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 stimulation of the STN is an effective treatment approach for some individuals with OCD. Another recent study also indicated that ventral cognitive circuit function can be improved by ventral capsular/ventral striatal (VC/VS) DBS targeting the ALIC [132]. Widge et al. [132] found that stimulation at this target resulted in significantly greater theta oscillations in prefrontal regions, including the IFG, during an inhibition task in patients with OCD and/or depression. These findings are consistent with recent connectomic analyses suggesting that a specific white matter network connecting frontal regions to the STN was associated with clinical response in ALIC, STN and other DBS techniques [70]. Future work should consider whether this form of treatment is mainly effective for those patients with response inhibition deficits.
