) will happen whenever the neutral stimulus appears. As this point the neutral stimulus becomes the conditioned stimulus, and the unconditioned response becomes the conditioned response. This fear will then be passed onto other stimuli similar to the conditioned stimuli via generalisation (i.e: fear of spiders generalised to all insects).

• In maintenance (operant conditioning- learning by trial and error) the phobic person avoids situations that may bring the individual with the phobia into contact with the phobic object. The consequence of this is that anxiety is reduced. This is a pleasant sensation which acts as a negative reinforcement (removal of negative stimulus).

• Social learning theorists suggest that learning can happen vicariously by observing models. Observing a fear response in others can then result in the same display of fear, especially if the behaviour results in reward for the model (i.e: attention).

• Example for acquisition of a phobia: Bees were originally a neutral stimulus for Laura, resulting in no fear response. However the pain of being stung (unconditioned stimulus) produced fear (unconditioned response). Bees (conditioned stimulus) became associated with the fear (conditioned response) due to the pain of the sting. So even when not stung there is now fear. However she now feels fear when seeing ants, moths, and spiders, even though she was never stung by them (generalisation).

• Example for maintenance of a phobia: Laura has been invited to a summer picnic. As she approaches the park she sees a number of bees. The thought of sitting near them causes her anxiety, so she calls her friends to say that an emergency has come up and she can’t make it. As she heads home, she is sad as she wanted to spend time with friends, but her anxiety decreases as she didn’t need to be around the bees and the phobia is thus negatively reinforced.

Evaluation

• Watson and Rayner (1920) used a child called little Albert to demonstrate how phobias could be induced in a child. They did this by making a loud noise (by hitting a metal bar behind the child’s head) when presenting a white rat to the child, and were able to generalise this fear to other white fluffy objects such as a rabbit.

• This study acts as evidence for the Two-process model via proving how acquisition and generalisation of phobias work, however it was a highly unethical study as it caused its participant (little Albert) emotional harm.

• Menzies and Clarke (1993) found that only 2% of children with a fear of water could recall a traumatic experience with water, suggesting that the behaviourist explanation cannot account for all phobias.

• Phobias of snakes, birds, and dogs had an evolutionary origin as our very early ancestors could have been hunted/attacked by these creatures. This could explain why these are common phobias, when phobias to objects that are more dangerous in the modern day (i.e: knives, cars) are rare. This is the evolutionary biological theory, however this nature explanation goes against the nurture explanation of the behavioural approach.

• Behaviourist theories of phobia formation and maintenance have lead to effective counter-conditioning treatments such as flooding and systematic desensitisation (see below), supporting the behaviourist explanation.

• Treating Phobias- Behaviourist therapies are based on the idea that phobias are learnt through association to fear, so therapies attempt to replace the fear association with one of relaxation/calm.

• Systematic desensitisation is an attempt to use the same classical conditioning techniques that are thought to have caused the phobia in a process to “counter condition” the phobia by replacing the association between the phobic object and fear with an association with relaxation/calm instead. 

• The process relies on the theory of reciprocal inhibition, that is, the idea that fear and relaxation are opposite emotions and so cannot coexist at the same time. Therefore if you feel calm around the phobic objects then you can’t simultaneously feel fearful around it, so the fear must have been eradicated.

• The first stage of systematic desensitisation is to break the phobia down into an anxiety hierarchy, ranking presentations of the stimulus from least feared (a picture of a bee) to most feared (being in a room with lots of bees).

• Relaxation techniques such as breathing exercises are then taught by the therapist. 

• As they are exposed to each stage of the anxiety hierarchy, clients are encouraged to relax at each stage in a stepped approach (once the client is able to relax at the stage they feel a bit anxious at, then moving on to the next slightly more anxiety-inducing situation ..etc). This gradual exposure leads to the extinction (loss of an association) of the fear association and formation of a new association with relaxation.

• Flooding counter conditions phobias by immediate full exposure to the maximum level of phobic stimulus (i.e: being put in a room with lots of bees). The scenario would be adjusted to make it safe (i.e: Laura given a beekeeper suit to prevent stings). This immediate exposure will cause temporary panic in the client while they are bombarded with fear, and they may even attempt to escape to avoid the phobic stimulus. The clinician’s job is to prevent avoidance by preventing the client from ending the treatment. Eventually temporary panic will stop and the client will calm down, anxiety will have receded and the fear will be extinguished due to exhaustion.

