Psychopathology

Any relatively usual behaviour or characteristic can be thought of ‘normal’ and any behaviour that is different to this is ‘abnormal’.

Because someone is not the statistical norm, does not necessarily mean that it is a condition that needs treatment. For example, abnormally high IQ scores (e.g. over 130) are abnormal, but that does not mean it needs to be treated and returned to normal. Therefore need to be careful in using this definition in making diagnoses.

Just because someone may be ‘abnormal’ does not mean that they will benefit from being labelled that way. For example, someone with a very low IQ but who was able to lead a relatively normal life may not benefit from a label as it could affect how others see them and therefore how they are treated, which could actually negatively impact them.

Easy to apply this definition in diagnosing conditions such as intellectual disability disorder. Also helpful in other mental disorders where severity is measured in an individual by comparing them to statistical norms.

When a person behaves in a way that is different from how we expect people to behave.

Whilst this definition is useful for diagnosing disorders such as antisocial personality disorder, there are other factors besides deviation from social norms that should be considered in diagnosing e.g. the distress to other people that results from antisocial personality disorder. Therefore this definition should not be used as a sole reason for defining abnormality.

This is the view that behaviour cannot be judged properly unless it is viewed in the context of the culture in which it originates. Social norms vary across cultures, meaning that what might be seen as abnormal in one culture would not be abnormal in each other – therefore this definition does not transfer well across cultures.

Too much reliance on deviation from social norms to understand abnormality can lead to systematic abuse of human rights. Looking at the historical examples of deviation, it is pretty clear that diagnoses such as drapetomania and *********** have been used in the past to maintain control over minority ethnic groups and women.

A person may be considered ‘abnormal’ when they cannot cope with the demands of everyday life and fail to function adequately.

A strength of this definition is that it attempts to include the subjective experience of the individual. It is therefore a useful definition as it at least acknowledges what the patient is experiencing is important too.

Someone has to judge whether a patient is distressed or distressing when deciding is someone is failing to function adequately. The problem is that some patients may say they are distressed but may not be judged as suffering. Methods such as the Global Assessment of Functioning Scale try to make this as objective as possible, but it is still down to a psychiatrist to make this judgement.

How can we tell if someone is genuinely failing to function or just deviating from social norms? E.g. alternative lifestyles such as extreme sports could be seen as failure to function because the individual does not necessarily have a permanent address or job and may be putting themselves at risk of harm. Treating these behaviours as ‘failures’ of adequate functioning risks limiting personal freedom and discrimination.

According to this definition of abnormality, someone can be classified as abnormal if they deviate from what we consider to be ideal mental health. Once we know what someone who is psychologically healthy should look like, we can start to work out if someone is deviating this and can therefore be considered ‘abnormal’.

A strength of this definition is that it is very comprehensive and covers a broad range of criteria for mental health. This sheer range makes it a good tool for thinking about mental health.

The criteria have been designed based on Western ideals, meaning that they do not apply very well to other cultures. For example, individualistic cultures would see a lack of personal autonomy as deviating from ideal mental health, but this does not apply as well to collectivist cultures that value the needs of the group over the needs of the individual.

It is unrealistic to expect an individual to be able to meet all criteria all the time. Therefore based on this approach, almost everyone could be diagnosed as abnormal. On the positive side, this allows people to see the ways in which they might benefit from seeking treatment to improve their mental health. However, deviation from ideal mental health is probably of no value in thinking about who might benefit from treatment against their will.

A phobia is an irrational fear of an object or a situation.

All phobias are characterized by excessive fear and anxiety, disproportionate to any real danger presented by the stimulus (an object, place or situation) that has triggered the phobia.

The DSM-5 recognizes the following categories of phobia and related anxiety disorder:

• Specific phobia – phobia of an object or a situation.
• Social anxiety (social phobia) – phobia of a social situation.
• Agoraphobia – phobia of being outside or in a public place.

Behavioural Characteristics of Phobias: We respond to things we fear by behaving in particular ways. The fear responses in phobias are the same we experience for any other fear, even if the fear is irrational (Panic, Fear, Endurance).

