Craniofacial muscle pain: review of mechanisms and clinical manifestations.
Epidemiologic surveys of temporomandibular disorders (TMD) have demonstrated that a considerable proportion of the population--up to 5% or 6%--will experience persistent pain severe enough to seek treatment. Unfortunately, the current diagnostic classification of craniofacial muscle pain is based on descriptions of signs and symptoms rather than on knowledge of pain mechanisms. Furthermore, the pathophysiology and etiology of craniofacial muscle pain are not known in sufficient detail to allow causal treatment. Many hypotheses have been proposed to explain cause-effect relationships; however, it is still uncertain what may be the cause of muscle pain and what is the effect of muscle pain. This article reviews the literature in which craniofacial muscle pain has been induced by experimental techniques in animals and human volunteers and in which the effects on somatosensory and motor function have been assessed under standardized conditions. This information is compared to the clinical correlates, which can be derived from the numerous cross-sectional studies in patients with craniofacial muscle pain. The experimental literature clearly indicates that muscle pain has significant effects on both somatosensory and craniofacial motor function. Typical somatosensory manifestations of experimental muscle pain are referred pain and increased sensitivity of homotopic areas. The craniofacial motor function is inhibited mainly during experimental muscle pain, but phase-dependent excitation is also found during mastication to reduce the amplitude and velocity of jaw movements. The underlying neurobiologic mechanisms probably involve varying combinations of sensitization of peripheral afferents, hyperexcitability of central neurons, and imbalance in descending pain modulatory systems. Reflex circuits in the brain stem seem important for the adjustment of sensorimotor function in the presence of craniofacial pain. Changes in somatosensory and motor function may therefore be viewed as consequences of pain and not factors leading to pain. Implications for the diagnosis and management of persistent muscle pain are discussed from this perspective.
Svensson
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P
Center for Sensory-Motor Interaction, Aalborg University, Fredrik Bajers Vej 7D-3, DK-9220 Aalborg E, Denmark. psv@smi.auc.dk
Graven-Nielsen
T
T
D000344:Afferent Pathways; D000818:Animals; D004576:Electromyography; D005157:Facial Pain / Q000503:physiopathology*; D006801:Humans; D006982:Hypertonic Solutions / Q000494:pharmacology; D008410:Masticatory Muscles / Q000187:drug effects / Q000503:physiopathology; D008954:Models, Biological; D009119:Muscle Contraction; D009619:Nociceptors; D017288:Pain Threshold; D013003:Somatosensory Cortex / Q000502:physiology
D006982:Hypertonic Solutions