Brainstem mechanisms underlying temporomandibular joint and masticatory muscle pain

Many trigeminal [V] brainstem nociceptive neurons receive convergent inputs from afferents supplying deep craniofacial sites [e.g., temporomandibular joint [TMJ]; muscle] as well as skin. These neurons appear to be involved i n mediating deep pain since very few of the nociceptive neurons exclusively receive deep afferent inputs; indeed, their extensive convergent input pat terns suggest their involvement also in pain spread and referral. Deep affe rent inputs evoked by application of the small-fiber excitant and inflammat ory irritant mustard oil [MO] to TMJ or muscle also induce a prolonged enha ncement of the cutaneous as well as deep receptive field properties of most nociceptive neurons. These neuroplastic changes appear to reflect a "centr al sensitization" and may be accompanied by MO-induced electromyographic ac tivity in the jaw muscles via interneurons in V subnucleus caudalis, and ma y be modulated by both peripheral and central N-methyl-D-aspartate, neuroki nin or opioid mechanisms. These findings underscore the functional plastici ty of the central V system and the particular effectiveness of deep nocicep tive inputs in inducing neuroplastic changes in brainstem nociceptive neuro ns that may be involved in the development of several conditions manifestin g pain and neuromuscular dysfunction, including temporomandibular disorders .