Psychopathology Shorter Version PDF

**Paper 2 Psychopathology** What is abnormal? **The definitions of abnormality** are 4 ways in which it can be defined. **Statistical infrequency (SI):** This defines abnormality as any behaviour that is rare or infrequent. Any relatively common or usual behaviour is seen as normal while behaviour...

**Paper 2 Psychopathology** What is abnormal? **The definitions of abnormality** are 4 ways in which it can be defined. **Statistical infrequency (SI):** This defines abnormality as any behaviour that is rare or infrequent. Any relatively common or usual behaviour is seen as normal while behaviour that is different to this is 'abnormal'. What is regarded as statistically rare depends on normal distribution -- people whose scores are in the top or bottom 2% of the population on any given variable are seen as abnormal. **Deviation from social norms (DSN)**: This defines abnormality as anything that goes against the accepted standards and desired behaviour in society. This definition draws a line between desirable and undesirable behaviours and labels individuals behaving undesirably as social deviants/abnormal. For example, robbing a bank goes against the norm of capitalism where people are allowed to keep what they've earned and stealing is undesirable and unacceptable/abnormal. "**Deviation from ideal mental health**" **(DIMH)** defines abnormality as when you **do not** possess certain 'normal' characteristics. - the ability to make sensible/normal individual choices - having normal resistance to stress (not too high or low) - having an accurate perception of reality - having reached **self-actualisation** - showing **empathy** and understanding towards others - having **environmental mastery** -- being competent in all aspects of life and able to meet the demands of any situation **Failure to function adequately** proposes that you are abnormal if you deviate from your normal pattern of behaviour and fail to cope with your job, family or relationships. There are **at least 5** indicators that you are or your behaviour is considered abnormal; - you cause yourself personal distress or discomfort - you cause others' (observers) distress or discomfort - you do anything maladaptive (something that hinders you from fitting in/adapting to your daily activities) - you do anything irrational (hard to understand) - you do something unexpected/unpredictable **Statistical Infrequency** **Strengths** 1. The definition gives an objective measure of what behaviours are normal -- no value judgements are made. A 'cut-off' point can be predetermined to establish whether someone is abnormal or not. 2. It has useful applications for intervention and assistance. - can provide medical professionals with statistics on what is developmentally normal at different ages to identify which children need intervention. **Limitations:** 1. This definition is **culture-dependent and era-dependent**. 2. **It fails to consider desirability of behaviour.** Not all rare behaviours are undesirable and abnormal - obtaining 15 A\*s at GCSE (!!) is very rare and would be considered abnormal by statistical infrequency - Jahoda's definition is useful as it favours desirable behaviour, labelling it 'normal' no matter how rare it might be. 3. Some undesirable behaviour is very frequent but we would not want it to be called 'normal'. For example depression affects 10% of the population and over-eating is more common than not **Deviation from social norms** **Strengths** 1. The definition considers the social setting of behaviour; a behaviour seen as abnormal in one setting (e.g. nudity in a public place) might be normal in another (on a nudist beach). 2. It also helps establish what behaviours are normal for different ages. For example wearing a nappy at age 2 might be acceptable but at age 12 it wouldn't be. **Limitations:** 1. By its very definition, this definition is **culture-dependent**.. E.g. in a collectivist society it would be seen as wrong to have banks and for different people to own different things. 2. It is also **era-dependent**. E.g. homosexuality was seen as a mental illness until the 1960's in the USA and was only removed from the DSM criteria in the 1990s. Also smoking was normal until 1964 when the World Health Organisation declared it to be dangerous! **Deviation from ideal mental health** 1. This conflicts with the statistical infrequency definition as rare behaviour such as obtaining 15 A\*s at GCSE would be considered normal, as it demonstrates you have very good ability to make sensible, good individual choices. For this reason, Jahoda's definition is useful as it favours desirable behaviour, labelling it 'normal' no matter how rare it might be. 2. It is also a very comprehensive definition as it covers a wide range of criteria for mental health -covers most of the reasons someone would seek help from mental health services or be referred for help, giving it useful applications. 1. The characteristics that are considered normal are very vague and **value-dependent.** For example choosing to cohabit before marriage would nowadays be considered a wise personal decision however in 1920 it would not have been as you could have been socially outcast. 2. Specific to Western cultures making it **culture-dependent**. - emphasis on personal achievement in the concept of self-actualisation would be considered self-indulgent and immoral in much of the world because the emphasis is on the individual rather that the family or community. 3. Also DIMH sets an **unrealistically high standard for mental health**. Most people do not meet all the ideals. Self-actualisation is only reached by a small percentage of people, leaving the vast majority abnormal! **Failure to function adequately** **Strengths** 1. It allows judgement by others of whether someone is functioning adequately. This might enable people to get help when they do not realise they need it themselves. 2. It considers the subjective experience of the individual/patient -- considering individual differences. **Limitations** 1. **Abnormality is not always associated with failing to function.** Harold Shipman was one of the most prolific serial killers in history, probably responsible for about 250 deaths and possibly many more. However, many people who knew him, including his former patients, described him as a good and caring family doctor. 