Brain as a Therapeutic and Research Target in Trigeminal Neuropathic Pain

Trigeminal neuropathic pain (TNP) disorders, such as classical trigeminal and post-surgical neuralgia, are debilitating chronic conditions with pain that is either spontaneous or that can be intensely evoked by light touch to the facial skin. Although neuroimaging techniques have provided insights into some brain mechanisms of experimental trigeminal pain in humans (DaSilva et al., 2002; Borsook et al., 2003), it is not well understood how structural and molecular mechanisms are affected during the course of TNP, and how they can be safely modulated for therapeutic and research purposes. Understanding these processes is crucial to determine the structures engaged in the development and persistence of TNP.

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.

Patient Inclusion Criteria:

• Daily chronic TNP for at least 6 months not adequately controlled by pervious medicine therapies;
• minimal average baseline pain score of 4 (moderate to severe) in the visual analogue scale (VAS);
• unilateral pain
• orofacial allodynic region to mechanical (light touch or palpation) or thermal stimulation (head or cold);

Patient Exclusion Criteria:

• pregnancy or planning to become pregnant
• local pathology (e.g. orofacial lesion)
• history of systemic disorders (e.g. MS)
• history of other chronic pain disorder (e.g. back pain)
• recent orofacial surgery or trauma (< 6 months)
• history of central origin disorders (e.g. stroke)