Temporomandibular disorders (TMD) affect ~ 7- 17% of the American adult population. The mechanisms that initiate and maintain TMD are not well understood; however, recent work suggests links to endocrine, autonomic and central nervous system function. This proposal will use recent advances in pain testing procedures in conjunction with functional magnetic resonance imaging (fMRI) to evaluate pathophysiological changes in the central nervous systems of human TMD patients and the association of these changes with muscle pain.
Aim 1 will use unique pain testing procedures, which offer a proven measure of control over distress, anxiety and other psychological factors, to evaluate why sensitivity in the faces of TMD sufferers is regional, i.e., how and why are some sites in muscles hypersensitive whereas other muscle sites are relatively 'normal' in pain response profiles.
Aim 2 involves developing a trigeminal pain testing methodology for use within the fMRI environment. Neural activity throughout central pain pathways in general and within the central trigeminal columns in particular will be studied in association with evoked pain to test the hypothesis that central circuitry is sensitized in symptomatically-specific ways. Particular attention will be paid to differences between relatively pain-free sites, relatively painful sites, and trigger point sites with pain referral patterns. The proposed studies will provide the first systematic neural imaging of trigeminal pathways in TMD sufferers. These studies could fundamentally change how such patients are evaluated and treated. The results will contribute to the knowledge base necessary for mechanistically-driven, non-invasive pain testing procedures for diagnosis, selection of treatments, and evaluation of treatment efficacy. These methods will also be useful in basic investigations of the biological basis of TMD, e.g., future work can use the evoked pain testing and neural imaging methods to study endocrine, sex hormone, genetic and other biological mechanisms that likely contribute to the etiology and pathophysiology of TMD. ? ? ?