2. It is a **subjective, value-dependent** judgement of abnormality -- someone must judge whether a person's behaviour is distressing or maladaptive. People who practise extreme sports could be accused of behaving in a maladaptive way because they lead an alternative, atypical lifestyle. **Phobias** **Emotional, behavioural and cognitive characteristics of phobias** **Emotional characteristics** -- these are cued by the presence or anticipation of a specific object or situation (e.g. spiders, flying, heights, seeing blood) and are out of proportion to the actual danger posed. \- Fear that is marked and persistent, and is likely to be excessive and unreasonable. \- Feeling of anxiety and panic. **Behavioural characteristics** \- Avoidance of the object or situation that creates fear. \- Freeze or faint. Freezing is an adaptive response because a predator may think the prey is dead. -Disruption in functioning and marked distress about having the phobia. **Cognitive characteristics** \- irrational thinking and resistance to rational arguments. -The person recognises that their fear is excessive or unreasonable, although this feature may be absent in children. -Selective attention to the phobic stimulus. A sufferer's focus fixates on the phobic stimulus. **The behavioural approach to explaining phobias: the two-process model, including classical and operant conditioning** Mowrer (1960) proposed the two-process model based on the behavioural approach to phobias. This states that phobias are acquired (learned in the first place) by classical conditioning and then are maintained because of operant conditioning. **Acquisition by classical conditioning** Classical conditioning involves learning to associate something of which we initially have no fear (called a neutral stimulus) with something that already triggers a fear response (known as an unconditioned stimulus). Watson and Rayner (1920) created a phobia in a 9-month old baby called 'Little Albert'. Whenever the rat was presented, they made a loud, frightening noise by banging an iron bar close to Albert's ear. This noise is an unconditioned stimulus (UCS) which produces an unconditioned response (UCR) of fear. When the rat (a neutral stimulus, NS) and unconditioned stimulus are encountered close together in time, the NS becomes associated with the UCS and both now produce a fear response-Albert became frightened when he saw a rat. The rat is now a learned or conditioned stimulus (CS) that produces a conditioned response (CR). This conditioning then generalised to similar objects. **Maintenance by operant conditioning** Operant conditioning maintains the phobia via negative reinforcement - an individual avoids a situation that is unpleasant (e.g. going to the park where there are dogs). Such a behaviour results in a desirable consequence (removal of the fear and anxiety), which means that the behaviour will be repeated. This reduction in fear reinforces the avoidance behaviour (e.g. not going to the park) and so the phobia is maintained. **Evaluation of the behavioural approach to explaining phobias/the two-process model** **Negative** **1. Issues with Watson and Rayner's study** \- only one participant and so we can't draw any general conclusions especially since Little Albert was not a very representative infant-he was 'stolid and unemotional' \- it is not clear that Little Albert developed a strong fear response - the researchers reported the following after several days of conditioning: 'Fear reaction slight...allowed the rat to crawl towards him without withdrawing'. \- it has proved hard to repeat the findings on Little Albert. One reason is probably the very limited and unscientific nature of the study. For example, Little Albert showed little or no fear during conditioning when he sucked his thumb. As Rolls (2010) pointed out, Watson and Rayner dealt with this problem by continually pulling his thumb out of his mouth.) **Positive** **1. Support for classical conditioning, DiNardo et al. (1988)** The theory predicts that phobic individuals would have experienced a triggering event at some point in their past-a moment in which a fear response was associated with the now phobic object/situation. This is supported by DiNardo et al. (1988), who found that over 60 per cent of people with a fear of dogs (cynophobia) could relate their fear to a particular frightening experience. **Negative** **2. Counter-evidence for classical conditioning, DiNardo et al., 1988** When it is possible to see that some people do indeed develop a phobia after an identifiable fearful incident, not all people do. In the DiNardo et al. (1988) study, for example, in a control group of participants without a phobia of dogs, a similar proportion of participants had experienced a fearful incident with a dog but had not developed a phobia. In any case, DiNardo only found that over 60 per cent of individuals with cynophobia could remember a fearful experience. That leaves a significant proportion of individuals who developed a phobia seemingly without being classically conditioned. **Positive** **2. Social learning can rescue the theory, Bandura and Rosenthal (1966)** Those who develop a phobia may also have done so through modelling the behaviour of others. An experiment by Bandura and Rosenthal (1966) supported the social learning explanation. In the experiment, a model acted as if he was in pain every time a buzzer sounded. Later on, those participants who had observed this showed an emotional reaction to the buzzer, demonstrating an 'acquired' fear response. **Negative** **3. Biological preparedness, Seligman (1970) and Bregman (1934)** The fact that phobias do not always develop after a traumatic incident may be explained in terms of biological preparedness. Seligman (1970) argued that animals, including humans, are genetically programmed to rapidly learn an association between potentially life-threatening stimuli and fear. These stimuli are referred to as ancient fears-things that would have been dangerous in our evolutionary past (such as snakes, heights, strangers). It would have been adaptive to rapidly learn to avoid such stimuli. This concept of biological preparedness would explain why people are much less likely to develop fears of modern objects such as toasters and cars that are much more of a threat than spiders. Such items were not a danger in our evolutionary past. For example, Bregman (1934) failed to condition a fear response in infants aged 8 to 16 months by pairing a loud bell with wooden blocks. It may be that fear responses are only learned with living animals such as rats, a link with ancient fears. This suggests that behavioural explanations alone cannot be used to explain the development of phobias. **The behavioural approach treating phobias: systematic desensitisation, including relaxation and use of hierarchy** Systematic desensitisation is derived