Obsessive Compulsive Disorder (3 page)

Another area of difficulty for the clinician is distinguishing OCD from stereotyped behaviour in children who have learning disabilities or autistic spectrum disorders. They may repeat actions for a number of other reasons such as the immediate pleasure of doing something well, or alleviating bore-dom rather than a feeling of preventing harm. In these instances, the ritual will be empty of meaning. However, people with autistic spectrum disorders can and do develop OCD so a careful description of the subjective experiences is necessary to determine the motivation behind the behaviour.

A 13-year-old boy with Asperger’s syndrome had developed a ritual of counting before he could open doors. When asked about this he explained that he had the feeling that something bad was going to happen if he did not open the door at just the right time. He was unable to identify a particular number that was involved, but he could explain that the anxiety or worrying thought came before he started to count. He also had other rituals such as getting dressed in a particular order which he described as being the right way to do things. These rituals he was able to modify under instruction, because they did not cause him distress. In this case, a diagnosis of OCD was made because he had the feeling that he had to do the counting ritual in order to prevent harm, whereas the dressing ritual seemed to be because he preferred to do things in a particular order.

Young people with OCD often have other psychological problems, with around 75 per cent experiencing difficulties that fulfil criteria for a diagnosis (March
et al.
, 2004; Swedo and Rapoport, 1989). This is not uncommon, as many other disorders have high rates of comorbidity (Caron and Rutter, 1991). However, while anxiety and depression have a high rate of occurrence in OCD, it is less common to find OCD co-occurring with depression or anxiety, when they are the primary presenting problem (Shear
et al.
, 2006).

Other anxiety disorders are common in OCD, such as generalised anxiety (worries that are not related to the OCD and may be around school, 8

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friendships, family, world affairs), separation anxiety (usually being away from their parents) and social anxiety (worrying about social situations).

The most recent British child mental health study (Heyman
et al.
, 2001) found that 52 per cent of young people with OCD had a comorbid anxiety disorder. There is considerable overlap in the phenomenology of cognitions in OCD and worry and they may be intrusive, similar in form, occur repeatedly and be persistent (Comer
et al.
, 2004). Therefore it is unclear whether the comorbidities reflect problems with the diagnostic systems or represent multiple pathologies. Nevertheless, the treatment of OCD with cognitive behaviour therapy (CBT) has a positive effect on other anxiety disorders (O’Kearney
et al.
, 2006).

The co-existence of depression or dysthymia in young people with OCD

is not uncommon, with studies suggesting that up to 20 per cent of young people with OCD also have a mood disorder (Heyman
et al.
, 2001). It appears likely that this is often a secondary problem, as the OCD begins to have a significant impact on the young person’s life. Whilst mild to moderate depression does not appear to have a significant impact on response to treatment, severe depression is associated with a poorer response (Abramowitz and Foa, 2000).

Young people with OCD may also experience externalising disorders, such as attention deficit hyperactivity disorder (ADHD), conduct disorder or oppositional defiant disorder. Different studies report different levels of comorbidity, ranging between 10 per cent and 44 per cent (Heyman
et al.
, 2001; Swedo and Rapoport, 1989; Thomsen, 1999). This is likely to be influenced by both catchment populations and how the behaviour is classified.

Many young people are in conflict with their parents as a result of the OCD

and this presents difficulties in diagnosis, since the conflict may be a consequence of their OCD or it may be a separate problem indicating a more deep-seated difficulty, such as oppositional defiant disorder. ADHD is also found in clinic populations and may represent a particular difficulty for psychological treatment. Careful planning may be needed to maximise engagement and reduce the effects of impulsivity and poor attention.

Young people or families often have concerns that their obsessional worries are a sign of madness. However, delusions do not develop from obsessional thoughts (Rachman and Hodgson, 1980), nor is there a link between OCD and psychotic disorders more broadly (Salkovskis, 1996b).

People with OCD generally have insight into their condition and recognise that their behaviour is irrational, whereas people with psychosis often lack insight.

There is evidence to suggest that tic disorders are linked to OCD. Nearly 50 per cent of young people with Tourette’s syndrome (TS) also develop obsessional behaviours and higher rates of OCD have been found in first-degree relatives of people with TS (Leckman, 1993; Pauls
et al.
, 1995). However, it is unusual to see individuals with OCD developing tics later. The compulsions seen in TS are more likely to consist of touching, tapping, rubbing, blinking and staring rituals, with less ordering, cleaning and washing compulsions (Hanna
et al.
, 2002). It is likely that obsessional behaviours
Introduction to obsessive compulsive disorder
9

often develop as a secondary problem, in that as the individual anticipates a tic they may become anxious and carry out a ritual to reduce their anxiety.

Up to 75 per cent of young people with OCD experience difficulties that fulfil criteria for additional diagnoses, such as anxiety disorders or depression.

Biological aspects of OCD

Heredity

The relative contributions of genes and the environment are not clearly understood. Studies suggest that in individuals with OCD, up to 10 per cent of their parents also meet criteria for a diagnosis (MacDonald
et al.
, 1992).

Twin studies (e.g. Carey and Gottesman, 1981) suggest that there is a genetic component, but that it is an inheritance of a general predisposition to anxiety rather than OCD per se. Any genetic component appears to be quite small in comparison with other anxiety disorders (Eley
et al.
, 2003).

In recent years there has been an increasing emphasis in the research literature on the effects of parental mental health problems and their effects on the child. ‘Top-down’ studies have looked at the children of parents with OCD. Black
et al.
(2003) carried out a two-year follow-up study and demonstrated that although the children of parents with OCD were likely to go on to develop an emotional disorder, it was not particularly likely to be OCD.

