Support for the utility of targeting neural circuitry underlying response inhibition in treatment for OCD was recently provided by Rappel and colleagues [130]. Recordings of oscillatory theta activity, a robust neurophysiological marker of inhibitory control processes [131], were taken from electrodes implanted in the STN for DBS treatment in patients with treatment-refractory OCD. STN theta oscillations were found to be smaller during failed inhibition trials of a Go/Nogo task and during OCD-symptom provocation prior to DBS stimulation. This pattern is consistent with the literature reporting that theta oscillations increase during successful response inhibition and decrease during inhibitory failures [131] and suggests that similar response inhibition failures were involved in the experience of OCD symptoms during provocation. Fluctuations in OCD symptom severity measured over 1-year post-DBS-activation were accompanied by and correlated with alterations in the level of theta oscillations; decreases in symptom severity co-occurred with increases in theta oscillations and vice versa [130]. This finding suggests that better function in neural mechanisms implicated in response inhibition are involved in OCD symptom improvement in (some) treatment-refractory patients. Furthermore, this study indicates that