Emotional Characteristics of Phobias: (Anxiety, Unreasonable Emotional Response).

Cognitive Characteristics of Phobias: (Cognitive Distortions, Irrational Beliefs, Selective Attention to Phobic Stimulus).

All forms of depression and depressive disorders are characterized by changes to mood.

The DSM-5 recognizes the following categories of depression and depressive disorders:

• Major depressive disorder – severe but often short-term depression.
• Disruptive mood dysregulation disorder – childhood temper tantrums.
• Persistent depressive disorder – long-term or recurring depression, including sustained major depression and what used to be called dysthymia.
• Premenstrual dysphoric disorder – disruption to mood prior to and/or during menstruation.

Behavioural Characteristics of Depression: (Lower Activity Levels, Disruption to Sleep and Eating Behaviour, Aggression and Self-Harm).

Emotional Characteristics of Depression: (Lowered Mood, Anger, Lowered Self-Esteem).

Cognitive Characteristics of Depression: (Poor Concentration, Attending to and Dwelling on the Negative, Absolutist Thinking).

The DSM-5 recognizes OCD and a range of related disorders. What these disorders all have in common is repetitive behavior accompanied by obsessive thinking.

OCD – characterized by obsessions and/or compulsions, although most people with a diagnosis of OCD have both.

Trichotillomania – compulsive hair pulling.

Hoarding Disorder – compulsive gathering of possessions and the inability to part with anything, regardless of its value.

Excoriation Disorder – compulsive skin picking.

Behavioural Characteristics of OCD: (Compulsions - Compulsions are repetitive and Compulsions reduce anxiety. Avoidance).

Emotional Characteristics of OCD: (Anxiety and Distress. Accompanying Depression. Guilt and Disgust). Conpulsions tend to bring relief from anxiety but this is temporary.

In the classic study of phobias, Watson and Rayner 1920) aimed to demonstrate that an irrational fear could be induced by use of classical conditioning. They used a placid baby boy, referred to as ‘Little Albert’ who, at 9 months, showed no fear of a laboratory white rat. At age 11 months they carried the following procedure aimed to induce fear. Whenever the rat was placed in Albert’s lap, Watson made a loud noise by banging together two steel bars behind Albert’s back. He did this a total of 7 times. In this procedure, the loud noise is an unconditioned stimulus and Albert’s response to it (crying) is an unconditioned response. Before conditioning the rat was a neutral stimulus. By the third trial Albert showed fear whenever he saw the rat. The rat was now a conditioned stimulus and Albert’s fear of it was a conditioned response. In his two-process model of phobia acquisition, Mowrer suggests that phobias are acquired as a result of classical conditioning and maintained by operant conditioning. A person who is terrified of spiders is likely to run away when they see one. The escape and consequent reduction of fear acts as a negative reinforcer, increasing the likelihood that they will continue to avoid spiders in future. In this way, the phobia is maintained. When an individual avoids a situation which is unpleasant, the behaviour results in a pleasant consequence which means the behaviour is likely to be repeated. Mowrer suggested that whenever we avoid a phobic stimulus we successfully escape the fear and anxiety that we would have suffered if we had entered its presence or remained there. This reduction in fear reinforces the avoidance behaviour and so the phobia is maintained.

The two-process model goes beyond Watson and Rayner’s concept of classical conditioning. It explains how phobias can be maintained over time, which has important implications for therapies because it explains why patients need to be exposed to the feared stimulus. Once a patient is prevented from practicing their avoidance behaviour the behaviour ceases to be reinforced and so it declines. Therefore a strength of the two-process model is its application to therapy.

Not all avoidance behaviour associated with phobias seems to be the result of anxiety reduction, at least in more complex phobias like agoraphobia. There is evidence to suggest that at least some avoidance behaviour appears to be motivated more by positive feelings of safety. This can explain why some patients with agoraphobia can leave their house with a trusted person and experience relatively little anxiety but not alone (Buck, 2010). This is a problem for the two-process model as it suggests that avoidance is motivated by anxiety reduction.

