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Axis I comorbidity
In terms of eating disorders, Rubenstein, using the SCID diagnostic interview, found that in 62 patients with OCD, the lifetime prevalence of anorexia nervosa or bulimia nervosa was 12.9%, with an additional 17.7% of subjects having had a subthreshold eating disorder at some time in their lives; these rates are far higher than those reported for the general population. Also of interest is that males with OCD were as likely as their females counterparts to have suffered from an eating disorder, in stark contrast to the uniform female excess of eating disorders in general population samples.
The high comorbid occurrence of OCD and anorexia/bulimia nervosa is worth considering further. Indeed, many of the features of these eating disorders could be construed as OCD symptoms. For example, the obsessional thinking about fatness and the often ritualised eating habits, calorie-counting and exercise, as well as the anxiety associated with the ‘fear of fatness’, would all be compatible with diagnoses of OCD or BDD, were it not for specific exclusion criteria in the DSM. But, it does beg the question, touched on above, of the relationship of these disorders to each other.
Having reviewed the internal and external boundaries of OCD, we now outline a putative model for subtyping OCD, on the basis of gender and age at onset. As a prelude, we examine these parameters in OCD, and also explore determinants of good and poor outcome of the disorder.
Obsessive–compulsive disorder in childhood
Obsessive–compulsive disorder and gender
For example, Bebbington, in reviewing epidemiological studies of OCD, concluded that the male : female ratio is ‘roughly 1:1.5’. This discrepancy between treated and epidemiological samples is presumably a reflection, in part at least, of differences between men and women in terms of help-seeking behaviour, the degree to which the impairment associated with OCD can be tolerated and accommodated by families in male and female family members and the degree of occupational impairment and gender differences in occupational expectations.
The extent to which these factors can explain the difference in gender ratio between treated and untreated samples, is difficult to assess. What is also probable is that males are more likely to get into treatment because they are relatively more prone to a severe form of OCD (although formal attempts to assess gender differences in severity of illness is inevitably complicated by the very fact that those who are most likely to be included in any such study, are those who have sought treatment). What is clear from both epidemiological and treated samples is that the symptoms of OCD tend to be somewhat different between the sexes. Thus, males tend to have more problems with ruminations, and females are more likely than males to be afflicted with cleanliness and checking rituals. It might be that this plays some part in determining the impact of the illness on the individuals’ daily functioning. Certainly, ruminations without rituals are notoriously difficult to treat.
Another issue of potential importance in determining the cause of gender differences in OCD, is age at onset differences between males and females with the disorder. In general, males tend to have a somewhat earlier onset than their female counterparts, and males predominate in cases of childhood OCD, as detailed above. In a study specifically of gender differences in OCD, Castle et al. assessed gender differences in a sample of 219 OCD patients, who had been referred to a tertiary treatment centre in London, UK. The male : female ratio was 1:1.35, and the mean age at onset was 22 years for males and 26 years for females (p = 0.003). Duration of illness prior to seeking help was 11.5 years for males and 9.2 years for females. Males exceeded females among those individuals whose onset of illness occurred before the age of 16 years, whereafter females predominated. This finding is compatible with the notion that there might be relatively discrete subtypes of OCD, to which males and females are differentially prone.
However, the recent long-term follow-up study of Skoog and Skoog is most enlightening. These authors personally followed up 122 of 251 OCD patients who had originally been admitted to hospital in Sweden between 1947 and 1953, over a mean period of 47 years from illness onset. For a further 22 patients, necessary information was obtained from informants and medical records, resulting in an overall 82% follow up of surviving patients. Subjects had received an array of different interventions, including psychosurgery (6 patients) and clomipramine (17 patients). Improvement was observed in 83% of subjects, with complete recovery in 20% and subclinical symptoms persisting in a further 28%. However, 48% of patients had had OCD symptoms for over 30 years. Associations with poor outcome included early illness onset, low baseline social functioning and having both obsessive and compulsive symptoms. This adds further to the notion that early onset of illness might be a characteristic of a particularly pernicious subtype of OCD. We now outline an integrative and interpretative model for subtyping of OCD.
A neurodevelopmental subtype of obsessive–compulsive disorder?
One of the parameters underpinning this hypothesis is that OCD has been shown, despite its historical ‘neurotic’ label, to be a disorder associated with brain dysfunction. The compelling evidence for serotonergic dysregulation in OCD, has been alluded to above. With the advent of modern neuroimaging techniques, further light is being shed on brain structural and functional abnormalities in OCD. In a recent review, Saxena et al. noted that structural and brain imaging studies of OCD patients generally suggest abnormalities in orbitofrontal and anterior cingulated cortex, and in parts of thalamus and striatum. These structures have historically been implicated as linked in a functional neuranatomic circuit. Functional neuroimaging studies have shown evidence of hypometabolism in the orbitofrontal cortex of OCD patients, and have found that this correlates with the severity of symptoms and normalises with treatment.
Of particular current interest is that the immune sequelae of infection by group A beta-haemolytic streptococcus can result in a variety of neuropsychiatric conditions in children, including tic disorder and OCD. These so-called paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are presumed to be consequent upon the formation of antibodies which cross-react with neural tissue. Again, this underlines the importance of brain insult in the pathogenesis of at least some cases of OCD. A further example of brain insult associated with obsessive–compulsive symptomatology is the occurrence of such symptoms as a sequel to encephalitis lethargica. Neurodevelopmental disorders are usually characterized by an early onset, severe symptoms and a poor longitudinal course; these disorders also tend to affect males more than females. As detailed above, those individuals whose onset of OCD occurs in childhood or early adulthood do indeed tend to be male. They also tend to have severe symptoms, significant disability and a poor outcome, with a relatively poor response to treatment. Furthermore, such individuals tend to have certain associated features which are also compatible with the notion that they have a disorder of neurodevelopment. These include an excess of ‘soft’ neurological signs, an excess of motor tics and poor performance on neuropsychological tests of visuospatial functioning. These strands have been brought together in a proposal that a neurodevelopmental form of OCD can be delineated, distinct from a putative ‘primary’ type, characterized by a later onset, a milder/episodic course and a favourable response to serotonergic agents; females are relatively more prone to this latter form of the illness. This subtyping has strong similarities with the models proposed for schizophrenia. Of course, much more research is required before accepting this proposed typology, and the mediating effect of gender and associated confounding factors must also be considered.
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