Obsessive-Compulsive Disorder Overview (Edexcel A-Level Psychology): Revision Notes

Obsessive-Compulsive Disorder Overview

Obsessive-compulsive disorder (OCD) is a common mental health condition that can have a major impact on a person's life. The World Health Organisation ranks it among the top ten most disabling illnesses in terms of impaired quality of life and loss of earnings. Most people may experience OCD-type symptoms at some point in their lives, usually during times of stress, but these are not as severe or pervasive as those experienced by individuals diagnosed with the disorder. Checking behaviours and fear of contamination are among the most common presentations of OCD.

Key terms

Obsessions are recurrent and persistent thoughts, urges or images that are experienced as intrusive or unwanted. These thoughts create anxiety and distress for the individual.

Compulsions are repetitive behaviours or mental acts that an individual feels compelled to perform in response to an obsession or according to rules that must be applied rigidly. The purpose of these behaviours is to reduce anxiety or prevent a feared outcome.

Tic disorder refers to uncontrolled spasms of muscles or vocal emissions that the individual cannot suppress.

Tourette's syndrome is a disorder characterised by unwanted and uncontrollable noises and movements (tics). Research has found links between Tourette's syndrome and OCD, particularly in the role of dopamine systems in the brain.

Symptoms

OCD is characterised by the presence of obsessions and/or compulsions. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) provides specific criteria for diagnosis:

• The obsessions cannot be ignored or suppressed and cause anxiety and/or distress. The sufferer may try to combat the obsession by performing compulsive behaviour that is not realistically connected to the obsession.

• The obsessions and/or compulsions are time-consuming, taking up more than one hour per day, and/or cause clinically notable distress or impairment to daily life.

• The symptoms cannot be explained by substance use or another medical condition, or by another mental disorder such as generalised anxiety disorder.

• The clinician must determine if the individual has good or fair insight into their disorder and recognises that the obsessive-compulsive beliefs are definitely or probably not true. Alternatively, they may have poor insight and believe their obsessions-compulsions are probably true, or they may have no insight and are completely convinced that their compulsions/obsessions are definitely true.

• The clinician should also establish if the individual has a current or past history of a tic disorder, as this can affect the severity of the disorder.

Features

Prevalence and demographics

The prevalence rate for OCD is between 1.1 and 1.8 per cent of the population. Females are more frequent sufferers as adults, although males are more commonly affected as children.

Age of onset

For most people, the age of onset is late teens or early twenties, but it is possible for symptoms to develop earlier or later. In 25 per cent of male sufferers, symptoms started before the age of 10. Generally, symptoms develop gradually, but in some cases they can be acute right from onset.

Risk factors

The risk is greater for people with higher negative emotionality, and for those who tend to internalise issues. OCD is also more frequent in those who suffered physical and sexual abuse in childhood.

There may be a genetic risk: the rate of OCD among first-degree relatives of adults with OCD is approximately twice that of those whose family have no history of the disorder.

Cultural considerations

OCD occurs across cultures at a similar rate and shows a similar age of onset and comorbidity with other disorders. There is a similar symptom structure involving cleaning, hoarding, taboo thoughts and symmetry. However, there are regional differences suggesting that cultural factors can affect the nature of the symptoms.

Biological explanation: neuroanatomical

Prevailing theories suggest that OCD is a biological disorder due to faulty functioning in the circuitry of an area of the orbitofrontal cortex. As with all biological explanations, there are several potential influences: genetic, structural differences and biochemical make-up. The focus in this section is on a structural explanation, although there is likely to be an interaction between all these factors.

Brain structure

The dominant view is that sufferers have faulty neuro-circuitry that links the orbitofrontal cortex to the thalamus. A key part of the circuit is the caudate nucleus, which normally inhibits the action of neurones that dampen the activity of the thalamus, acting as a kind of brake for thalamic activity.

In OCD, the caudate nucleus is overactive, which impedes the dampening function, leading to an overactive thalamus. The overactive thalamus causes a cascade reaction in the orbitofrontal cortex which, via the cingulate gyrus, connects to the caudate nucleus, thus increasing its stimulation and causing a loop of hyperactivity.

Hypothetically, the hypothalamus might be hardwired to produce primitive cleaning and checking behaviour, and the role of the orbitofrontal cortex is to alert the brain when something seems odd, causing anxiety, which promotes checking behaviour consistent with the obsessions and compulsions in OCD.

Biochemical explanation

The biochemical explanation focuses on the serotonin system and argues that dysregulation in this system leads to the development of OCD symptoms. This is largely due to evidence that SSRI drugs (which stop the reuptake of serotonin from the synapse, thus increasing serotonergic activity) are effective in reducing symptoms. Further research has implicated the dopamine systems in the production of the symptoms of tics and Tourette's syndrome.