from the behavioural approach and is based on classical conditioning. Fear is overcome by introducing the feared stimulus gradually. This is based on the principle of **counterconditioning** - Individuals learn to relax in the presence of stimuli that had once made them unbearably nervous and afraid. The two responses of relaxation and fear are incompatible (called **reciprocal inhibition**) and the fear is eventually dispelled. **The different steps** Step 1: Patient is taught how to relax their muscles completely. (A relaxed state is incompatible with anxiety.) Step 2: Therapist and patient together construct a fear hierarchy consisting of a list of situations or objects producing fear in the client, starting with those causing only a small amount of fear and moving on to those causing increasingly great levels of fear. Step 3: Patient gradually works his/her way through the fear hierarchy, visualising each anxiety-evoking event (covert desensitisation) while engaging in the competing relaxation response. In some cases, the actual object/situation may be presented (in vivo desensitisation). Step 4: Once the patient has mastered one step in the hierarchy (i.e. they can remain relaxed while imagining it), they are ready to move onto the next. Step 5: Patient eventually masters the feared situation that caused them to seek help in the first place. The phobia is said to be 'cured' when the person is able to remain relaxed in the presence of their most feared situation or stimulus. **Evaluation of systematic desensitisation** **Positive** ** ** **1. Evidence for its effectiveness, Gilroy et al. (2003)** Research has shown that systematic desensitisation is effective in the treatment of specific phobia. For example, Gilroy et al. (2003) followed up 42 patients who had been treated for spider phobia in three 45-minute sessions of systematic desensitisation. Spider phobia was assessed on several measures including the Spider Questionnaire and by assessing response to a spider. A control group was treated by relaxation without exposure. At both three months and 33 months after the treatment, the systematic desensitisation group were less fearful than the relaxation group. This is a strength because it shows that systematic desensitisation is helpful in reducing the anxiety in spider phobia and that the effects are long-lasting. **2. Appropriateness-it is more acceptable than flooding** A strength of systematic desensitisation is that patients prefer it; those given the choice of systematic desensitisation or flooding tend to prefer the former. This is largely because it does not cause the same degree of trauma as flooding. It may also be because systematic desensitisation includes some elements-learning relaxation procedures- that are actually pleasant. This is reflected in low refusal rates and low attrition rates. **Negative** **1. Not effective...counterevidence, Choy et al. (2007), McGlynn et al. (2004)** Most evidence (Choy et al., 2007), indicates that flooding (or exposure therapy even) is more effective than systematic desensitisation in the treatment of phobias. This helps to explain why there has been a large reduction in the use of systematic desensitisation over the years (McGlynn et al., 2004). **2. Appropriateness-This form of therapy may be too superficial**   The assumptions of the behavioural approach, that all behaviour is learned through relatively simple conditioning principles, means that therapy targets these learnt associations. There is no attempt to address any deeper psychological or emotional issues related to the disorder, i.e. these therapies focus on symptoms rather than any deeper underlying causes. **3. Systematic desensitisation may not be appropriate for all phobias** Behavioural therapies are most effective when it is possible to identify a particular object or situation as the source of phobia. For example, it would be possible to treat arachnophobia (fear of spiders) quite quickly and effectively with systematic desensitisation but not a social phobia where the particular source of the phobia cannot be identified. **Flooding** Flooding also involves exposing phobic patients to their phobic stimulus but without a gradual build-up in an anxiety hierarchy. Instead flooding involves immediate exposure to a very frightening situation. Flooding sessions are typically longer than systematic desensitisation sessions, one session often lasting two to three hours. Sometimes only one long session is needed to cure a phobia. **How does it work?** Flooding stops phobic responses very quickly. This may be because, without the option of avoidance behaviour, the patient quickly learns that the phobic stimulus is harmless. In classical conditioning terms this process is called extinction. A learned response is extinguished when the conditioned stimulus (e.g. a dog) is encountered without the unconditioned stimulus (e.g. being bitten). The result is that the conditioned stimulus no longer produces the conditioned response (fear). In some cases, the patient may achieve relaxation in the presence of the phobic stimulus simply because they become exhausted by their own fear response. In recent years, flooding has been developed into virtual reality flooding, in which a computer program produces a virtual environment stimulating the phobic situation. The patient typically has a head-mounted display that allows for visual and auditory input. **Reciprocal inhibition** also applies here -- fear and exhaustion cannot be felt at the same time, hence the fear is replaced with exhaustion and eventually relaxation. **Evaluation of flooding** **Positive** **1. Effectiveness-research support for flooding, Kaplan and Tolin (2011), Choy et al. (2007)** Flooding is consistently effective. For example, single-session flooding has proved very successful in treating specific phobia. Kaplan and Tolin (2011) reported that 65% of patients with specific phobia given a single session of flooding showed no symptoms of specific phobia 4 years later. In addition, traditional flooding and virtual reality flooding are both often more effective than systematic desensitisation (Choy et al., 2007) **2. Appropriateness-quick and the only possible psychological treatment for some** Behavioural therapies in general are quick and require less effort on the patient\'s part when it comes to phobias than other psychotherapies where patients must play a more active part in their treatment. Behavioural therapies may be the only psychological treatments possible for certain groups of people, for example for some individuals with severe learning difficulties. **3. Appropriate-it