In this paper we report dysfunctions in distinct neurocircuits, which we propose may underlie different clinical profiles in OCD. Yet, the complex phenomenology of the condition likely reflects widespread abnormalities across multiple brain regions and circuits encompassing a variety of emotional, cognitive, and behavioral domains, like most psychiatric disorders [5, 7]. A single mechanism is therefore unlikely to explain such a heterogeneous disorder, and the different clinical profiles of OCD we present here will overlap, interact, and co-occur in individual patients. Likewise, CSTC circuits are interconnected rather than fully segregated and activity (or dysfunction) in one circuit will affect the integrity of the others [13]. Moreover, OCD symptoms wax and wane and change in type over the lifespan. Consequently, a patient may have different circuit abnormalities at different stages of development. Such developmental variations have not been captured in previous neuroimaging studies, which have mostly been cross-sectional rather than longitudinal. The stage and chronicity of disease and effects of past and current treatments on brain neuroplasticity have also not been adequately addressed in neuroimaging work [16].
