Effect Of Pain And Decreased Function / Range Of Motion On Chewing, Speaking, Or Mouth Opening

Effect Of Pain And Decreased Function / Range Of Motion On Chewing, Speaking, Or Mouth Opening

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Sessle proposed a pain-adaptation model to explain the presence of pain and decreased function/range of motion on chewing, speaking, or mouth opening in a TMD patient (Sessle ed 2008). His model rests on three postulates. First, chronic pain creates a general effect on the motor system, including body posture and avoidance of physical work. Second, nociceptors have a similar effect on the orofacial motor system independent of the tissue of origin. Specifically, activation of nociceptors from the articular disc, skin, muscle, or teeth create the same resultant effect. The resultant effect is the third premise, which is the inhibition of agonist muscles and the activation of antagonist muscles via modification of output from the central pattern generators. Though commonly viewed as dysfunction, reduced range of motion and pain on activity is viewed as adaptive because these prevent further damage. Sessle’s model can be used to explain the symptoms of a TMD patient as described in the question, that is patients with TMD complain of pain upon chewing, speaking or opening their mouth. Neck and shoulder pain can also be explained by this model, as accessory muscles of mastication, such as the suprhyoid and the infrahyoid muscles and postural muscles of the head and neck are considered agonist muscles, which are inhibited.
Sensory innervation in the orofacial region is mainly provided by the trigeminal cranial nerve. Trigeminal sensory afferent nerves do not relay information through the dorsal horn as their location is above the spinal cord. However, the nerve relay circuit is analogous to the dorsal horn system in function and anatomy. In the peripheral sensory system, primary afferent nerves have their cell bodies outside of the spin...

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...tex, where information is perceived in a somatotopic manner. This concept has been the basis of nociceptive pathway in both the periphery and the orofacial region. However, evidence in primates suggest the existence of an ipsilateral somatosensory pathway through the thalamus. Nash et al investigated this in human subjects, in which hypertonic saline is injected into the right masseter. Through the use of functional MRI, they found bilateral activation of neurons in the ventral posterior thalamus as well as the face region in the somatosensory cortex upon noxious stimulation (Nash et al 2010). If noxious information from the trigeminal sensory region is carried bilaterally to the brain, it is not difficult to postulate that a derangement of neurons through central sensitisation can cause referred pain and secondary hyperalgesia to the contralateral side of the face.

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