<qa>  What is the primary goal of this study?The primary goal of this study is to examine the physiological effects of BoNT therapy and to advance the understanding of the pathophysiology of dystonia. BoNT therapy is commonly perceived to induce peripheral muscle weakness through inhibition of acetylcholine release at the neuromuscular junction. However many argue that this is not likely the only or primary mechanism of action, as many subjects have improvement in dystonia without discernible muscle weakness and others have significant weakness and no improvement in their dystonia. Indeed, BoNT has been proposed to induce central effects possibly related to modulation of the muscle spindle afferent feedback or a retrograde transport of toxin to the central nervous system. A leading theory underpinning the pathophysiology of dystonia is loss of motor inhibition or increased excitability at the level of the spinal cord, brainstem and the motor cortex. Thus, modulation of pathology in these central pathways is critical for control of dystonia. Transcranial magnetic stimulation TMS is a noninvasive physiological technique for assessment of motor cortex excitability. Paired-pulse TMS paradigms, such as short-interval intracortical inhibition SICI and intracortical facilitation ICF are well established paradigms for evaluation of motor cortex excitability. 