is cheap** Flooding is at least as effective as other treatments for specific phobias. Studies comparing flooding to cognitive therapies (e.g. Ougrin 2011) have found that flooding is highly effective and quicker than alternatives. This quick effect is a strength because it means that patients are free of their symptoms as soon as possible and this makes the treatment cheaper. **Negative** **1. Appropriateness - Behavioural therapy may be too superficial**   The assumptions of the behavioural approach, that all behaviour is learned through relatively simple conditioning principles, means that therapy targets these learnt associations. There is no attempt to address any deeper psychological or emotional issues related to the disorder, i.e. these therapies focus on symptoms rather than any deeper underlying causes. **2. It is less effective for some types of phobias** Although flooding is highly effective for treating simple phobias, it appears to be less so for more complex phobias like social phobias. This may be because social phobias have cognitive aspects. For example, a sufferer of a social phobia does not simply experience an anxiety response but thinks unpleasant thoughts about the social situation. This type of phobia may benefit more from cognitive therapies because such therapies tackle the irrational thinking. **3. Appropriateness-the treatment can be traumatic for patients** Perhaps the most serious issue with the use of flooding is the fact that it is a highly traumatic experience. The problem is not that flooding is unethical (patients give consent) but that patients are often unwilling to see it through to the end. This is a limitation of flooding because time and money are sometimes wasted preparing patients only to have them refuse to start or complete treatment. **Depression** **Emotional, behavioural and cognitive characteristics of depression** **Emotional characteristics** Negative mood states or an absence of positive mood states (e.g. reduced pleasure) including: -depressed mood i.e. an ever present and overwhelming feeling of sadness/hopelessness -irritability -reduced pleasure in most activities -feelings of guilt and worthlessness **Behavioural characteristics** -Loss of energy i.e. depressed people can have reduced amounts of energy resulting in fatigue, lethargy, and high levels of inactivity -Changes in eating behaviour (weight going up or down) -Sleep pattern disturbance i.e. depression is often characterised by constant insomnia or oversleeping -Less effective behaviour in social areas i.e. reduced levels of social interaction with friends and relations -Poor personal hygiene i.e. depressed people often have reduced incidence of washing, wearing clean clothes etc. -Less effective behaviour in professional and educational areas **Cognitive characteristics** -thoughts of death or suicide -an impaired ability to think, poor concentration and indecisiveness -in some cases, poor memory -some depressives will experience delusions, generally concerning guilt, punishment, worthlessness or disease. Some will also experience hallucinations, which can be auditory, visual, olfactory (smell) or haptic (touch) **The cognitive approach to explaining and treating depression: Beck's negative triad** **Biased thinking** Beck (1967) developed a cognitive explanation for depression. He believed that depressed individuals feel as they do because their thinking is biased towards negative interpretations of the world and they lack a perceived sense of control. **Negative schemas and their causes** Depressed people have acquired a negative schema during childhood-a tendency to adopt a negative view of the world. This may be caused by a variety of factors, including parental and/or peer rejection and criticisms by teachers. These negative schemas (e.g. expecting to fail) are activated whenever the person encounters a new situation (e.g. an exam) that resembles the original conditions in which these schemas were learned. Negative schemas lead to systematic cognitive biases in thinking. For example, individuals over-generalise, drawing a sweeping conclusion regarding self-worth on the basis of one small piece of feedback. +-----------------------------------+-----------------------------------+ | **The negative triad** | Negative schemas and cognitive | | | biases maintain what Beck calls | |  | the negative triad, a pessimistic | | | and irrational view of three key | | | elements in a person's belief | | | system. | | | | | | -The self; depressed people see | | | themselves as helpless, worthless | | | and inadequate. | | | | | | -The world; they interpret events | | | in the world in an | | | unrealistically negative and | | | defeatist way, and they see the | | | world as posing obstacles that | | | can't be handled. | | | | | | -The future; they see the future | | | as totally hopeless because their | | | worthlessness will prevent their | | | situation from improving. | +-----------------------------------+-----------------------------------+ **Other cognitive biases** **-Arbitrary inference:** Conclusions drawn in the absence of sufficient evidence. For example, a man concluding he's worthless because it's raining the day he hosts an outdoor party. **-Overgeneralisation:** Sweeping conclusions drawn on the basis of a single event. For example, a student regarding poor performance on one test as a proof of his worthlessness. **-Magnification and minimisation:** Exaggerations in evaluation of performance. For example, a man believing he's ruined his car due to a small scratch (maximisation) or a woman believing herself worthless despite many praises (minimisation). **Evaluation of Beck's negative triad** **Positive** **1. Evidence to support Beck's theory, Boury et al., 2001** Boury et al. (2001) monitored students' negative thoughts with the Beck depression inventory (BDI), finding that depressives misinterpret facts and experiences in a negative fashion and feel hopeless about the future, giving support to Beck's cognitive explanation. **Negative** **1. Issues of causality** The fact that such studies suggest that there is a link between negative thoughts and depression does not mean that negative thoughts cause depression. It may be that, for example, a depressed individual develops a negative way of thinking because of their depression rather than the other way around. It may be that a sufferer develops depression because of the genes they have inherited and their negative thoughts are a symptom of this genetic disorder. **Positive** **2. Evidence establishing cause and effect, Lewinsohn et al. 2001** Evidence that negative thinking can be involved in the development of major depressive disorder was obtained by Lewinsohn et al. 2001. They measured negative thinking (e.g. 