|
 
 |
| ORIGINAL HYPOTHESIS |
|
| Year : 2016 | Volume
: 7
| Issue : 3 | Page : 94-99 |
|
Temporomandibular pain and jaw movement: The hybrid model
Talal H Salame
Jaw Function and Orofacial Pain Research Unit, Westmead Centre for Oral Health, Westmead Hospital, Sydney, Australia
| Date of Web Publication | 14-Sep-2016 |
Correspondence Address:
Talal H Salame
Department of Prosthodontics, Faculty of Dentistry, Hadath Campus, The Lebanese University, Beirut, Lebanon
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2155-8213.190484
Introduction: TMD sufferers are not able to move their jaw normally. Several theories tried to demonstrate the relation between pain and movement in patients with TMD. The Vicious Cycle Theory (VCT) suggested that a sore muscle caused by prolonged contraction would lead to more muscle activity which would lead to more pain and a continuation of the vicious cycle. The Pain Adaptation Model (PAM) suggested that a decreased activity of a sore muscle responsible for producing movement is more likely in order to reduce speed and the detrimental effect of movement and promote healing. The hypothesis: The Hybrid model, developed in 2006, suggested that both the VCT and the PAM are valid and applicable in orofacial pain patients, depends on the origin of the pain whether from the muscle or from the joint. Evaluation of the hypothesis: The data from a study on pain and movement showed that both increased and decreased activities of masticatory muscles are possible in the presence of pain as the system reacts differently if the pain originates from the muscle or from the joint. In case of muscle pain, the data showed decreased activity of agonistic muscles during movement and this is conformed to the PAM. When the pain is in the joint, both decreased and increased activities were observed throughout the movement. Neurophysiological mechanisms that govern the relationship between pain and movement, as well as clinical manifestation of the pain, are different if the pain arises from the muscle or from the joint. Finding new treatment approaches that deal with the muscle pain and joint pain as two different entities seems to be of utter importance in orofacial pain patients. The Hybrid model could play an important role in this direction. Keywords: Chronic pain, jaw movements, orofacial pain, temporomandibular disorders, TMD
How to cite this article:
Salame TH. Temporomandibular pain and jaw movement: The hybrid model. Dent Hypotheses 2016;7:94-9 |
| Introduction | |  |
Temporomandibular disorders (TMD) "is a collective term concerning a number of clinical problems involving the masticatory musculature and/or the temporomandibular joint." [1],[2],[3] They consist of a range of specific signs and symptoms, and are associated with pain and/or dysfunction and limitation of jaw movements. [4] Signs and symptoms of TMD could be unilateral or bilateral and they could affect the joint alone, the masticatory muscles alone, or both. Epidemiological surveys showed that an estimated 12-59% of the population are aware of some temporomandibular disorders. [5] Okeson reported that TMD has a prevalence rate of approximately 12% of the general population, with 5% having symptoms severe enough to seek treatment. [6]
TMD sufferers are not able to move their jaw normally. [7] Normal joint function is usually obtained by the active contraction of muscles specific to the proposed movement, and constrained by a passive contraction of the opposing muscles and other soft tissues. At the level of the masticatory system, the muscles are considered to act as a functional unit when evaluating mandibular position and movement, [8] and together with the joints, surrounding bones and teeth constitute a homogeneous system that could control and constrain the movement of the jaw at all times. [9],[10] It is, therefore, expected that pain in any of these structures could affect the function in another and may lead to more and diffuse pain throughout the musculoskeletal unit. [9]
Several theories have tried to demonstrate the relation between pain and jaw movement in patients with TMD. The Vicious Cycle Theory (VCT), described first by Laskin, suggested that a sore muscle caused by prolonged contraction or muscle overuse would excite the nociceptors inside the muscle, [11] which would lead to more muscle contraction, represented by increased activity, more pain, and a continuation of the vicious cycle. [12]
More recently, the Pain Adaptation Model (PAM) was proposed by Lund to replace the VCT for the relation between pain and dysfunction. [13] According to this model, when there is an injury, the main goal for the injured part is to prevent movement to prevent more injury, and consequently promote healing. Thus, a decreased activation of the muscle responsible for producing movement will reduce speed and the detrimental effect of movement on an injured part and consequently promote healing.
| The Hypothesis | | |
Between the years of 2002 and 2006 the effect of pain on jaw movement and masticatory muscles activity was extensively studied by the author in order to evaluate the validity and applicability of both the VCT and the PAM in patients with orofacial pain. Electromyographic (EMG) activity of some masticatory muscles, namely the temporalis and the masseter as jaw closing muscles, the inferior head of the lateral pterygoid muscle, and the digastric as jaw opening muscles, was recorded from patients suffering chronic orofacial pain due to TMD as clinically diagnosed following the research diagnostic criteria of TMD (RDC/TMD) set by Dworkin and Leresche. [14] The recording was made while patients were moving their jaw in different speeds and directions. Simultaneously, the detailed movement of the jaw was recorded in three dimensions with the aid of the Jaws-3D system. Both the EMG activity and the jaw movement were analyzed subsequently, and were compared to the activity and jaw movement of pain-free individuals who were following the same protocol.
During the experiments, participants were asked to reach a previously set target during different types of lateral movements such as protrusion and contralateral (i.e., opposite to the pain side). All non-pain participants were able to reach the target precisely. However, when pain patients, who showed increased pain perception during movement, were asked to reach the target, the results were not similar. For instance during protrusion, most of the pain patients were overshooting the target indicating an increase in muscle activity, as suggested by the VCT. While during contralateral movement, the range of movement decreased in pain patients and most of them were undershooting the target which suggested decreased muscle activity supporting the PAM. The author concluded that both the PAM and VCT are valid, applicable, and work in conjunction in chronic orofacial pain patients, which gave rise to the "Hybrid Model" that suggested that the pattern of muscle function, or dysfunction, in TMD patients could be presented as an increase in activity some times and decrease in activity some other times and depends on the origin of the pain, whether from the muscle or from the temporomandibular joint.
| Evaluation of the Hypothesis | | |
There is evidence that sensory receptors in and around the joints have an important role in locomotion and kinesthesia, [15],[16] and that there is mechanical relation between joint movement and muscle activity either directly, [17] or through the central nervous system. [18]
A study on shoulder kinematic in patients suffering pain from disc impingement showed alteration of shoulder movements during rotation and translation in a manner similar to the alteration of jaw movement in TMD pain patients. [19] Another study on lower limbs concluded that the motor control of a muscle adjacent to a painful joint was modulated by chronic pain in the joint itself. [20]
Orofacial pain patients overshot their targets during protrusive movement. In the TMJ, high threshold type III and IV and a few type II nociceptive afferents are distributed in the periphery of the capsule and are reactive to intense mechanical and/or noxious stimuli. [21],[22] However, their sensitivity may increase resulting in peripheral and central sensitization causing pain. [7],[22],[23] Biomechanical studies suggest that the TMJ is compressively loaded during function, such as during protrusion, [24] and that the load on the articular surfaces is transmitted to the disc, [25] which will be compressed between the condyle and temporal bone. [25],[26] As such a painful TMJ, and in order to put the joint away from the source of pain and prevent further pain, could cause increased activity of surrounding muscles during movement, as suggested by the VCT, and produce high level of agonistic muscles contraction, and this could explain why the range of movement was increased during protrusion in pain patients.
Orofacial pain patients undershot their target during contralateral movement. The PAM suggested that pain would reduce the activity of agonistic muscles and increase the activity of antagonistic muscles during movement. This would be an adaptive way for the masticatory system to prevent further damage from fast and forceful contraction of the muscle and promote healing. [27] During contralateral movement, the contralateral condyle (i.e., contralateral to the proposed movement), which is the condyle in the painful side, moves downward and away for the painful capsule. [28] Thus the limitation of movement seen during contralateral movement could not be caused by joint pain but by muscle pain only. If the pain is in the corresponding agonistic muscles, the system would decrease the activity of these muscles, as suggested by the PAM, in order to limit their movement to prevent further injury and pain; this could explain why pain patients undershot their target during contralateral movement.
It has been concluded that the VCT and PAM are both applicable in TMD pain patients during different movements, depending on the origin of the pain either from the muscle or from the joint; this supports the hypothesis of the Hybrid Model. In fact, the increase in the activity of the agonistic muscles during protrusion shown above as application of the VCT could also be explained as an adaptive mechanism against pain and further injury as suggested by the PAM.
| Clinical Implications | | |
Clinically, TMDs represent the most common non-odontogenic orofacial pain conditions that could confront the dentist. [1],[29] In 2011, the International Association for the Study of Pain stated that TMD-related facial pain has been reported in 4-12% of the population. [30] Symptoms include pain and/or tenderness in the periauricular area and/or in the masticatory muscles; a reduction and/or an alteration of the range of joint motion; clicking or crepitus during mandibular movements and headache are also common. [31],[32],[33]
Most internationally recognized orofacial pain classification schemes, such as The Research Diagnostic Criteria for Temporomandibular Disorders RDC/TMD, [22] The International Association for the Study of Pain, [34] The International Classification of Headache Disorders second edition and The American Academy of Orofacial Pain, [35],[36] divide orofacial pain conditions into muscles disorders and joints disorders. However, current treatment approaches are still random, not evidence-based, and do not differentiate between joint pain and muscle pain. This may result in undesirable effects and sometimes irreversible drastic consequences.
As an example, one of the common approaches currently applicable worldwide is to apply heat pack on the TMD region and the surrounding muscles. While this treatment modality would be effective in treating ischemic muscle pain caused by repeated contraction, it could be harmful and contraindicated for pain originating from the joint itself. This is because ischemic muscle pain usually results from repeated muscle contraction due to abnormal muscle activity such as clenching and bruxing. Repeated and prolonged muscle contraction results in occlusion of the vessels entering the muscle and prevent normal inward blood flow. [12] Applying heat packs on the affected muscle helps in restoring normal blood flow to the muscle and reduces pain. However, the mechanism of pain originating from the TMJ is different. It has been shown that pain from TMJ is triggered by inflammatory process, rather than ischemia, due to repeated microtrauma caused by hyperfunction. Inflammatory mediators released in the TMJ sensitize the surrounding nociceptors in the TMJ capsule and result in pain. [37] Applying heat packs would increase the blood flow to the affected areas and would amplify the inflammatory process and increase pain. Although some studies suggested that heat therapy could increase local tissues metabolism and promote healing, [38] others suggested that one aim of physical therapy should be decreasing the intraarticular temperature because high temperatures could increase the breakdown of tissues that contain collagen, and therefore, could damage the articular disk composed of collagen fibres solely. [39]
| Discussion | | |
Neurophysiological mechanisms
Peripheral receptors are nerve ending units that exist in both muscle and joint tissues as well as other body organs and are responsible to receive, in a discriminative manner, external (exteroceptive) or internal (proprioceptive) impulses induced by physical (mechanoreceptors) and/or thermal (thermoreceptors) afferents or by pain (nociceptors). Transduction is the activation of the peripheral receptors by one or more of the previously described stimulus. Impulses from the peripheral part of the receptors are transmitted by their axons through the spinal cord to their central end by what is called the conduction process. Transmission is the synaptic transfer of these impulses from one axon to another between the spinal cord, the brainstem, the thalamus, and the cerebral cortex where sensation is perceived (perception). [40],[41] When the sensation is perceived in the brain as intense or unpleasant, it is pain, and the whole process of transduction, conduction, transmission, and perception is termed nociception. Such sensations are usually linked to a specific stimulus associated with danger that we learn to avoid through a certain regulatory process controlled by the brain. [41] However, the response of the system to pain could be different if the pain is originating from the joint or from the muscle, and the whole regulatory process could change.
The effect of joint and muscle pain on jaw movements
Movement is controlled centrally by a feedforward mechanism that is modulated by feedback. [42] According to the feedforward model, the set of muscle activations required to execute precise limb movement is centrally defined by a motor plan prior to the onset of the movement. [42],[43],[44] Studies on the movements of the limb and back demonstrated that the feedforward mechanism is altered in patients with a history of pain or during experimentally induced pain. [45],[46] Clinical and experimental evidence suggested that noxious stimuli may sensitize central neural structures involved in pain perception. [23],[47] Changes in the feedforward mechanism in low back pain has been suggested to be due to altered processing within the central nervous system (CNS) in order to prevent damage to the spine. [45] This is consistent with leg movements in patients with chronic knee pain, where it was concluded that neuroplastic mechanisms within the CNS modulate the motor control of the quadriceps muscle to protect the knee and minimize painful sensations. [20] Thus, when the pain exists in the TMJs, central neuroplastic changes are expected to regulate the movement behavior of the masticatory system to prevent joint pain. This regulation occurs by increasing muscle activity sometimes and decreasing it some other times in order to put the joint in a safer position, as suggested by the PAM. In fact, a study by Clark and Lynn (1986) found that, in patients with TMJ pain alone (i.e., without the presence of muscle pain), the velocity of the jaw during retrusion was significantly lower than that in controls. [48] This would represent a protective action of the jaw agonistic muscles to prevent a rapid return of the condyle toward the injured and painful joint, however, in this instance the decreased activity of the muscles is due to joint rather than muscle pain.
It seems that the regulatory process is different when the pain arises from the muscle rather than the joint. In addition to moving body parts, the main role of the muscles is to generate force in order to execute the desired movement or to complete other force requiring vital tasks such as chewing. Muscle spindles are responsible to produce signals to the muscles regarding their actual length and the length needed for new movement. Golgi tendons are responsible to inform the muscles regarding the force needed to execute the required contraction. A Group of Ib fibers, that have their cell bodies in the dorsal root ganglia and project in the spinal cord to synapse with the Ib inhibitory interneuron, innervate the Golgi tendon organ and are activated when tension is applied to a muscle. [49]
When a muscle is subjected to excessive or continuous force that threatens to cause pain or injury, the Golgi tendon sends signals to the spinal cord through what is called autogenic inhibitory reflex that acts on the Ib inhibitory interneurons to reduce the activation of the motorneurons and relax the muscle. [50] Multiple studies have suggested that this process represents a protective mechanism to prevent a potential damage to the muscle itself caused by the excessive contraction force. [51],[52],[53] It has been suggested that masticatory muscle pain is usually caused by acute, sustained, or repeated overload of the muscle such as during bruxism or jaw clenching. [12],[54] Thus, the autogenic inhibitory reflex would constitute the best explanation for the decrease in muscle activity shown in TMD patients with muscle pain.
Clinical manifestation and assessment of muscles and joints pain
According to The Guidelines of the American Academy of Orofacial Pain and the Research Diagnostic Criteria, pain in TMJ arthralgia occurs over the TMJ during mandibular movement. [14],[32] In addition, pain on palpation of the lateral pole of the condyle surface or via the external auditory meatus without crepitus confirms the TMJ arthralgia. [32],[55] Because of its nociceptive and inflammatory nature, as described above, joint pain is typically well localized, constant, and often with an aching or throbbing quality. [56]
Meanwhile, masticatory muscle pain has been described as dull aching and cramping pain that increases with palpation or muscle function. [12],[54],[57] Furthermore, myofascial pain, which is clear RDC/TMD diagnostic criteria, has also been considered as a form of myalgia with trigger points and spread or migration of pain on palpation. [57] Trigger points are described as sites of focal tenderness in a palpable taut band of muscle fibres that can produce pain on mechanical stimulus, and have been reported in approximately 18% of patients with different chronic muscle pain syndromes (e.g., fibromyalgia). [58]
Following the recently updated RDC/TMD criteria by Schiffman et al. (2012), joint pain is normally much localized to the TMJ area and occurs during digital palpation of the lateral pole of the condyle or after inserting the little finger in the external auditory meatus. Meanwhile, muscle palpation usually reveals more spreading pain over the entire area of the muscle and toward the surrounding structures sometimes, or the presence of small local nodules in the palpated muscle indicating the presence of trigger points. [55]
In addition, and based on the author's personal clinical experience, although both joint pain and muscle pain occur and aggravate during mandibular jaw movement, joint pain usually occurs during different types of movement and continuously throughout the movement, whereas muscle pain occurs during certain types of movements and usually close to the end of the ongoing movement, such as maximum assisted or unassisted opening, when the pressure on the muscle fibres is in its higher end.
| Conclusion | | |
In conclusion, it seems obvious that the system reacts differently toward pain when it arises from the joint or from the muscle. These differences occur at the level of neurophysiological mechanisms as well as clinical manifestation and assessment. It would be of significant importance to develop new treatment approaches that apply standard and reliable methods of clinical pain management in patients with orofacial pain and deal with joints pain and muscles pain as two different entities. The Hybrid Model could play an important role in this direction.
Acknowledgements
The "Hybrid Model" was developed by the author in 2006 while he was undertaking a research program for a PhD degree in the Department of Prosthodontics at the Faculty of Dentistry, University of Sydney, Australia. The research was supported by the National Health and Medical Council of Australia (NHMRC) and the Bela Schwartz Foundation.
The Author would like to thank Professor Iven Klineberg, head of the department of Prosthodontics at The University of Sydney and the staffs of the Jaw Function and Orofacial Pain Research Unit.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | McNeil C. Temporomandibular disorders: Guidelines for classification, assessment and management. Illinois: Quintessence; 1993.  |
| 2. | Okeson JP. Bell′s orofacial pains. Chicago: Quintessence; 1995. |
| 3. | Krogstad BS, Jokstad A, Dahl BL, Vassend O. Relationships between risk factors and treatment outcome in a group of patients with temporomandibular disorders. Pain 1996;10:48-53. |
| 4. | DeBoever JA, Carlsson GE. Etiology and differential diagnosis. In: Zarb GA et al., editors, Temporomandibular joint and masticatory muscles disorders. Copenhagen: Munksgaard; 1994 |
| 5. | Dworkin SF, LeResche L. Assessing clinical signs of TMD: Realibility of clinical examiner. J Prosthet Dent 1990;63:571-9. |
| 6. | Okeson JP. Diagnosis of temporomandibular disorders. In: Management of temporomandibular disorder and occlusion. 5 th ed. Mosby, St Louis; 2003. p. 321-64. |
| 7. | Lund J, Sessle B. Neurophysiological mechanisms. In: Zarb G et al., editors, Temporomandibular joint and masticatory muscle disorders. Copenhagen: Munksgaard; 1994. |
| 8. | Harper RP, de Bruin H, Burcea I. Muscle activity during mandibular movements in normal and mandibular retrognathic subjects. J Oral Maxillofac Surg 1997;55:225-33. |
| 9. | Allan DA. Structure and physiology of joints and their relationship to repetitive strain injuries. Clin Orthop Relat Res 1998;351:32-8. |
| 10. | Koolstra JH. Dynamics of the human masticatory system. Crit Rev Oral Biol Med 2002;13:366-76. |
| 11. | Laskin DM. Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 1969;79:147-53. |
| 12. | Mense S, Simons DG. Muscle pain: Understanding its nature, diagnosis, and treatment. Ottawa: Lippincott Williams and Wilkins; 2001. |
| 13. | Lund JP, Donga R, Widmer CG, Stohler CS. The pain-adaptation model: A discussion of the relationship between chronic musculoskeletal pain and motor activity. Can J Physiol Pharmacol 1991;69:683-94. |
| 14. | Dworkin SF, LeResche L. Research diagnostic criteria for temporomandibular disorders: Review, criteria, examinations and specifications, critique. J Craniomandib Disord 1992;6:301-55. |
| 15. | Freeman MA, Wyke B. Articular contribution to limb muscle reflexes. Br J Surg 1966;53:61-9. |
| 16. | McMahon TA. Reflexes and motor control. In: McMahon TA editor, Muscles, Reflexes, and Locomotion. New Jersey: Princeton University Press; 1984. |
| 17. | Koolstra JH, van Eijden TM. Combined finite-element and rigid-body analysis of human jaw joint dynamics. J Biomech 2005;38:2431-9. |
| 18. | Gribble PL, Ostry DJ. Compensation for interaction torques during single- and multi-joint limb movement. J Neurophysiol 1999;82:2310-26. |
| 19. | Ludewig PM, Cook TM. Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement. Phys Ther 2000;80:276-91. |
| 20. | On AY, Uludag B, Taskiran E, Ertekin C. Differential corticomotor control of a muscle adjacent to a painful joint. Neurorehabil Neural Repair 2004;18:127-33. |
| 21. | Sessle BJ. The neurobiology of facial and dental pain: Present knowledge, future directions. J Dent Res 1987;66:962-81. |
| 22. | Hannam AG, Sessle BJ. Temporomandibular neuroscensory and neuromuscular physiology. In: Zarb GA et al., editors. Temporomandibular joint and masticatory muscles disorders. Copenhagen: Munksgaard; 1994. |
| 23. | Sessle BJ. Acute and chronic craniofacial pain: Brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol Med 2000;11:57-91. |
| 24. | Koolstra JH, van Eijden TM. Biomechanical analysis of jaw-closing movements. J Den Res 1995;74:1564-70. |
| 25. | Sindelar BJ, Herring SW. Soft tissue mechanics of the temporomandibular joint. Cells Tissues Organs 2005;180:36-43. |
| 26. | Koolstra JH, van Eijden TM. Combined finite-element and rigid-body analysis of human jaw joint dynamics. J Biomech 2005;38:2431-9. |
| 27. | Lund JP. Pain and Movement. In: Lund JP et al., editors. Orofacial pain: From basic science to clinical management. Illinois: Quintessence Publishing Co., Inc.; 2001. |
| 28. | DuBrull EL. The craniomandibular articulation. In: Sicher editor. Sicher and DuBrull′s oral anatomy. Tokyo: Ishiyako EuroAmerica, Inc.; 1980. |
| 29. | Yap AU, Dworkin SF, Chua EK, List T, Tan KB, Tan HH. Prevalence of temporomandibular disorder subtypes, psychologic distress, and psychosocial dysfunction in Asian patients. J Orofac Pain 2002;17:21-8. |
| 30. | International Pain Summit of the International Association for the Study of Pain. Declaration of Montreal: Declaration that access to pain management is a fundamental human right. J Pain Palliat Care Pharmacother 2011;25:29-31. |
| 31. | Sharav Y, Benoliel R. Orofacial pain and headache. Edinburgh; New York: Mosby; 2008. |
| 32. | Leeuw RD, American Academy of Orofacial Pain. Orofacial pain: Guidelines for assessment, diagnosis, and management. Chicago: Quintessence; 2008. |
| 33. | Tanaka E, Tanne K, Sakuda MA. Three dimensional finite element model of the mandible including the TMJ and its application to stress analysis in the TMJ during clenching. Med Eng Phys 1994;16:316-22. |
| 34. | Merskey H, Bogduk N. Classification of chronic pain, IASP Task Force on Taxonomy. Seattle, WA: International Association for the Study of Pain Press; 1994. |
| 35. | Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders. Cephalalgia: An international journal of headache 2004;24:9. |
| 36. | Okeson JP. The classification of orofacial pains. Oral Maxillofac Surg Clin North A 2008;20:133-44. |
| 37. | Nawaz-Khan A, Ul Haque S, Macdonald S, Saeed S, Bibi N, Ribeiro N. Temporomandibular joint meniscus abnormalities. emedicine, 2005. Available: www.emedicine.com. [Last accessed on 2007 Jan 20]. |
| 38. | Nadler SF, Weingand K, Kurse RJ. The physiologic basis and clinical applications of cryotherapy and thermotherapy for the pain practitioner. Pain Physician 2004;7:395-9. |
| 39. | Fredrikus GJ, Oosterveld FG, Rasker JJ. Treating arthritis with locally applied heat or cold. Semin Arthritis Rheum 1994;24:82-90. |
| 40. | Cadden SW, Orchardson R. The neural mechanism of oral and facial pain. Dent Update 2001;28:359-67. |
| 41. | Woolf CJ. Pain: Moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004;140:441-51. |
| 42. | Ferrell WR, Gandevia SC, McCloskey DI. The role of joint receptors in human kinaesthesia when intramuscular receptors cannot contribute. J Physiol 1987;386:63-71. |
| 43. | Milner TE. A model for the generation of movements requiring endpoint precision. Neurosci Res 1992;49:487-96. |
| 44. | Desmurget M, Grafton S. Forward modeling allows feedback control for fast reaching movements. Trend Cogn Sci 2000;4:423-31. |
| 45. | Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain: A motor control evaluation of transversus abdominis. Spine 1996;15:2640-50. |
| 46. | Falla D, Jull G, Hodges PW. Feedforward activity of the cervical flexor muscles during voluntary arm movements is delayed in chronic neck pain. Exp Brain Res 2004;157:43-8. |
| 47. | Coderre TJ, Katz J, Vaccarino AL, Melzack R. Contribution of central neuroplasticity to pathological pain: Review of clinical and experimental evidence. Pain 1993;52:259-85. |
| 48. | Clark GT, Lynn P. Horizontal plane jaw movements in controla and clinic patients with temporomandibular dysfunction. J Pros Dent 1986;55:730-5. |
| 49. | Knierim J. Neuroscience Online Chapter 2: Spinal Reflexes and Descending Motor Pathways; 1997. |
| 50. | Chalmers G. Strength training: Do Golgi tendon organs really inhibit muscle activity at high force levels to save muscles from injury, and adapt with strength training? Sport Biomech 2002;1:239-49. |
| 51. | Earle RW, Barchle R. Resistance training and spotting techniques. In: Essentials of strength training and conditionning. Earle R, editor. Champaign, IL: Human Kinetics; 2000. p. 343-94. |
| 52. | Brooks GA, Fahey T, White T, Baldwin K. Exercise Physiology: Human Bioenergetics and Its Applications. 3 rd ed. Mountain View, CA: Mayfield 2000; 2000. |
| 53. | Powers SK, Howley ET. Exercise Physiology: Theory and Application to Fitness and Performance. Exerc Metab 2001;7:51-71. |
| 54. | Clark G, Takeuchi H. Temporomandibular dysfunction, chronic orofacial pain and oral motor disorders in the 21 st century. W VA Dent J 1996;70:17-9, 21-3, 27. |
| 55. | Schiffman E, Ohrbach R, List T, Anderson G, Jensen R, John MT, et al. Diagnostic criteria for headache attributed to temporomandibular disorders. Cephalalgia 2012;32:683-92. |
| 56. | Nicholson B. Differential diagnosis: Nociceptive and neuropathic pain. Am J Manag Care 2006;12:S256-62. |
| 57. | Greenwood LF. Masticatory muscles disorders. In: Zarb GA. et al., editors. Temporomandibular joint and masticatory muscles disorders. Copenhagen: Munksgaard; 1994. |
| 58. | Wolfe F, Simons DG, Fricton J, Bennet RM, Goldenberg DL, Gerwin R, et al. The fibromyalgia and myofascial pain syndromes: A preliminary study of tender points and trigger points in persons with fibromialgia, myofascial pain syndrome and no disease. J Rheumatol 1992;19:944-51. |
|
Search Pubmed for