Evaluation

Perhaps the most conclusive support is for the structural explanation. Menzies et al. (2007) found that scans of people suffering from OCD compared to healthy controls showed differences in the amount of grey matter in brain areas, including the orbitofrontal cortex, suggesting a physical difference in the areas implicated in this explanation. Other scanning studies show abnormally small caudate nuclei in sufferers of OCD.

When people with OCD are shown objects that bring on their symptoms, such as a dirty piece of clothing in someone with a cleaning compulsion, activity increases in the orbitofrontal cortex, the caudate nucleus and the anterior cingulate (McGuire et al., 1994). Furthermore, surgical lesioning of the cingulate gyrus is a successful intervention for most patients for whom other treatments have not worked; this would break the loop of hyperactivity suggested by this model.

Support for the biological explanation comes from research that shows a genetic link, because it suggests that physiological factors underlie the development of the disorder in many people. For example, twin studies typically (although not inevitably) show a higher concordance rate in MZ twins compared to DZ twins. Furthermore, many studies back this up, but in many cases sufferers have no family history at all, suggesting that genes alone cannot be an explanation, although this does not necessarily exclude other biological causes.

Promising research comes from animal studies such as that of Feng et al. (2007), who bred mice to show symptoms consistent with OCD (excessive grooming and anxious behaviour), when a targeted gene is missing. This gene is one that is expressed in the brain areas associated with planning and initiation of action, potentially indicating a clear link to the formation of compulsions. However, although humans and mice share 97 per cent of their DNA, there is still a massive difference in how these genes are expressed. Extrapolation to humans may therefore be unreliable, but there are findings from human research which suggest that there is a genetic marker for early onset OCD (Murphy et al., 1997).

When the disorder is present in the children of sufferers, it is found that their symptoms differed from those of their parents. This suggests that the cause of OCD is unlikely to be social learning, leading us back towards a biological cause. This idea is supported by findings that show antidepressants that alter the chemistry of the brain, especially those that raise serotonin levels, relieve the symptoms of OCD, suggesting a physical cause for the disorder.

One non-biological explanation: cognitive theory

Cognitive explanations centre on faulty information processing as being at the root of the disorder. The perceptions or thoughts we have about our experiences will trigger an emotional response, which then triggers behaviour to deal with the emotion. If we change the original perception, then what follows will also change. An influential theorist in this area is Paul Salkovskis, who has been developing and refining cognitive models of OCD for many years.

In the case of OCD, early childhood experiences could cause a general negative belief system about how the world works. For example, the world is full of threats. This leads to intrusive thoughts (obsessions) in response to events that happen. These thoughts are misinterpreted and made important, causing anxiety. To deal with the anxiety, the person adopts counterproductive behaviour such as thought suppression, or they feel compelled to perform neutralising rituals (compulsions) that give temporary relief. This serves to reinforce the faulty thought pattern at the root of the sequence. Unless a link in this sequence is broken, it becomes self-perpetuating.

One further theory is that a lack of confidence in memory may explain checking behaviours. For example, it is not that the person does not have a memory for checking that they turned the oven off; it is that they do not trust their recall and feel compelled to check again. Woods et al. (2002) conducted a meta-analysis of studies that aimed to test how memory relates to checking and found that those suffering from OCD had a slightly worse memory for recalling stimuli that had been presented, but they felt that their memory was inadequate compared to those who do not have OCD.

Another idea is that people with OCD may be hypervigilant (Williams et al., 1997). This means they are constantly scanning for threats in the environment and have an attentional bias towards potential threats. These threats form the basis of their obsessions. The detection of threat then triggers anxiety, which in turn triggers compulsive behaviour designed to reduce the anxiety level. Rahman (2004) reports a case study showing that someone with OCD centred on blood could, due to hypervigilance, recall all the times in her past that she had come into contact with blood.

Evaluation

Therapy based on a general cognitive explanation is used successfully in many cases, suggesting some validity behind the explanation. Van Balkom et al. (1996) found it to be just as effective as a drug treatment, which lends support to the view that the cause of OCD may lie in faulty cognitive function, because if it were purely biological then the drugs would have been a more effective treatment.

The Pediatric OCD Treatment study (POTS, 2004) compared treatments in a randomised investigation and found that CBT was more effective than drug treatment, but that there was a minor improvement when CBT was combined with the drug therapy. This suggests that when CBT is done well, it is the most appropriate treatment for children and adolescents.

Further support comes from studies that show what happens when sufferers try to engage in thought suppression in order to block the obsessions. Rather than this stopping the cycle, it suspends it temporarily. For example, Salkovskis and Kirk (1997) conducted a diary study of people with OCD. On some of the days of the study, they were told to deliberately suppress the obsessive thoughts but on others they were allowed free rein. It was found that the frequency of intrusive thoughts was much higher on the days they tried to suppress them.

A more eclectic explanation would involve combining the cognitive with other theories in order to increase its explanatory power. For example, a fuller explanation might involve the orbitofrontal cortex hyperactivity loop, which affects how the person processes information.