• Flooding can be in vivo (real life stimulus) or in vitro (situation is imagined by patient).

Evaluation

• While both SD and flooding may be effective in the clinical setting, it may be that the effect is not generalised to the outside world.

• McGrath et al. (1990) found that 75% of patients with phobias were successfully treated using systematic desensitisation, when using in vivo techniques (see below). This shows that systematic desensitisation is effective in treating phobias.

• Further support comes from Gilroy et al. (2002) who examined 42 patients with arachnophobia (fear of spiders). Each patient was treated using three 45-minute systematic desensitisation sessions. When examined three months and 33 months later, the systematic desensitisation group were less fearful than a control group (who were only taught relaxation techniques). This provides further support for systematic desensitisation, as a long-term treatment for phobias.

• However, systematic desensitisation is not effective in treating all phobias. Patients with phobias which have not developed through a personal experience (classical conditioning) for example, a fear of heights, are not effectively treated using systematic desensitisation. Some psychologists believe that certain phobias, like heights, have an evolutionary survival benefit and are not the result of personal experience, but the result of evolution. These phobias highlight a limitation of systematic desensitisation which is ineffective in treating evolutionary phobias.

• Systematic desensitisation is often thought to be more successful than flooding as the client is in control of their progress, not the therapist.

• Flooding is not appropriate for older people, people with heart conditions, children, or abuse victims due to ethical concerns, whereas systematic desensitisation is ethically suitable for almost all people. There are ethical concerns as flooding exposes participants to emotional harm, and it could also end up reinforcing the phobia if treatment is ended too soon.

• One strength of flooding is it provides a cost effective treatment for phobias. Research has suggested that flooding is comparable to other treatments, including systematic desensitisation and cognition therapies (Ougrin, 2011), however it is significantly quicker. This is a strength because patients are treated quicker and it is more cost effective for health service providers.

• Although flooding is considered a cost effective solution, it is highly traumatic for patients and causes a high level of anxiety. Although patients provide informed consent, many do not complete their treatment because the experience is too stressful and therefore flooding is sometimes a waste of time and money as many patients do not finish their therapy. Systematic desensitisation has a higher completion rate, perhaps because it is a more pleasant experience.

• Although flooding is highly effective for simple (specific) phobias, the treatment is less effective for other types of phobia, including social phobia and agoraphobia. Some psychologists suggest that social phobias are caused by irrational thinking and are not caused by an unpleasant experiences (or learning through classical conditioning). Therefore, more complex phobias cannot be treated by behaviourist treatments and may be more responsive to other forms of treatment, for example cognitive behavioural therapy (CBT), which treats the irrational thinking.

• Alternative treatments for phobias exist, such as drug treatments. These are often used as a short term solution before talking therapies. Examples are anxiety disorder tranquilisers such as Benzodiazepines, and beta blockers such as Propranolol. Antidepressants can also be prescribed, but all of these drugs simply suppress the symptoms without addressing the underlying cause, and can also cause side-effects. As talking therapies are more effective in the long term they are the preferred treatment plan.

• Both systematic desensitisation and talking therapies take a number of sessions to complete and require 1:1 time with the therapist, resulting in a substantially higher cost than for drug treatments.

The cognitive approach to explaining and treating depression: Beck’s negative triad and Ellis’s ABC model; cognitive behaviour therapy (CBT), including challenging irrational thoughts

• Cognitive explanations for depression- The cognitive approach suggests that depression results from faulty cognition/faulty information processing/negative thinking about events (so disturbances in thinking).

• Cognitive psychologists say that we have a mental framework for objects and events (schemas) that work as shortcuts in understanding the world. This includes schemas about ourselves. Depression can result from our self-schemas being negative.

• One cognitive explanation for depression is Beck’s negative triad. It states that events are seen by the sufferer with a pessimistic/negative bias due to the development of negative schemas about the world, the self, and the future. This can lead to overgeneralisation (problems in one situation being seen as a problem in others), magnification of problems (seeing them as more important than they are), selective perception (focusing on the negative), and absolutist thinking (all or nothing).

Overly magnificent shellfish ass

• Another explanation is Ellis’ ABC model. This model states that people respond in different ways to stresses and challenges in life. Ellis suggests that this difference depends on their beliefs, resulting in different consequences for different people. The activating event (A) is the external situation that there will be a reaction to. The belief (B) is why the individual thinks that the activating event happened (rational or irrational). The consequence (C) is the behaviour and emotions caused by the person’s beliefs about the activating event. In depression the activating event is blamed for the unhappiness felt.