Sometimes an individual may develop a phobia even if they are not aware of having had a related bad experience. The two-process model cannot explain why someone who has never even encountered a snake, let alone been frightened by one, may then develop a phobia of them.

The two-process model is good as it explains all of the behavioral characteristics of phobias. However, we know that phobias have a cognitive element as well, which the two-process model does not explain. Therefore the two-process model is limited as it cannot fully explain how phobias develop or all of the characteristics associated with phobias.

Bounton (2007) points out that evolutionary factors probably have an important role in phobias but the two-factor theory does not mention this. For example, we easily acquire phobias of things that have been a source of danger in our evolutionary past e.g. snakes, the dark, and it is adaptive to acquire such fears. Seligman (1971) called this biological preparedness – the innate predisposition to acquire certain fears. However it is rare to develop fear of things like cars or guns, which are actually more dangerous now – perhaps because they have only existed recently? Therefore appears that there is more to acquiring phobias than just conditioning, which the two-process suggests.

Behavioural Therapy designed to gradually reduce phobic anxiety through the principle of classical conditioning. If the sufferer can learn to relax in the presence of the phobic stimulus, they will be cured. A new response to the phobic stimulus is learned – the phobic stimulus is paired with relaxation instead of anxiety. This learning of another response is called counterconditioning. It is also impossible to be afraid and relaxed at the same time, so one emotion prevents the other – this is called reciprocal inhibition.

The anxiety hierarchy: Put together by the patient and therapist. This is a list of situations related to the phobic stimulus that provoke anxiety arranged in order from least frightening to most frightening.

Relaxation: The therapist teaches the patient to relax as deeply as possible. This might involve breathing exercises, meditation or mental imagery techniques. Alternatively, drugs might be used to achieve relaxation.

Exposure: The patient is exposed to the phobic stimulus while in a relaxed state. The patient starts at the bottom of the anxiety hierarchy and moves up a level when they can stay relaxed in the presence of the phobic stimulus. When the patient can stay relaxed in situations high on the anxiety hierarchy, treatment is successful.

Gilroy et al (2003) looked at 42 patients treated for spider phobia using systematic desensitisation, compared with control group who was treated by relaxation but without exposure. At both three months and 33 months after the treatment, the SD group were less fearful than the relaxation group. Therefore there is research support that shows SD is helpful as a long-lasting and effective treatment of specific phobias.

Some alternative treatments such as flooding or cognitive therapies may not be suitable to all patients – SD works well with a range of individuals and is therefore an appropriate treatment for many individuals.

Patients prefer SD – largely because it does not cause the same level of trauma as alternative treatments such as flooding. This is shown in the low level of refusal rates and attrition rates in SD.

Flooding also involves exposing phobic patients to their phobic stimulus – however flooding involves immediate exposure to a very frightening situation. Flooding sessions typically last longer than SD sessions, often two to three hours – sometimes only one session is needed to cure a phobia. Flooding works by stopping phobic responses very quickly. Without the option of avoidance behaviour, the patient very quickly learns that the phobic stimulus is harmless. In classical conditioning this is called extinction. A learned response is extinguished when the conditioned stimulus is encountered without the unconditioned stimulus, resulting in the conditioned stimulus no longer producing the conditioned response.

It is at least as effective as other treatments for phobias. Compared to cognitive therapies (Ougrin, 2011) flooding has been found to be highly effective and quicker than alternatives.

It is effective for treating simple phobias but appears to be less effective for more complex phobias e.g. social phobias. This may be because social phobias have cognitive aspects, and so this kind of phobia might benefit more from cognitive therapies.

It is a highly traumatic experience. Patients give consent, but many are often unwilling to see it through to the end, meaning that time and money can be wasted preparing patients only for them to refuse to start or complete treatment.

Aaron Beck (1967) suggested a cognitive approach to explaining why some people are more vulnerable to depression than others. In particular, it is a person’s cognitions (the way they think) that creates this vulnerability. Beck suggested there were three parts to this cognitive vulnerability: Faulty information processing, negative self-schemas, the negative triad.

