The conventional view is that obsessive–compulsive disorder (OCD) is driven by irrational beliefs, which are a putative basis of obsessions. Compulsions are considered a coping mechanism, which neutralize anxiety or reduce the likelihood that these fears will be realized. Contrary to this view, recent data suggest that compulsions in OCD are a manifestation of a disruption in the neurobiologically well-defined balance between goal-directed action and automatic habits.

The habit hypothesis of OCD is neurobiologically plausible; goal-directed control (which protects against habits) relies upon the integrity of two key brain regions implicated in the pathophysiology of OCD, the caudate nucleus and medial orbitofrontal cortex (Gillan et al, 2014). Neurobiological models of obsessions, on the other hand, are lacking. One promising model implies that obsessions may be a consequence of dysfunction in fear conditioning processes in OCD, whereby patients cannot adequately extinguish fears that accompany normal intrusive thoughts and worries. In support of this, impairments in extinction recall are evident in OCD, and the respective neural correlates also overlap on regions thought to be involved in the disorder (Milad et al, 2013). However, patients with post-traumatic stress disorder (PTSD), for example, have similar deficits in fear-extinction recall, but do not typically present with obsessions. In this light, fear-conditioning abnormalities in OCD may more parsimoniously reflect concomitant anxiety in OCD, rather than obsessions.

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