OCD And Comorbidity

Now, to continue the topic of OCD and potential comorbidities, I will present results from a series of scientific articles, in the order in which they were published.

Overbeek et al (2002) presented their findings regarding the occurrence of OCD and what is in all probability its main concomitant ‘other’ mental disorder: depression. As for this article, one can safely speak of major depressive disorder, because this group was alert to avoid incidental symptoms relating to depression; they went for the syndrome of depression itself.

More than 90% of patients with an anxiety disorder such as OCD, they write, have a lifetime history of other psychiatric problems. Co-occurrence of any anxiety disorder with depression is therefore very common. In fact, major depressive disorder (MDD) that presents in OCD, general anxiety disorder (GAD), or social anxiety disorder (SAD), does so in higher rates than might be expected purely in terms of chance.

Theoretical ideas emerge from such a prevalence. There may be shared pathogenic and/or genetic factors at work. If comorbid disorders occur consecutively in similar fashion (one before the other in most cases), then the hypothesis of causality could be put forward. Another point is that an anxiety disorder is clinically often more resistant to therapy than the anxiety alone.

The lifetime prevalence for OCD is 2-3%; that for MDD is around 8-12%. MDD is the most frequent complication of OCD. The comorbidity estimate varies wildly, from 19 to 90% of all cases of OCD; according to the authors, the variation is largely a matter of semantics (i.e. what one defines as OCD and MDD precisely). More apt estimates center around 1 in 3 cases of MDD in OCD for all OCD patients, and 2 in 3 in patients that are assessed in the clinic. In 38% of comorbity cases, OCD clearly precedes MDD; and in only 11% it is the other way around. Such statistics usually have implications for research into proper treatment, and also into considerations about how such disorders may initially arise and are associated with abnormalities in one’s brain (the pathophysiology).

Carter et al (2004) mainly confirmed what Overbeek et al wrote. They performed their study in a family context, and found that comorbidity of anxiety (OCD, panic disorder, or GAD) with MDD happens more frequently than may be predicted from pure chance alone.

Fineberg et al (2005) already went for finer differentation; they asked: is comorbid depression in OCD patients different from depression alone? Their answer was that in OCD patients, there is considerably more inner tension and there are stronger pessimistic thoughts. On the other hand, comorbid MDD showed less sleeping problems, and less lack of appetite. Their discussion, finally, is about the possible neurobiological differences of ‘pure’ MDD compared to MDD as a comorbid disorder. For instance, in cases of OCD only modern antidepressants of the SSRI type (which increase availability of serotonin, a messenger molecule in our brain) are efficent; in pure MDD there are more different medications that work well. This group also refers to a study done by Saxena et al (2001); here it was suggested that in pure MDD, abnormalities in the brain that are important in this disorder are different from the abnormalities of depression in co-morbidity. Fineberg et al by the way nicely confirm that 1 in 3 to 2 in 3 OCD patients develops MDD symptoms (see Overbeek et al, above).

Hasler et al (2005) in turn go one step further. When they  published this article, there was more clarity about the different symptom dimensions in OCD (contamination/washing; symmetry/ordering; et cetera). They asked: can we link different symptom dimensions of OCD to specific comorbid disorders? (I must add one point here: there have always been slight differences between different research groups and projects as to the labelling of symptom dimensions; the general idea is the same, but individual categories may be named differently, or put into a different order. Here, if each defined dimension can be repeatedly linked to one and the same comorbid disorder, that is additional evidence that that dimension as a constant was identified correctly.)

Hasler et al defined a ‘factor I’ cluster of obsessions and compulsions as: sexual, religious, aggressive, somatic (i.e. referring to the body) and with checking compulsions. Here, depression and anxiousness were prominent comorbidities.

Their ‘factor II’ cluster contained symmetry and repetitive obsessions, with counting, ordering and arranging compulsions. These co-occurred with bipolar disorder, panic disorder, and agoraphobia as comorbidities.

Cluster ‘factor III’ was the familiar contamination obsession and washing compulsion. Intriguingly, eating disorders were prominent here.

Finally, factors I and II were significantly associated with early onset OCD. Takent together, these results are a good starting ground for further research into so-called subtyping of OCD, and investigating the genetic aspects of OCD dimensions. I would go so far as to say that in the more distant future, OCD as a ‘defining’ may fall apart altogether, because its different dimensions (or clusters of symptoms, factors) could turn out to be so different in all aspects, that a series of autonomous disorders may emerge (imagine: different genes, different brain areas affected, different sensitivities to treatment, different susceptibilities to environmental aspects, trauma, and so on and so on). That is why OCD is known as a very heterogeneous disorder: it presents itself in many, many guises.

Besiroglu et al (2007) basically returned to looking at onset of MDD after that of OCD again, but applied more advanced statistics to the riddle compared to those used in earlier studies. They conjectured that pathological processes mediated by specific obsessions, anxieties and fears render neural circuits more vulnerable to the development of depression. As we will see later, when we will look at specific brain regions involved in these disorders, and into the qualitative deterioration of nerve tissue in disease (and its regeneration!), this idea is pretty obvious at first sight… were it not that OCD and MDD share unique features which provides this hypothesis with a credibility that is linked to what we see in depressed persons, or animal models of depression.

Now take good notice of this: Besiroglu et al discovered that depression in OCD cannot be solely explained as a secondary complication to the disability resulting from OCD. That is something unexpected. It seems only natural that someone ‘taken out of normal life’ by the burden of OCD develops symptoms of depression after a while. But this group calculated that the severity of depression in OCD does not associate (or correlate, if you will) with the severity of the compulsions. And the latter is just what you would expect to see confirmed, as in: the graver and more time-consuming the rituals, the deeper the depression. Which doesn’t hold true according to this study.

Lastly, the group of Besiroglu reported that mainly obsessions of the aggressive type, and generalized anxiety disorder (GAD) are linked to MDD.



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