• Ellis suggests that Musturbatory thinking (thinking in absolutes and that the world must be a certain way for us) is a common type of belief that leads to unhappiness.

Evaluation

• Hammen and Krantz (1976) found support for negative cognitive distortions in depressed female undergraduates compared to a female undergraduate non-depressed control group when presented with a short story, with the depressed females showing more errors in logic when interpreting the narrative.

• Cognitive explanations for depression have been used to develop successful and widely used CBT and REBT (see below) treatments. The success of these treatments is shown by March et al (2007) who compared CBT with medication and found an effectiveness rate of 81% for both treatments, suggesting that the underlying cognitive theory that depression is due to faulty cognitions is valid as the treatment based on that idea is effective.

• The cognitive explanation cannot explain why some depressive patients have manic phases in which they exhibit a large amount of energy and confidence in short burst before returning to their depressive state. Also many patients have significant anger management issues, which the cognitive explanation also fails to explain.

• Placing the responsibility for depression in the hands of the patient could either empower the patient to help themselves or potentially be a cause of ‘blaming the victim’, especially if there are contributing factors like grieving or poverty.

• There is significant evidence that biological factors play a large role in depression, with some people being genetically vulnerable and a neurochemical factor being apparent from the effectiveness of antidepressant medication. This means that the cognitive explanation cannot be a full explanation.

• The cognitive approach to treating depression- Cognitive behavioural therapy (CBT) is a talking therapy that focuses on identifying and challenging irrational thoughts. Activities are set to change behaviours.

• Beck’s CBT is a 16-20 week program that focuses on present experiences and issues. The therapist trains the patient in thought-catching, that is identifying and recording their automatic negative/irrational thoughts. Once identified the negative thoughts are challenged and reconstructed to avoid distortion due to the negative triad.

• The patient can reality-test their irrational thoughts by carrying out homework tasks such as testing new ways of thinking/behaving and then evaluating the evidence with the therapist. Diaries may also be used as evidence.

• Patients are encouraged to take part on enjoyable activities that those with depression often avoid in a process called behavioural activation. This improves emotions and challenges irrational thoughts.

• Another form of CBT is Ellis’ Rational Emotive Behavioural Therapy (REBT). In this therapy Ellis’ ABC model is developed to the ABCDE model, with D being disputation of irrational beliefs, and E being effective change resulting from the changed beliefs. REBT is characterised by intensive disputation (arguing against assumptions underlying irrational beliefs). These arguments can either be logical (do the beliefs make sense) or empirical (is there evidence for this belief).

Evaluation 

• March et al (2007) compared three groups: those with medication only, those with CBT only, and those with both over 36 weeks using 327 participants. Found both CBT and medication alone had 81% effectiveness for depression alone and 86% when combined. Suggests that CBT is as effective as medication.

• CBT is not appropriate for patients who are severely depressed as they are unwilling/unable to engage with the difficult psychological work. In these cases it is more appropriate to take medication until they improve their mood enough to engage in therapy.

• 16-20 sessions with a trained professional is a considerable investment of time and has considerable costs associated with it. This may mean that access is limited in a health service, with limited funds making CBT a less viable treatment compared to cheaper and more accessible antidepressants.

• CBT could be seen as empowering the patient as in the therapy they act as an engaged and active force in their own recovery, whereas antidepressant medication places the patient into a passive role.

• The success of CBT as a treatment has likely had a positive impact on the wider economy. People being more in control of their mental health results in fewer sick days and improves their productivity whilst at work.

The biological approach to explaining and treating OCD: genetic and neural explanations; drug therapy

• Genetic explanations of OCD-  The genetic explanation suggests that OCD may be inherited, as gene markers predict its presence.

• Individual genes such as Gene 9, COMT, and SERT seem to be present with OCD, however there may be as many as 230 separate genes that may be involved in the development of OCD meaning that the disorder is polygenic. It is also aetiologically heterogeneous as because there are many candidate genes, different gene combinations could lead to OCD.

• The COMT gene is associated with the regulation of the neurotransmitter dopamine. One variation of the COMT gene results in higher levels of dopamine and this variation is more common in patients with OCD, in comparison to people without OCD.