'My life is wasted unless I am a success') in adolescents not having a major depressive disorder at the outset of the study. One year later, Lewinsohn et al. assessed the negative life events experienced by the participants over the 12-month period and also assessed whether they were suffering from major depressive disorder. Those who had experienced many negative life events had an increased likelihood of developing major depressive disorder only if they were initially high in negative attitudes. Since these negative attitudes were assessed before the onset of depression, they seem to be a risk factor for developing that disorder when exposed to stressful life events. **Positive** **2. Practical applications in therapy** Both cognitive explanations have been applied to CBT. CBT is consistently found to be the best treatment for depression especially when used in conjunction with drug treatments (e.g. Cuijpers et al., 2013). If depression is alleviated by challenging irrational thinking then this suggests such thoughts had a role in the depression in the first place. **The cognitive approach to explaining and treating depression: Ellis's ABC model** Ellis (1962) was the first therapist to adopt the cognitive approach with his rational emotive therapy. He argued that anxiety and depression occur as the final stage in a three-point sequence. According to his ABC model, depression does not occur as a direct result of unpleasant events but rather is produced by the irrational thoughts triggered by unpleasant events. A (for adversity or activating event): an unpleasant event occurs at point A. For example, you get fired at work. B (for beliefs): At point B, the individual puts his/her own interpretation on this unpleasant event. This may be rational or irrational. For example: 'The company was overstaffed' or 'I was sacked because they've always had it in for me'. C (for consequences): If the interpretation is negative or self-defeating, the individual experiences depression (or anxiety) at point C. However, if the individual interprets the unpleasant event in a positive or realistic way, this greatly reduces the amount of depression (or anxiety) experienced. **Mustabatory thinking** The source of irrational beliefs lies in mustabatory thinking-thinking that certain ideas or assumptions must be true in order for an individual to be happy. Ellis identified the three most important irrational beliefs: -I must be approved of or accepted by people I find important. -I must do well or very well, or I am worthless. -The world must give me happiness, or I will die. **Evaluation of Ellis's ABC model** **Positive** **1. Further evidence that negative thinking may lead to depression, Lloyd and Lishman, 1975** In a study by Lloyd and Lishman (1975), participants with depression were presented with stimulus words in response to which they were required to recall pleasant or unpleasant experiences from their past. They found that those with low-level depression responded faster when recalling pleasant memories than those participants with deeper depression. Those with deeper depression were quicker to recall unpleasant memories. This supports the idea that depressed people display irrational negative thinking. **Negative** **1. Issues of cause and effect** Ellis's ABC model provides only a sketchy account of some factors that might explain the existence of depression. For example, suppose we assume that Ellis is correct in arguing that depression is associated with negative and self-defeating interpretations of unpleasant events. It is very hard to know whether these negative interpretations cause depression or whether depression causes negative interpretations. **Positive** **2. Practical applications in therapy** Both cognitive explanations have been applied to CBT. CBT is consistently found to be the best treatment for depression especially when used in conjunction with drug treatments (e.g. Cuijpers et al., 2013). If depression is alleviated by challenging irrational thinking then this suggests such thoughts had a role in the depression in the first place. **Negative** **1. Irrational beliefs may be realistic AKA Depressive Realism** Not all irrational beliefs are 'irrational', they may simply seem irrational. In fact, Alloy and Abrahamson (1979) suggest that depressive realists tend to see things for what they are (with normal people tending to view the world through rose-coloured glasses). They found that depressed people gave more accurate estimates of the likelihood of a disaster than 'normal' controls, and called this the sadder but wiser effect.) **2. Alternative explanations** The biological approach to understanding mental disorder suggest that genes and neurotransmitters may cause depression-for example research supports the role of low levels of the neurotransmitter serotonin in depressed people and has also found that a gene related to this is 10 times more common in people with depression (Zhang et al. 2005). The success of drug therapies for treating depression suggests that neurotransmitters do play an important role. At the very least a diathesis-stress approach might be advisable, suggesting that individuals with a genetic vulnerability for depression for depression are more prone to the effects of living in a negative environment, which then leads to negative irrational thinking. **Cognitive behaviour therapy (CBT), including challenging irrational thoughts -- treating depression** **What is meant by CBT?** Cognitive-behavioural therapy started life as cognitive therapy, based on the view that the way we feel is partly dependent on the way we think about events (i.e. cognition) and then treatment involves identifying the irrational thinking. Cognitive therapy grew into cognitive-behavioural therapy because, once irrational cognitions are identified, coping strategies need to be developed (i.e. behavioural change). **Ellis's CBT-REBT** **The basic idea** In the 1950s, Albert Ellis was one of the first psychologists to develop a form of CBT. The main aim of his therapy is to turn irrational thoughts into rational ones. Ellis named his therapy rational emotional behaviour therapy (REBT) as the therapy also resolves both emotional and behavioural problems. **Challenging irrational thoughts** REBT challenges mustabatory thinking (outlined above). Depressed individuals suffer serious emotional consequences when they fall short of their irrational beliefs. As a consequence, REBT focuses on disputing these musts and replacing them with effective rational beliefs that are more flexible **Ways of challenging irrational beliefs** Two ways to combat irrational beliefs are: **-Empirical disputing-**self-defeating beliefs may not be consistent with reality (e.g. 