We read with great interest the article published by Ni et al reporting the effect of pallidal deep brain stimulation (DBS) on cortical excitability and plasticity in patients with primary cervical dystonia. 1 Interestingly, the authors found two peaks (the first with a latency of 10ms and the second of 25ms) of cortical evoked potentials in the ipsilateral motor cortical areas in response to internal globus pallidus (GPi)-DBS. In addition, transcranial magnetic stimulation with a conditioning-test paired-pulse paradigm demonstrated that GPi-DBS had a facilitatory effect on the motor evoked potentials at the interstimulus interval of 6 to 12ms, preceding an inhibitory, negative cortical peak at 22 to 26ms.Considering the short latency, facilitatory effect at 6ms between the GPi and motor cortical areas and given that GPi-DBS does not activate directly the corticospinal fibers, it is possible to hypothesize a fast, direct interplay between the GPi and the motor-related cortical areas. Although the traditional view of the basal ganglia circuitry does not assume the existence of a fast route between the cerebral cortex and the GP, this has been recently hypothesized and proved both in animals and humans. 2 Recent studies have indeed identified a direct GABAergic projection from the GP to the cerebral cortex, 3,4 as well as a glutamatergic cortico-pallidal projection. 5 The findings of Ni and associates are also in line with recent human structural connectomics data 6 showing that precentral and postcentral gyri, the paracentral and superior parietal lobules, are connected with GP paralleling the direct, indirect, and hyperdirect pathway. 2,7 The existence of a direct cortico-pallidal connection is also corroborated by the presence of a robust band of beta coherence between the sensorimotor areas and GPi in dystonic patients with GPi-DBS. 7,8 On the other hand, we cannot exclude the possible involvement of cholinergic facilitatory neurons, which are dispersed around the GPi. 1 Despite the high clinical relevance of GPi-DBS in reducing the abnormal plasticity driven within the cortico-basal ganglia network and in improving symptoms in patients with dystonia, several questions are still to be answered.It is likely that the cortico-pallidal system may act as an important node involved in the functional interactions of beta signaling in the cortex-basal ganglia-cortex loops contributing to abnormal sensory-motor plasticity and motor learning in dystonia. 7 This should be the focus of future studies aimed to design new therapeutic strategies in dystonia.