Simulation paradigms can induce plastic changes in brain excitability. Paired associative stimulation (PAS) with an interstimulus interval of 25 ms (PAS25) induces a long-term potentiation (LTP)-like effect while that at an interval of 10 ms (PAS10) induces a long-term depression (LTD)-like effect. The LTP-like effect induced by PAS25 is exaggerated in patients with focal dystonia. The LTD-like effect with PAS10 is also increased in focal dystonia but not in the target area of PAS. Depotentiation refers to the reversal of LTP by which LTP is abolished by a following procedure that has no effect when it is given alone. Brain-derived neurotrophic factor has a variety of roles in modulating both LTP and LTD. The Val66Met single nucleotide polymorphism is related to abnormal cortical plasticity. In this protocol, we propose a study to test the hypothesis that depotentiation is weaker in focal dystonia patients compared to healthy controls. In addition, motor cortical inhibition is decreased in focal dystonia. We will test the changes in motor cortical inhibition following different interventional procedures in focal dystonia. We will also test the relationship between depotentiation and LTP/LTD-like effects in focal dystonia patients.