Obsessive Compulsive Disorder (26 page)

• We have some understanding of maintenance but little information about the origins of OCD and so much of our limited theoretical understanding has to come from generalisations of the theory.

• We need to establish an empirical basis of causal factors in order to facilitate treatment and prevention.

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Understanding comorbidity

From clinical experience we know that individuals rarely present to services with one clear-cut psychological problem. This is supported by research which indicates that young people with OCD often have other psychological problems. Studies suggest that three-quarters of young people also meet criteria for other diagnoses (March
et al.
, 2004; Swedo and Rapoport, 1989), with anxiety disorders and depression especially common. Despite this, our understanding of comorbidity is poor. There appears to be considerable overlap in the thinking patterns in OCD and other phenomena such as worry and yet it is unclear as to whether these really are different, distinct pathologies or, as seems likely, whether by using a diagnostic system we are making artificial divisions.

In terms of treatment (and to some extent theory), comorbidity is probably best dealt with by formulation. The patterns involved vary. We have been able to identify situations where a single factor causes multiple problems (e.g. clinical perfectionism as a vulnerability factor for OCD, eating disorders and depression; cf Shafran
et al.
, 2003). Most commonly, one problem triggers another (e.g. as OCD makes more and more inroads into the young person’s life and prevents them from engaging in normal activities, they become more and more demoralised until they meet clinical criteria for depression). Rarer, but importantly, another problem is primary and OCD is secondary; for example, depression and grief trigger obsessional symptoms. In such instances, establishing the timeline is crucial in order to decide which problems should be treated first. In some instances, comorbidity simply represents the person having two separate problems, in the way that it is possible to have both influenza and chickenpox at the same time. The complication in such instances can be that although initially func-tionally independent, the problems may begin to interact as time goes by.

Young people with OCD often have other psychological problems and this comorbidity is probably best dealt with by individual case formulation.

Establishing the role of biological factors

The literature on obsessional problems in general and childhood OCD in particular emphasises the idea that OCD is a ‘neurodevelopmental disorder’.

‘Theoretical’ papers emphasising biological explanations abound. Curiously, this enthusiasm for biological approaches has not resulted in coherent biological theories and the evidence for biological discontinuity for OCD is largely absent.

A common clinical justification for the use of biological explanations is that in some way it is ‘good for the patient’. Those advocating this position 144

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argue that biological disease models are destigmatising and empowering relative to psychological models. Promoting the view that mental health problems have biological causes has become an established part of many programmes with the declared intention of reducing stigma. However, the promotion of biological factors is not necessarily in the best interest of those with mental health problems and their families. For example, genetic factors may be promoted (or overpromoted) as causal with little regard for the potential impact that such ideas may have (Rimes and Salkovskis, 1998).

Clinicians, sufferers and carers who uncritically consider genetic factors are likely to overestimate these. Once a person is identified as having OCD, relatives will recall great uncle George who was funny about being clean.

Cousin Emily was diagnosed as having OCD. The young person’s grand-mother recalls an aunt who checked a lot. Three cases in a family, that sounds like a lot. However, the context is that the collective recollection of family members of several generations can draw upon a potential pool of information about almost 200 relatives; OCD is likely to occur at normal lifetime rates in at least eight of those. If obsessional symptoms are included the figure would rise to somewhere in the region of 30. None of the examples given are first-degree relatives. Note also that genetic and biological explanations may have the effect of alleviating feelings of blame and guilt not in the young person but in the parents.

Biological accounts can be problematic because they may have the unwanted effect of inducing pessimism regarding likely treatment outcome in young people, their carers and the general public. Attributing mental health problems to ‘brain disease’ and biological causes additionally affects the extent to which sufferers are regarded as unusually unpredictable, potentially antisocial or even frankly dangerous by and to themselves and others.

The brain is commonly understood to be the organ of the mind and the ‘seat of the self ’; a diseased brain for many comes to mean a diseased mind and diseased ‘self ’.

Research in an adult community sample highlighted that ‘psychological’

but not ‘biological’ labels resulted in more positive views of mental health problems relative to controls (Lam
et al.
, 2005). Anxious and depressed patients have also been shown to be similarly susceptible to biological labelling effects in experimental studies (e.g. Lam and Salkovskis, 2007). The importance of clinicians’ attitudes to causal factors in mental health problems lies both in their own expectations of patients’ response to treatment (Lam
et al.
, submitted) and in the extent to which their causal beliefs are transmitted to patients. The way in which patients understand and accept such causal explanations may in turn affect not only their expectation of change, but also their engagement and response in treatment. Understanding how causal labelling might affect younger people with mental health problems is thus an important next step in research terms. To our knowledge, there are no data on children’s reaction to causal labelling. OCD has been an area in which such labelling has been particularly prominent since the publication of the popular book
The Boy Who Couldn’t Stop Washing
(Rapoport, 1989).

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In order to understand OCD in young people better, we may need to consider neuroscience-based approaches to establishing the role of biological/genetic factors and their interaction in the type of way that has been done in complex trait research (Kovas and Plomin, 2006). Disease/neuropsychiatric models (e.g. comparing OCD to neurological disease such as epilepsy or genetic problems such as Huntington’s disease) have failed to help our understanding and may well have been damaging in terms of stigma. Currently, biological theories struggle to account for the specific phenomenology of OCD and the effectiveness of psychological treatment.

This is not to say that biological factors are not relevant, as all psychological processes have a physiological substrate. The mistake, in our view, is to presume a pathophysiological basis of OCD.