Faulty Information Processing: When depressed, we tend to attend to the negative aspects of a situation and ignore the positives. We also tend to blow small problems out of proportion and think in ‘black and white’ terms.

Negative Self-Schemas: A schema is a ‘package’ of ideas and information developed through experience. They act as a mental framework for the interpretation of sensory information. A self-schema is therefore the package of information we have about ourselves. We use schemas to interpret the world, so if we have a negative self-schema we interpret all information about ourselves in a negative way.

Negative Triad: A person develops a dysfunctional view of themselves because of three types of negative thinking that occur automatically, regardless of the reality of what is happening at the time. These three elements are called the negative triad. When we are depressed, negative thoughts about the world, the future and oneself often come to us.

Albert Ellis (1962) suggested an alternative cognitive explanation of depression. He proposed that good mental health is the result of rational thinking, defined as thinking in ways that allow people to be happy and free of pain. To Ellis, conditions like anxiety and depression (poor mental health) result from irrational thoughts. Ellis defined irrational thoughts not as illogical or unrealistic thoughts, but as any thoughts that interfere with us being happy and free of pain. He used the ABC model to explain how irrational thoughts affect our behaviour and emotional state.

Activating Event: According to Ellis we get depressed when we experience negative events and these trigger irrational beliefs.

Beliefs: Ellis identified a range of irrational beliefs. He called the belief that we must always succeed or achieve perfection ‘musturbation’. ‘I-can’t-stand-it-itis’ is the belief that it is a major disaster whenever something does not go smoothly. Utopianism is the belief that life is always meant to be fair.

Consequences: When an activating event triggers irrational beliefs there are emotional and behavioural consequences. For example, if you believe you must always succeed and then fail at something, this can trigger depression.

A strength of Beck’s explanation of depression is that there is research to support the idea that depression is associated with faulty information processing, negative self-schemas and the cognitive triad. For example Grazioli and Terry found that women that were more cognitively vulnerable when assessed before and after giving birth were more likely to suffer post-natal depression. In addition, Clark and Beck (1999) conducted a review of research into depression and concluded there is solid support for all these cognitive vulnerability factors. This is important as it shows that these cognitive factors exist before an individual develops depression, suggesting that they do play a role in causing depression in real life situations.

One limitation of both Ellis’s and Beck’s explanations of depression is that they cannot explain the more complex aspects of depression. For example these theories cannot explain the extreme anger, hallucinations, bizarre beliefs or Cortard syndrome that some depressed patients suffer. However these symptoms are part of the experience that individuals with depression go through, and therefore it is important that any theories of depression can explain this. Therefore, these theories can be seen as incomplete and unable to adequately explain depression.

A limitation of Ellis’s theory of depression is that it only partially explains depression. Some cases of depression do follow an activating event, but this is known as reactive depression and is seen as different to depression that arises without an obvious cause by psychologists. This means that Ellis’s theory can only be used to explain reactive depression, but may not be able to explain why depression arises in individuals without an obvious cause. Therefore this theory is limited as it cannot fully explain all types of depression.

A strength of both Beck’s and Ellis’s theories of depression is that they have practical real-life applications. These theories have led to the development of successful therapies for treating depression, such as CBT and REBT. These theories work to challenge irrational beliefs to reduce depression, a concept which has been supported by research (Lipsky et al. 1980). This again lends support to the theory, as it indicates that irrational thinking does play a role in depression.

CBT is the most commonly used psychological treatment for depression and a range of other mental health problems. If you see a clinical psychologist for a mental health problem, the chances are you will receive CBT. CBT begins with an assessment in which the patient and the cognitive therapist work together to clarify the patient’s problems. They jointly identify goals for the therapy and put together a plan to achieve them. CBT then involves working to change negative and irrational thoughts and finally put more effective behaviours into place.