'Where is the proof that this belief is accurate?'). **-Pragmatic disputing-**emphasises the lack of usefulness of self-defeating beliefs (e.g. 'How is this belief likely to help me?'). Effective disputing helps the client feel better, and eventually become more self-accepting. **Homework** Clients are often asked to complete assignments between sessions. This might include asking a person out on a date when they had been afraid to do so before for fear of rejection or asking friends to tell them what they really think of them. Such homework is vital in testing irrational beliefs against reality and putting new rational beliefs into practice. **Behavioural activation** A characteristic of many depressed people is that they no longer participate in activities that they previously enjoyed. In CBT, therapist and client identify potentially pleasurable activities and anticipate and deal with any cognitive obstacles (e.g. 'I won't be able to achieve that'). This is based on the common-sense idea that being active leads to rewards that act as an antidote to depression. **Evaluation of CBT** **Positive** **1. Effectiveness-positive support for REBT, Cuijpers et al., 2013 and Hollon et al. (2006)** REBT, and CBT in general, have done well in outcome studies of depression. For example, Hollon et al. (2006) found that 40% of moderately to severely depressed patients treated with CBT for 16 weeks relapsed within the following 12 months, compared to a relapse rate of 45% for patients treated for the same period with drug therapy and 80% for those given a placebo drug. i.e. CBT works better than drugs in the long term. **Negative** **1. Mixed support for CBT, Robinson et al., 1990** In a review of 57 studies into the effectiveness of treatments for depression. Robinson et al., 1990 found that psychological therapies were better than no treatment at all. However, they could find no significant evidence that CBT was more effective than other forms of psychological therapy or drug therapy. Interestingly, while CBT was better than no treatment, Robinson et al. found that CBT was no more effective in reducing depressive symptoms than a placebo treatment (a dummy treatment). This fits in with a criticism of psychological therapies in general-that it is a relationship with a therapist that is important rather than any particular therapeutic technique. -- **[relies heavily on therapist competence]** **2. Less effective for some -- relies heavily on patient cooperation** CBT appears to be less suitable for people who have high levels of irrational beliefs that are both rigid and resistant to change (Elkin et al., 1985). Ellis also explained a possible lack of success in terms of suitability-some people simply do not want the direct sort of advice that CBT practitioners tend to dispense. They prefer to share their worries with a therapist without getting involved in the cognitive effort that is associated with recovery (Ellis, 2001). **3. Alternative treatments (or a combination with CBT) may be more appropriate** The most popular treatment for depression is the use of antidepressants such as SSRIs. Drug therapies have the advantage of requiring less effort on the part of the client (note that Ellis required 27 sessions of REBT). They can also be used in conjunction with a psychotherapy such as CBT. This may be useful as a distressed client may be unable to focus on the demands of CBT but the drug treatment enables them to cope better. The same review by Cuijpers et al. (2013) found that CBT was especially effective if it was used in conjunction with drug therapy. **Positive** **1. Appropriateness-CBT seems to fit the disorder** Since many of the symptoms of depressed patients are basically cognitive, it seems entirely appropriate for therapy to have as its central focus the changing of their negative and irrational attitudes into ones that are more positive and realistic. **The behavioural, emotional and cognitive characteristics of obsessive-compulsive disorder (OCD)** **The general idea** Obsessive-compulsive disorder (OCD) is classed as an anxiety disorder. The disorder typically begins in young adult life and has two main components-obsessions and compulsions. Obsessions are persistent thoughts and compulsions are repetitive behaviours. Wilner et al. (1976) found that 69% of OCD patients had both obsessions and compulsions, 25% had obsessions only, and 6% had compulsions only. **Behavioural characteristics of OCD** **Compulsions** The **behavioural** component of OCD is compulsive behaviour. Two elements to compulsive behaviours are: **1. Compulsions are repetitive** Typically sufferers of OCD feel compelled to repeat a behaviour. A common example is hand washing. Other common compulsive repetitions include counting, praying and tidying/ordering groups of objects such as CD collections (for those who have them) or containers in a food cupboard. **2. Avoidance** The behaviour of OCD sufferers may also be characterised by their avoidance as they attempt to reduce anxiety by keeping away from situations that trigger it. Sufferers of OCD tend to try to manage their OCD by avoiding situations that trigger anxiety. For example, sufferers who wash compulsively may avoid coming into contact with germs. However, this avoidance can lead people to avoid very ordinary situations, such as emptying their rubbish bins, and this can in itself interfere with leading a normal life. **Emotional characteristics of OCD** **1. Anxiety and distress** OCD is regarded as a particularly unpleasant emotional experience because of the powerful anxiety that accompanies both obsessions and compulsions. Obsessive thoughts are unpleasant and frightening, and the anxiety that goes with these can be overwhelming. The urge to repeat a behaviour (a compulsion) creates anxiety. **2. Accompanying depression** OCD is often accompanied by depression, so 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. **3. Guilt and disgust** As well anxiety and depression, OCD sometimes involves other negative emotions such as irrational guilt, for example over minor moral issues, or disgust, which may be directed against something external like dirt or at the self. **Cognitive characteristics of OCD** **1. Obsessive thoughts** (in around 90% of sufferers) Obsessive thoughts recur over and over again and are always unpleasant. Examples of recurring thoughts are worries of being