 The VSVC and STN are both stations in the neural circuitry thought to be dysfunctional in OCD. The pre-eminent neurobiological model of OCD implicates abnormalities of orbitofrontal cortex OFC, anterior cingulate cortex ACC and ventral striatum. These structures are integral to limbic cortico-striatal-thalamo-cortical circuitry whereby cortical outputs synapse successively in ventral striatum, ventral pallidum and mediodorsal nucleus of thalamus before projecting back to cortex; within this system, the pallidum projects to thalamus either directly or indirectly via the subthalamic nucleus. It is therefore possible that the observed clinical improvement in OCD with DBS is due to high frequency electrical stimulation disrupting abnormal activity in the limbic circuit and that this can be obtained at either of the two target sites. However, the ventral striatum and STN are thought to have separate functions, important in different ways for modulating information processing in the cortico-striatal-thalamo-cortical circuitry essential for the control of behaviour. Thus, although both VSVC and STN DBS affect the same neural circuit, their mechanism of action may be quite different and stimulation at each of these locations may have unique effects on the symptom dimensions of OCD. 