CBT - Beck's Cognitive Therapy: Application of Beck’s cognitive theory of depression. The idea is to identify automatic thoughts about the self, world and future. Once identified, these thoughts must be challenged. As well as challenging these thoughts directly, cognitive therapy aims to help patients test the reality of their negative beliefs. They might therefore be set homework such as to record when they enjoyed an event or when people were nice to them. This is sometimes referred to as the ‘patient as scientist’. In future sessions if patients say that no one is nice to them or there is no point going to events, the therapist can then produce this evidence and use it to prove the patient’s statements are incorrect.

One strength of CBT is that it is supported by research. For example, March et al (2007) compared the effects of CBT with antidepressant drugs and found that after 36 weeks 81% of the CBT group, 81% of the antidepressants group and 86% of the CBT + antidepressants group were significantly improved. This shows that CBT is just as effective as medication and helpful alongside medication. Therefore a strength of this theory is that it has been shown to be an effective treatment of depression.

One limitation is that CBT may not be appropriate for all individuals. In some cases depression can be so severe that patients cannot motivate themselves to engage with the hard cognitive work of CBT. They may not even be able to pay attention to what is happening in a session. Where this is the case, it is possible to treat patients with antidepressant medication and commence CBT when they are more alert and motivated. Although it is possible to work around this by using medication, this is a limitation of CBT as it cannot be used as the sole treatment for all cases of depression.

One limitation of CBT is that the success may not be a result of the therapy but because of the relationship between the patient and the therapist. Rosenzweig (1936) suggested that the differences between different methods of psychotherapy such as between CBT and systematic desensitisation, may actually be quite small. All psychotherapies share one essential ingredient – the therapist-patient relationship. It may be the quality of this relationship that determines success rather than any particular technique that is used.Many comparative reviews (e.g. Luborsky et al. 2002) find very small differences, which supports the view that simply having an opportunity to talk to someone who will listen could be what matters most. Therefore a limitation of this treatment is that it may not actually be down to the therapy that patients improve.

One limitation of CBT is that it focuses too much on cognition. As a result, there is a risk that because of its emphasis on what is happening in the minds of the individual patient CBT may end up minimizing the importance of circumstances in which a patient is living (McCusker 2014). A patient living in poverty or suffering abuse needs to change their circumstances, and any approach to therapy that emphasizes what is happening in the patient’s mind rather than their environment can prevent this. A limitation of CBT therefore is that the techniques, when used inappropriately, can demotivate people to change their situation.

Some mental disorders appear to have a stronger biological component than others and OCD is a good example of a condition that may be largely understood as biological in nature. One form of biological explanation is the genetic explanation. Genes are involved in individual vulnerability to OCD. Lewis (1936) observed that of his OCD patients, 37% had parents with OCD and 21% had siblings with OCD. This suggests that OCD runs in families, although what is probably passed on from one generation to the next is genetic vulnerability not the certainty of OCD. According to the diathesis-stress model certain genes leave some people more likely to suffer from a mental disorder but it is not certain – some environmental stress (experience) is necessary to trigger the condition.

Diathesis – biological. An individual may have genes that makes them more vulnerable to OCD.

Stress – eenvironmental. Not everyone that is vulnerable to OCD will develop the disorder – however if an individual experiences the right stressors in their environment, this may result in the individual developing OCD.

Researchers have identified genes, which create vulnerability for OCD, called candidate genes. Some of these genes are involved in regulating the development of the serotonin system. For example the gene 5HT1-D beta is implicated in the efficiency of transport of serotonin across synapses.

However, 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. Genes that have been studied in relation to OCD included those associated with the action of dopamine as well as serotonin, both neurotransmitters believed to have a role in regulating mood.

One group of genes may cause OCD in one person but a different group of genes may cause the disorder in another person. The term used to describe this is aetiologically heterogeneous, meaning that the origin (aetiology) of OCD has different causes (heterogeneous). There is also some evidence to suggest that different types of OCD may be the result of particular genetic variations, such as hoarding disorder and religious obsession.