contaminated by dirt and germs or certainty that a door has been left unlocked and that intruders will enter through it or impulses to hurt someone. **2. Cognitive strategies to deal with obsessions** Obsessions are the major cognitive aspect of OCD, but people also respond by adopting cognitive coping strategies. For example, a religious person tormented by obsessive guilt may respond by praying or meditating. This may help manage anxiety but can make the person appear abnormal and can distract them from everyday tasks. **3. Insight into excessive activity** People suffering from OCD are aware that their obsessions and compulsions are not rational. In fact, this is necessary for a diagnosis of OCD. If someone really believed their obsessive thoughts were based on reality that would be a symptom of a quite different form of mental disorder. However, in spite of this insight, OCD sufferers experience catastrophic thoughts about the worst case scenarios that might result if their anxieties were justified. They also tend to be hypervigilant i.e. they maintain constant alertness and keep attention focused on potential hazards. **The biological approach to explaining OCD: genetic explanations** **The basic idea** A popular explanation for mental disorders is that they are inherited. This would mean that individuals inherited specific genes from their parents that are related to the onset of OCD. **The COMT gene** The COMT gene may contribute to OCD. It is called the COMT gene because it is involved in the production of catechol-O-methyltransferase, or COMT for short. In turn, COMT regulates the production of the neurotransmitter dopamine that has been implicated in OCD. High levels of dopamine lead to compulsions. All genes comes in different forms (alleles) and one form of the COMT gene has been found to be more common in OCD patients than people without the disorder. This variation produces lower activity of the COMT gene and higher levels of dopamine. **The SERT gene** Another possible candidate gene is the SERT gene (also called 5-HTT) which affects the transport of serotonin, creating lower levels of this transmitter. Low levels of serotonin affect the worry circuit in the brain.\* One study found a mutation of this gene in two unrelated families where six of the family members had OCD (Ozaki et al., 2003). \* making it hard for an OCD patient to 'calm down' their worry circuits, leaving them over-active -- we can easily see how this might lead to the emotional characteristic 'anxiety' and the cognitive characteristic 'obsessions'. **OCD seems to be polygenic** Like many conditions, OCD seems to be polygenic. This means that OCD is not caused by one single gene but that several genes are involved. Taylor (2013) has analysed findings of previous studies and found evidence that up to 230 different genes may be involved in OCD. As seen above, genes that have been studied in relation to OCD include those associated with the action of dopamine as well as serotonin and both neurotransmitters are believed to have a role in regulating mood AND compulsive behaviours -- we can clearly see how such genes might cause emotional characteristics of OCD such as anxiety and depression or compulsions (a behavioural characteristic). **Evaluation of genetic explanations of OCD** **Positive** **1. Supporting evidence from twin studies, Miguel et al., 1997** Twin studies provide a precise way of assessing the extent of genetic influences on behaviours. In these, scientists look at the concordance rates of these influences-the correlation between the scores of a pair of twins on a specified variable. Since monozygotic (identical) twins are genetically identical there should be a higher concordance rate than dizygotic (non-identical) twins, who share 50 percent of their genes. Miguel et al. (1997) found a 53 to 87 per cent concordance rate for OCD in monozygotic twins compared with 22 to 47 per cent in dizygotic twins. **Negative** **1.** **Concordance rates not 100% for monozygotic twins** Twin studies also provide much ammunition for those arguing that environmental factors are important. If genetic factors were all important, the concordance rate for identical twins would be 100%, if diagnosis were perfect. Indeed it is the occurrence of OCD that seems to run in families rather than the specific symptoms (such as obsession with dirt), which shows that there is at least an environmental contribution to OCD in terms of the symptoms. **2. Environments are more similar** One reason why the concordance rate is higher for identical than for fraternal twins may because the environments in which identical twins are brought up tends to be more similar than those in which fraternal twins are brought up. This is arguably a more serious point than the above point as it could entirely invalidate a genetic explanation. **Negative** **3. You cannot discount, environmental factors (that we have more control over), Cromer et al., 2007** Environmental factors may trigger or increase the risk of developing OCD and should be seen in conjunction with any genetic abnormality. For example, Cromer et al. (2007) found that over half the OCD patients in their sample had a traumatic event in their past, and that OCD was more severe in those with more than one trauma. This suggests that OCD cannot be entirely genetic in origin, at least not in all cases. It may be more productive to focus on the environmental cause because we are more able to do something about these (and it's more acceptable ethically to do so). **Neural explanations** **i. Abnormal levels of neurotransmitters** Dopamine levels are thought to be abnormally high in people with OCD. This is based on animal studies-high doses of drugs that enhance levels of dopamine induce stereotyped movements resembling the compulsive behaviours found in OCD patients (Szechtman et al., 1998). Contrastingly, lower levels of serotonin have been associated with OCD. Serotonin has a role in preventing repetition of tasks, and a lack of serotonin therefore results in the loss of a mechanism that helps to suppress task repetition. **ii. Abnormal brain circuits** Several areas in the frontal lobes of the brain are thought to be abnormal in people with OCD. The orbitofrontal cortex (OFC) sends signals to the thalamus about things that are worrying, such as a potential germ hazard. The caudate nucleus (located in the basal ganglia) normally suppresses signals from the OFC. When the **caudate nucleus** is damaged, it fails to suppress minor 'worry' signals and the thalamus is alerted, which in turn sends signals back to the OFC, acting as a worry circuit. This