In attempting to understand the mechanism of pain production in tic douloureux, one must account for the myelination pathology seen in the primary afferent fibers, the cases where trigger is in a different division than the pain, the frequent lack of a fixed neurologic deficit, the effective trigger stimuli corresponding to large caliber axons which would not seem to involve the small axons usually associated with pain production, and similar puzzling features of the disease. We present a theory which satisfactorily predicts, or is consistent with, most known features of tic; it is based upon two mechanistic assumptions, both of which have strong experimental foundations in the literature. The first is the trigeminal dorsal root reflex, and the second is the creation of extra action potentials at sites of altered myelination.