One strength of the genetic explanation of OCD is that there is research support for it. Nastadt et al. (2010) reviewed previous twin studies and found that 68% of identical twins shared OCD as opposed to 31% of non-identical twins. This strongly suggests a genetic influence on OCD. On the other hand, if OCD was purely down to genetics, there should be a 100% concordance rate as identical twins share 100% of their DNA. Overall however, the genetic explanation for OCD is strong as there is evidence to support for the influence of genes in the development of OCD.

One limitation of the genetic explanation is that it is incredibly difficult to identify all the genes involved in causing OCD. Psychologists have not been successful at pinning down all of the genes involved in OCD. One reason for this is because it appears several genes are involved and that each genetic variation only increases the risk of OCD by a fraction. The consequence is that a genetic explanation is unlikely to ever be very useful because it provides little predictive value. Therefore the genetic explanation of OCD is limited as it may not be useful in identifying individuals at risk developing of OCD.

One limitation to the genetic explanation of OCD is that it only considers the biological factors involved in OCD. It also appears that environmental factors can also trigger or increase the risk of developing OCD (diathesis-stress model). 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 causes because we are more able to do something about this. Therefore the genetic explanation of OCD is limited as it does not consider all factors that may be involved.

One explanation for OCD concerns the role of the neurotransmitter serotonin, which is believed to help regulate mood. Neurotransmitters are responsible for relaying information from one neuron to another. If a person has low levels of serotonin then normal transmission of mood-relevant information does not take place and mood – and sometimes other mental processes – are affected. At least some cases of OCD may be explained by a reduction in the functioning of the serotonin system in the brain.

Some cases of OCD, and in particular hoarding disorder, seem to be associated with impaired decision making. This in turn may be associated with abnormal functioning of the lateral of the frontal lobes of the brain. The frontal lobes are responsible for logical thinking and making decisions. There is also evidence to suggest that an area called the left parahippocampal gyrus, associated with processing unpleasant emotions, functions abnormally in OCD.

One strength of this explanation is that there is evidence to support the role of some neural mechanisms in OCD. For example, some antidepressants work purely on the serotonin system, increasing levels of this neurotransmitter. Such drugs are effective in reducing OCD symptoms and this suggests that the serotonin system is involved in OCD. Also OCD symptoms form a part of a number of other conditions that are biological in origin, for example Parkinson’s Disease (Nestasdt et al. 2010). This suggests that the biological processes that cause the symptoms in those conditions may also be responsible for OCD. Therefore a strength of this theory is that it is supported by research.

One limitation of neural explanations is that it is not clear exactly what mechanisms are involved. Studies of decision making have shown that these neural systems are the same systems that function abnormally in OCD (Cavedini et al. 2002). However research has also identified other brain systems that may be involved sometimes but no system has been found that always plays a role in OCD. Therefore it is a limited explanation of OCD as we cannot use this explanation to identify those most at risk of developing OCD.

Drug Therapies: Drug therapy for mental disorders aims to increase or decrease levels of neurotransmitters in the brain or to increase/decrease their activity. When explaining OCD from the biological perspective, we saw that low levels of serotonin are associated with OCD. Therefore drugs work in various ways to increase the level of serotonin in the brain.

SSRIs: The standard medical treatment used to tackle the symptoms of OCD involves a particular type of antidepressant drug called a Selective Serotonin Reuptake Inhibitor (SSRI). SSRIs work on the serotonin system in the brain, preventing the reuptake of serotonin in the synapse by the pre-synaptic neuron where it is broken down and re-used. By preventing the re-absorption and breakdown of serotonin SSRIs effectively increase its levels in the synapse and thus continue to stimulate the postsynaptic neuron, which compensates for whatever is wrong with the serotonin system in OCD.

Combining SSRIs With Other Treatments: Drugs are often used alongside CBT to treat OCD. The drugs reduce a patient’s emotional symptoms, such as feeling anxious or depressed. This means that patients can engage more effectively with the CBT.

Alternatives to SSRIs: Where an SSRI is not effective after three to four months the dose can be increased or it can be combined with other drugs. Sometimes different antidepressants are tried. Patients respond very differently to different drugs and alternatives work well for some people and not at all for others.