• The SERT gene (also known as the 5-HTT gene) is linked to the neurotransmitter serotonin and affects the transport of the serotonin (hence Serotonin Transporter), causing lower levels of serotonin which is also associated with OCD (and depression).

• Lewis (1936) examined patients with OCD and found that 37% of the patients with OCD had parents with the disorder and 21% had siblings who suffered. Research from family studies, like Lewis, provide support for a genetic explanation to OCD, although it does not rule out other (environmental) factors playing a role.

• Neural explanations of OCD-  Neural explanations of OCD focus on neurotransmitters as well as brain structures in the development of OCD.

• Neurotransmitters- The neurotransmitter serotonin is believed to play a role in OCD. Serotonin regulates mood and lower levels of serotonin are associated with mood disorders, such as depression. It may be that serotonin prevents the repetition of tasks, and that if it is in too low a level, or is removed too quickly from the synaptic systems, before it is able to inhibit the repetition of an action, and this may result in obsessive thoughts.  Furthermore, some cases of OCD are also associated with the reduced levels of serotonin, which may be caused by the SERT gene (see above). Further support for the role of serotonin in OCD comes from research examining anti-depressants, which have found that drugs which increase the level of serotonin are effective in treating patients with OCD.

• In addition, the neurotransmitter dopamine has also been implicated in OCD, with higher levels of dopamine being associated with some of the symptoms of OCD, in particular the compulsive behaviours.

• Brain structures- Two brain regions have been implicated in OCD, including the basal ganglia and orbitofrontal cortex.

• The basal ganglia is a brain structure 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. Furthermore, 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.

• Another brain region associated with OCD is the orbitofrontal cortex, a region which converts sensory information into thoughts and actions. It predicts future events and controls impulses from the limbic system. PET scans have found higher activity in the orbitofrontal cortex in patients with OCD. One suggestion is that the heightened activity in the orbitofrontal cortex increases the conversion of sensory information to actions (behaviours) which results in compulsions. The increased activity also prevents patients from stopping their behaviours.

• There is also abnormal activity in the parahippocampal gyrus, which regulates unpleasant emotions.

Evaluation

• One strength of the biological explanation of OCD comes from research from family studies. Research from family studies, like Lewis, provide support for a genetic explanation to OCD.

• While evidence from family studies seem to indicate a strong genetic factor, these studies cannot fully control for the influence of shared environmental factors such as diet and social learning theory in their methods. Conversations about and awareness of OCD will be more common with a sufferer in the household, making other family members more likely to seek treatment, making this genetic link seem greater than it already is.

• Further support for the biological explanation of OCD comes from twin studies which have provided strong evidence for a genetic link. Nestadt et al. (2010) conducted a review of previous twin studies examining OCD. They found that 68% of identical twins and 31% of non-identical twins experience OCD, which suggests a very strong genetic component.

• Support for the neural explanations of OCD come from research examining biological treatments including antidepressants.

• Hu (2006) found genetic differences between 169 OCD sufferers and 253 controls that impacted the function of serotonin transporters in the brain, supporting genetic and neural explanations.

• Antidepressants typically work by increasing levels of the neurotransmitter serotonin. These drugs are effective in reducing the symptoms of OCD and provide support for a neural explanation of OCD.

• However, no twin study has found a concordance rate of 100% in identical twins, which means that biological factors are not the only factor contributing to OCD and there must be environmental factors which also contribute to this disorder.

• Effectiveness of drug treatments (SSRIs, see below) indicate that the neural explanations are valid, but drugs that work on the serotonin system simply cover up symptoms and don’t treat the root cause.

• The biological explanation could be seen as biologically deterministic as it suggests that OCD is due to uncontrollable genetic and neuronal factors. However cognitive explanations say that OCD is due to faulty information processing, and can be cured by the use of conscious thought in challenging irrational beliefs. Some psychologists suggest that OCD may be learnt through classical conditioning and maintained through operant conditioning stimulus (for example, dirt) is associated with anxiety and this association is then maintained through operant conditioning, where a person avoids dirt and continually washes their hands. This hand washing reduces their anxiety and negatively reinforces their compulsions. As OCD symptoms has been shown to be reduced by cognitive therapies such as CBT, the validity of this deterministic viewpoint can be questioned.

Drug therapy- Biological treatments for OCD aim to restore biological imbalances, such as too little serotonin. Drug treatments are based on the assumption that chemical imbalances are the main cause of the problem. Two types of drug are used for the treatment of OCD: (1) antidepressants and (2) anti-anxiety drugs.

