 We will test the hypothesis that chronicity of TNP is sustained by changes at cellular and molecular levels in neural circuits associated with pain perception and modulation, rather than by the initial peripheral etiology, and that this dysfunction can be safely targeted and modulated as a therapeutic approach by transcranial direct current stimulation tDCS. To achieve this goal we will use a neuroimaging technique, PET, employing a mathematical model that permits the quantification of opioid receptor availability in vivo. 