One strength is that there is clear evidence for the effectiveness of SSRIs in reducing the severity of OCD symptoms and so improving quality of life for individuals with OCD. Soomro et al (2009) reviewed studies comparing SSRIs to placebos in the treatment of OCD and concluded that all 17 studies reviewed showed significantly better results for the SSRIs than for placebo conditions. Effectiveness is greatest when SSRIs are combined with a psychological treatment (often CBT). Symptoms decline significantly for about 70% of patients taking SSRIs. Of the remaining 30 alternative drug treatments or combinations of drugs and psychological treatments will be effective for some, so drugs can help most patients with OCD. Therefore a strength of this treatment is that there is support for its effectiveness as a treatment.

One strength of drug treatments is that they are cost effective. Drug treatments are cheap when compared to psychological treatment, which is therefore good value for a public health system. In addition, SSRIs are non-disruptive to patients’ lives when compared to psychological therapies, as individuals can simply take the drugs until their symptoms decline, without having to engage with the hard work of psychological therapy. This is a strength of drug treatments therefore, as it allows more individuals to be treated for a lower cost.

One limitation is that a significant minority of individuals with OCD will get no benefit from taking drugs like SSRIs.  Some patients also suffer side-effects such as indigestion, blurred vision and loss of sex drive. For those taking Clomipramine, side-effects are more common and can also be more serious. For example, more than 1/10 patients suffer erection problems, tremors and weight gain. More than 1/100 become more aggressive and suffer disruption to blood pressure and heart rhythm. Therefore the effectiveness of the medication is reduced because people stop taking it.

One limitation of drug treatments is that the supporting research might not be trustworthy. Some psychologists believe that the evidence favouring drug treatments is biased because the research is sponsored by drug companies who do not report all the evidence (Goldacre, 2013). Therefore, the research used to support the effectiveness of drug treatments may not give a full picture of the treatments.  This is a limitation as it may mean that individuals are being treated with drugs that they believe are effective, due to research not being entirely honest, when in fact the drugs may not be helping.

One limitation of drug treatments of OCD is that it may not be effective for all cases of OCD. OCD is widely believed to be biological in origin, meaning it makes sense to treat OCD biologically. However, OCD can have a range of other causes and in some cases OCD is a response to traumatic life event.  Therefore it is questionable whether a biological treatment is the most appropriate treatment in these cases.

CBT - Ellis' Rational Emotive Behavioural Therapy:  REBT extends the ABC model to an ABCDE model (D stands for dispute and E for effect). The central technique of REBT is to identify and dispute (challenge) irrational thoughts. For example, a patient might talk about how unlucky they have been or how unfair things seem. An REBT therapist would identify these as examples of utopianism and challenge this as an irrational belief. This would involve a vigorous argument. The intended effect is to change the irrational belief and so break the link between negative life events and depression. This vigorous argument is the hallmark of REBT. Ellis identified different methods of disputing.

Another limitation of CBT is that it focuses too much on the present. One of the basic principles of CBT is that the focus in therapy is on the present and future, not the patient’s past, unlike some other forms of psychological therapy. Some patients are aware of the link between their childhood experiences and current depression and want to talk about their experiences. As a result, they find this ‘present-focus’ very frustrating. Therefore, CBT is limited as it does not consider the role of other factors outside the present in developing depression.

One limitation of this explanation is that it is unclear if neural mechanisms cause OCD or are a result of it. There is evidence to suggest that various neurotransmitters and structures of the brain do not function normally in patients with OCD. However this is not the same as saying that this abnormal functioning causes the OCD. This is a limitation as biological abnormalities could be a result of OCD rather than its cause.

One limitation of this explanation is that the link between serotonin and OCD may be due to co-occurring depression. Many people who suffer OCD become depressed – having two disorders together is called co-morbidity. This depression probably involves disruption to the serotonin system. Therefore, a limitation of this explanation is that it could simply be that the serotonin system is disrupted in many patients with OCD because they are depressed as well.