• Antidepressant drugs- The biological explanation suggests that OCD (and depression) is the result of low levels of the serotonin in the brain. SSRIs (selective serotonin reuptake inhibitors) are one type of antidepressant drug, which include drugs like Prozac.

• When serotonin is released from the presynaptic cell into the synapse, it travels to the receptor sites on the postsynaptic neuron. Serotonin which is not absorbed into the postsynaptic neuron is reabsorbed into the sending cell (the presynaptic neuron). SSRIs increase the level of serotonin available in the synapse by preventing it from being reabsorbed into the sending cell. This increases level of serotonin in the synapse and results in more serotonin being received by the receiving cell (post-synaptic neuron).

• If SSRIs are ineffective then non-selective reuptake drugs called tricyclics (such as clomipramine) may be used, as may SNRIS that influence noradrenaline, however these are often second choice due to their more intense side effects.

• Antidepressants (like anti-anxiety drugs) improve mood and reduce anxiety which is experienced by patients with OCD.

• Anti-anxiety drugs- Benzodiazepines (BZs) are a range of anti-anxiety drugs, which include trade names like Valium and Diazepam.

• BZs work by enhancing the action of the neurotransmitter GABA (gamma-aminobutyric acid).

• GABA tells neurons in the brain to ‘slow down’ and ‘stop firing’ and around 40% of the neurons in the brain respond to GABA. This means that BZs have a general quietening influence on the brain and consequently reduce anxiety, which is experienced as a result of the obsessive thoughts.

• In severe cases that don’t respond to drugs patients can have surgery to alter the communication between the orbital frontal cortex and other areas of the brain (psychosurgery), stopping the loop of continuous checking behaviour. A new experimental technique is deep brain stimulation, where electrodes are placed within the brain to interfere with or enhance the function of certain brain regions.

Evaluation

• In a meta-analysis by Greist (1995) reviewed placebo-controlled trials of the effects of four drugs on OCD using a total of 1520 participants. All four drugs were found to be significantly more effective than the placebo, with Clomipramine being the most effective (the others were fluvoxamine, fluoxetine, and sertraline). So biological treatments for OCD often have strong evidence such as highly controlled drug trials to show the effectiveness of biological treatments.

• Soomro et al. (2008) conducted a review of the research examining the effectiveness of SSRIs and found that SSRIs were more effective than placebos in the treatment of OCD, in 17 different trials. This supports the use of biological treatments, especially SSRIs, for OCD.

• Cognitive neuroscience applied to OCD is now producing biological treatments that involve direct deep brain stimulation using electrodes to affected areas of the brain to reduce the presence of obsessions. It is hoped that these treatments will be able to replace drugs in severe cases.

• Publication bias is an issue when considering the effect of drug treatments, as positive results are more likely to be published than negative, so it is argued that drug companies often run trials with the financial incentive to show that their drug is effective, potentially leading to researcher bias and demand characteristics in participants.

• Another strength of biological treatments is their cost. Biological treatments, including anti-depressants and anti-anxiety drugs, are relatively cost effective in comparison to psychological treatments, like cognitive behavioural therapy (CBT). Consequently, many doctors prefer the use of drugs over psychological treatments, as they are a cost effective solution for treating OCD (and depression), which is beneficial for health service providers.

• In addition, psychological treatments like CBT require a patient to be motivated. Drugs however are non-disruptive and can simply be taken until the symptoms subside. As a result, drugs are likely to be more successful for patients who lack motivation to complete intense psychological treatments.

• However, one weakness of drug treatments for OCD is the possible side effects of drugs like SSRIs and BZs. Although evidence suggests that SSRIs are effective in treating OCD, some patients experience mild side effects like indigestion, while other might experience more serious side effects like hallucinations, erection problems and raised blood pressure. BZs are renowned for being highly addictive and can also cause increased aggression and long-term memory impairments. As a result, BZs are usually only prescribed for short-term treatment. Consequently, these side effect diminish the effectiveness of drug treatments, as patients will often stop taking medication if they experience these side effects.

• Finally, drug treatments are criticised for treating the symptoms of the disorder and not the cause. Simpson (2004) found relapse (symptoms returning) in 45% of OCD cases within 12 weeks of stopping medication, compared to only 12% of cases for CBT patients, suggesting that the drugs are not a long term solution as they do not treat the underlying cause of OCD.