To progress our understanding of OCD, biological accounts need to be conceived of in a more subtle way. The fact that psychological theories and research are so well developed should provide a useful starting point, allowing consideration of the psychological/neurophysiological interface. Such theories may be able to generate specific predictions based on the phenomenology of OCD and therefore provide evidence to evaluate them. It thus seems extremely unlikely at this stage that OCD will be identified as a primarily biological abnormality, making the interface between normal biological and psychological factors and how these normal processes can produce disordered reactions of the type seen in OCD the primary area of interest. Such research may suggest ways in which psychological and pharmacological treatments might be combined synergistically in particular types of problem. Note that at present CBT is the first line treatment, with the combination of psychological and pharmacological treatment being of uncertain value.

• Although ‘theoretical’ papers emphasising biological explanations abound, this has not resulted in coherent biological theories.

• Biological accounts can be problematic in that they may have the unwanted effect of inducing pessimism regarding likely treatment outcome and lead to stigma.

• The primary area of interest may be the interface between normal biological and psychological factors and how these processes can produce disordered reactions as seen in OCD.

Understanding family involvement

Unsurprisingly, research on treatment of young people with OCD suggests that family factors may be relevant in understanding the problem and seeking to change it. There is evidence that families of young people with OCD are more likely to be characterised by high levels of criticism and 146

Salkovskis, Waite and Williams

overinvolvement (Hibbs
et al.
, 1991) and lower levels of emotional support (Valleni-Basile
et al.
, 1995). Families of young people with OCD have demonstrated less use of positive problem solving and been less likely to reward independence in their children (Barrett
et al.
, 2002). There may also be other factors that are important, such as families holding strong and rigid belief systems (e.g. overvaluing cleanliness or setting overly high standards).

However, it is unclear how these factors are involved in the development and maintenance of the problem. It is possible that these factors contribute towards the development of OCD, in that if young people are given less responsibility and support, they may be less able to use their own resources effectively to deal with difficulties. Alternatively, these factors may be involved more in the maintenance of the problem, as OCD disrupts family relationships and functioning and families often find themselves in a vicious cycle, where they accommodate the OCD and become involved in providing reassurance or carrying out compulsions. The stress of having a family member suffering from OCD may distort family relationships, rendering them more abnormal and stressful for the sufferer, which in turn may exacerbate the obsessional problem.

What is clear is that there is little evidence of direct transmission of OCD from parents to children. Surprisingly few children of parents suffering from OCD develop this problem either as a child or later. Direct copying of symptoms is unlikely to be an explanation of childhood OCD. Challacombe and Salkovskis (submitted) evaluated children of women with OCD, finding little evidence of elevated anxiety levels relative to healthy controls and an anxious comparison group. Observation of parent–child interaction revealed some differences in terms of the granting of autonomy which might be expected to predispose the child to the experience of anxiety symptoms later in their development. However, it seems likely that the level of risk to children of women suffering from OCD is rather low.

Although family factors have been put forward as relevant in understanding OCD, it remains unclear how they are involved in both the development and maintenance of OCD.

Future opportunities

Prevention

As we develop a greater understanding of the nature and development of OCD, the clear implication is that this understanding may provide opportunities for prevention or the development of primary or secondary prevention strategies. Quite what form this should take is unclear, but at this stage leading candidates would be to teach young people about the nature of
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intrusive thoughts and to learn to ignore them rather than to think of them as meaningful and occurrences to be ‘neutralised’. Learning about the uncontrollability of intrusive thoughts, images and doubts and the controllability of responses to them may be able to prepare young people to deal with intrusions more effectively. If we can understand the kind of things which mark the transition from normal intrusive thoughts to obsessional disorders, we may be able to help and support them to deal with these situations, thereby reducing the likelihood of OCD developing. The clearest examples of triggers in young people include bullying, peer relationship problems and illness or death within the family. Previously held or newly developed beliefs (such as overly rigid moral codes, ideas about thought– action fusion) are a further obvious target of preventative interventions.

More broadly, if we were to teach young people some of what they would learn in CBT (such as normalising of intrusions) and to use some of the techniques such as behavioural experiments to test out predictions about the way their thinking and behaviour impacts on the world, it may be possible to reduce the rate of people going on to develop different disorders.

Historically, these questions are left unanswered as research of this kind is difficult to do. This is because the prevalence of OCD is around 1 per cent or less in teenagers and so in order to determine whether prevention programmes have any real effect, sample sizes would need to be extremely large or risk predictions particularly strong. Nevertheless, it makes good sense to work with young people to enable them to deal effectively with distressing thoughts, worries and their reactions to adverse life events through educational settings, youth groups and other environments, as well as through print and broadcast media.

As we develop a greater understanding of the nature and development of OCD, this may provide opportunities for primary and secondary prevention strategies.

Developing and refining treatment

Despite the success of CBT, many young people with OCD fail to make progress in treatment or have difficulty maintaining progress over the longer term. In order to improve treatment, we need to understand better what might define the problems experienced by those young people who do poorly in therapy. Rachman (1983) describes how in some cases the individual does not improve because the treatment is inadequate or not adequately delivered, which he calls ‘technical treatment failures’. This is a kind way of indicating that some therapists do not do treatment very well. In other cases, treatment may be delivered adequately but the individual makes limited progress and these are described as ‘serious treatment failures’. Clearly identifying factors likely to result in relatively poorer outcomes will, in research terms, allow research to turn failure into success.