supported by PET scans of patients with OCD, taken while their symptoms are active (e.g. when a person with a germ obsession holds a dirty cloth). Such scans show heightened activity in the OFC. **Evaluation of neural explanations of OCD** **Negative** **1. Issues of cause and effect** Many studies supporting neural explanations of OCD just show that there is an association between elevated activity in certain brain areas and OCD. Since it is only an association, it doesn't show that those brain areas play a role in causing the disorder. It is very possible that having obsessive compulsive symptoms leads to increased brain activity in areas concerned with thinking and action. **Positive** **1. Evidence linking OCD to abnormalities in the orbitofrontal cortex, Menzies et al., 2007** Menzies et al., 2007 used MRI to produce images of brain activity in OCD patients and their immediate family members without OCD (a sibling, parent or child) and also a group of unrelated healthy people. OCD patients and their close relative had reduced grey matter in key regions of the brain, including the OFC. This supports the view that anatomical and so neural differences may be linked the disorder. Indeed the fact that healthy relatives displayed this anatomical differences counters the previous criticism that symptoms may then lead to change in neurology. **Negative** ** ** **2.  Studies have not established that serotonin causes OCD** Studies in which serotonin levels in OCD patients have been assessed have typically found no differences between them and healthy controls. In addition, there is no evidence that patients with relatively low levels of serotonin respond better to drug therapy than patients whose serotonin levels are higher. **3. Issues of cause and effect for serotonin** Even if there were an association between OCD and low serotonin levels, that wouldn't prove that low serotonin levels hep to cause OCD-the causality might go in the other direction. **Negative (for genetic and neural)** **Alternative explanations, the two-process model** There is quite strong competition from behavioural explanations. First, fear in OCD patients is triggered by stimuli (e.g. unwashed hands; obsessional thoughts) that are very unlikely to cause harm. Second, these patients manage to reduce their level of fear by compulsive rituals (e.g., hand washing), and this behaviour is reinforced or rewarded by fear reduction. **The biological approach to treating OCD: Drug therapy** **SSRIs** The most common drugs used in the treatment of OCD are selective serotonin re-uptake inhibitors (SSRIs e.g. Prozac). Neurotransmitters are chemicals that are released by one neuron and then taken up by another neuron. Neurotransmitters that are not taken up by other neurons are taken up by the same neurons that released them in the first place. This process is called 're-uptake'. In essence, SSRI's inhibit the re-uptake of serotonin which means that more serotonin is available to be taken up by other neurons. The end result is that there is an increased concentration of serotonin. If a deficiency in serotonin is associated with the development and maintenance of OCD (in the 'worry circuit', in particular), it is reasonable to expect that drugs correcting that deficiency should prove effective in treatment of that condition. Increasing serotonin availability, as an inhibitory neurotransmitter, also might help suppress an OCD patient's urges to repeat tasks (compulsions). **Evaluation of drug therapy for OCD** **Positive** **1. Evidence for its effectiveness, Soomro et al., 2008** There is considerable evidence for the effectiveness of drug treatments. Soomro et al., 2008 reviewed 17 studies (a meta-analysis) of the use of SSRIs with OCD patients and found them to be more effective than placebos in reducing the symptoms of OCD **up to three months after treatment** i.e. in the short term. **Negative** **1. They may only work in the short term, Simpson et al., 2004** One of the issues regarding the evaluation of treatment is that most studies are only of three to four months duration, and therefore little long-term data exists. Indeed, Simpson et al. (2004) compared groups of patients with OCD who were administered behavioural therapy or drug therapy and who responded well to treatment. During the 12 weeks following the end of the active treatment**, 45% of patients who had received clomipramine relapsed back into the disorder compared to only 12% of those who had received exposure and response prevention**. Thus the beneficial effects of drug therapy **often don't last long after treatment has ceased.** **2. Drug therapy is palliative, not curative** It has been pointed out that treatments can be effective in two different senses. Some effective treatments are palliative - they suppress the symptoms of a disorder while applied but don't focus on the processes producing the disorder. Other effective treatments are curative - they reduce and eliminate the symptoms of the disorder as well as the underlying processes. Drug therapy doesn't affect the underlying mechanisms responsible for OCD. As a result, drug therapy reduces the symptoms of the disorder while patients take drugs but often fails to produce benefits that continue after. **3. Side effects, Abramowitz et al., 2009** Nausea, headache and insomnia are common side effects of SSRIs. These may not seem that terrible but are often enough to make the patient prefer not to take the drug. **Drop out is a real problem with SSRIs.** Abramowitz et al., 2009 reviewed several studies and found that the **drop-out rate varied between 24% and 89%.** Leaving a substantial number of people who the drugs will be ineffective on (because they have failed to complete the course). **Positive** **2. Drug therapies have practical benefits** Drug therapies **require little effort from the user and little input in terms of time;** considerably less than is required for therapies such as CBT, where the patient has to attend regular meetings and put considerable thought into tackling their problems. From the point of view of the health service, they are also cheaper because they require little monitoring and are cheap compared to psychological treatments. Furthermore, patients may still benefit from the fact that simply talking with a doctor during consultations may help. **[This means drug treatment for OCD (and other psychological illnesses) has positive implications for the economy -- research into this area could save the economy billions of pounds in sick leave, keeping the majority fit and well for work and paying taxes rather than receiving benefits. ]**