Other ‘bottom-up’ studies have investigated the parents of children with OCD and Derisley
et al.
’s (2005) study found that children with OCD were more likely to have parents with an anxiety disorder. Again there was little evidence of specificity of transmission. However, Hanna
et al.
(2005) identified higher rates of OCD in the close relatives of children with OCD than in the close relatives of children with no diagnosis. More distant relatives showed no higher an incidence of OCD, suggesting only a minor role for heredity.

Although there appears to be a genetic component, this is quite small in comparison with other anxiety disorders and appears to be a general predisposition to anxiety, rather than OCD specifically.

Paediatric autoimmune neuropsychiatric disorder associated

with streptococcal infection

Studies in the United States have drawn attention to the association between OCD and particular infections (Swedo
et al.
, 1998). Streptococcal bacteria, 10

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which typically cause sore throats, may trigger an autoimmune response in susceptible individuals (Snider and Swedo, 2004). Swedo and her colleagues have described five features which together indicate a paediatric autoimmune neuropsychiatric disorder associated with streptococcal infection (PANDAS): presence of OCD and/or a tic disorder, prepubertal age of onset, abrupt onset, a relapsing course, and association with neurological symptoms during exacerbations. While the range of symptoms does not differ from other early onset patients, the age of onset is earlier. In addition, the course of the disorder is characterised by sudden and severe deteriorations which remain for a few weeks before declining again. Preliminary indications are that a number of physical treatments such as particular antibiotics or therapeutic plasma exchange are effective in both treatment and prophylaxis (Snider and Swedo, 2004).

A recent quasi-epidemiological study found that 6 per cent of children with OCD had evidence of streptococcal infections within three months of the onset of the disorder (Mell
et al.
, 2005). This is three times more common than in children with no disorder but the rate of streptococcal infections in young people with other mental health problems is unknown and so we cannot be sure how specific the link is.

Further research is required to detail the specific link between streptococcal infections and OCD.

Neuropsychology

Given that young people report problems with decision-making and memory, it is not surprising that researchers have proposed that there may be cognitive deficits in OCD. Although there is little research on neuropsychological functioning in young people with OCD, there have been studies of neuropsychological functioning in adult populations. This suggests that OCD may be characterised by executive deficits (which includes abilities such organisa-tion, planning and shifting from one way of thinking or rule to another), attention and memory difficulties and visuospatial and visuoconstructional impairments (e.g. Aronowitz
et al.
, 1994; Boone
et al.
, 1991; Christensen
et al.
, 1992; Head
et al.
, 1989). However, much of this research has been carried out on non-clinical or subclinical samples, sample sizes are often small and many studies do not include normal or clinical (especially anxious) control groups. In addition, studies have struggled to find associations between specific cognitive deficits and actual symptom subtypes, such as memory difficulties in compulsive checkers, or a relationship between impairments and symptom severity.

An alternative to the cognitive deficit theory is that patients try too hard to control their cognitive functioning and consequently other cognitive functions suffer as a result of competition for processing resources (Salkovskis,
Introduction to obsessive compulsive disorder
11

1996a). Radomsky
et al.
(2001) suggested that the development and persist-ence of OCD may be related to a lack of confidence in memory rather than deficits in memory and found that young people with OCD had less confidence in their memory only for threat-relevant material under a high responsibility condition. Cougle
et al.
(in press) also found that checkers performed similarly to a non-clinical control group in their recall of actions and that their accuracy of recall was correlated with their confidence in memory. They hypothesised that there may be a high level of concern about making a mistake and so checking then becomes a way of trying to be sure that they have not caused harm.

Brain structure and chemistry

Biological accounts of OCD have sought to explain OCD in terms of general deficits in specific areas of the brain or in differences in neurotransmitters. Studies have focused particularly on serotonin, the neurotransmitter that is known to modulate mood, emotion, sleep and appetite and is implicated in the control of numerous behavioural and physiological functions.

The finding that particular medications which act as serotonin reuptake inhibitors (SSRIs) can be effective in reducing OCD symptoms led to the initial hypothesis that there may be an abnormality in serotonin and studies have reported different levels of serotonin in OCD (e.g. Insel
et al.
, 1985; Zohar
et al.
, 1988). In addition, brain scanning studies have been used to suggest that there are biological differences in OCD, such as differing metabolic rates in the part of the brain known as the fronto-striatal system (e.g.

Baxter
et al.
, 1988). However, just because differences are found does not necessarily mean that there is a deficit or abnormality. Baxter
et al.
(1992) demonstrated that the anomalies detected through brain scanning can resolve through medication or behaviour therapy, suggesting that any neurological changes are reversible.

If OCD is caused by biological factors, theories need to be able to account for the effectiveness of treatment and to explain how psychological therapy may work. Theories must also be able to account for the phenomenology of OCD more broadly, such as why memory and decision-making problems only occur in situations linked to the obsessional problem. To progress our understanding, biological accounts of OCD need to be able to generate specific predictions based on the phenomenology of OCD and must be able to provide evidence to evaluate them.

Biological theories have been very influential in the literature on OCD.

However, biological approaches have lacked well-elaborated theories and have struggled to account for the phenomena of OCD.

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Psychological aspects of OCD

Causes

Salkovskis
et al.
(1999) have suggested five mechanisms for the development of inflated responsibility which they propose are critical for the development of OCD. These include: