Obsessive compulsive disorder (OCD) is a common and disabling psychiatric illness, characterized by intrusive thoughts and ritualistic behaviors, that often fails to respond to currently available treatments. Although the disorder tends to emerge during childhood or adolescence, the brain abnormalities associated with pediatric OCD have not been well-studied. In adult patients, hyperactivity of the anterior cingulate cortex (ACC) has been found to occur at rest, to increase with symptom provocation and to normalize with effective treatment, but the functional significance of these findings is not well-understood.
Neuroimaging work in healthy subjects suggests that the midline prefrontal cortex (MFC)—including the ACC—mediates inhibitory and error processing along a dorsal to rostral continuum, which is especially relevant for OCD, given patients’ apparent failure to inhibit intrusive thoughts and behaviors and their excessive concern that errors have been made. Indeed, hyperactivation of the ACC in its rostral subdivision for errors, and more dorsally for correct response inhibition, has recently been demonstrated in adult OCD patients, suggesting that functional abnormalities of both inhibitory and error processing within discrete MFC subregions may exist in OCD. Because the normal mediation of inhibitory and error processing by the MFC develops dramatically during the time period in which OCD typically has its onset, mid-childhood through adolescence, it is possible that aberrant development of these functions may be associated with the emergence of OCD in youth. This possibility is consistent with the association of increased ACC volumes, symptom severity, and deficits of response inhibition in pediatric OCD patients. However, whether functional abnormalities of inhibitory and/or error-processing can be mapped to the MFC in pediatric OCD has not been directly tested.
To do so, we are conducting a functional magnetic resonance imaging (fMRI) study using the Multisource Interference Task (MSIT) to test for abnormalities of inhibitory and/or error processing within the MFC in youth with OCD. In a pilot sample of healthy children and adolescents, we have found the MSIT to yield robust activation of the dorsal MFC during correct interference and error trials, with additional activation in the rostral ACC only during errors, making it a reliable probe of this region’s function in youth. We predict that altered activation of the MFC during both inhibitory and error-processing will occur in pediatric OCD patients compared to matched healthy control subjects, and anticipate that this work will help to define the primary neurobiological correlates of the disorder.
Ultimately, the study of brain function in youngsters with who are near illness onset will contribute to the framework on which a neurodevelopmental model of OCD can be built, which, in turn, will guide the development of better treatments, and possibly even preventative strategies.