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The Relationship Between Pain and Movement
CLINICAL PRACTICE
PA I N U P D AT E
The relationship between pain and movement Christopher C. Peck, PhD, MScDent, BDS
CLINICAL PROBLEM
patient underwent a lengthy crown preparation five days ago and returned to the dentist’s office the day after the procedure complaining of limited mouth opening and difficulty eating and speaking. The right masseter muscle was severely tender to palpation, and the dentist prescribed analgesics. The patient returns today having experienced a vast improvement in the pain, but with similar limited opening and eating and speaking difficulties. A clinical assessment revealed no pathology causing this functional impairment. How does pain affect the jaw muscles and consequently jaw movement?
A
EXPLANATION
It is not unusual for pain to affect movement; for example, consider an episode of low back pain, which often transforms a person from walking tall to being a slow shuffler whose every step is taken with caution. Similarly, people with jaw pain arising, for example, from a needle injury of the medial pterygoid muscle or as a result of pericoronitis commonly eat more slowly and complain of reduced jaw opening and limitations in other jaw movements. However, slower and smaller movements are not always seen in patients with pain; this is demonstrated by competitive athletes who continue to perform with seemingly no problems, although they may have undergone extreme tissue trauma and are experiencing severe pain. This paradoxical observation is explained below. Vicious-cycle theory. Researchers have proposed two key theories to explain how musculoskeletal pain affects movement: the vicious-cycle
theory (VCT)1 and the pain-adaptation model (PAM).2 Adherents of the VCT propose that an initiating factor (such as an abnormality in posture or structure, stress or excessive movement) produces pain that leads to excessive muscle activity (muscle hyperactivity) and fatigue. This results in further muscle pain, which perpetuates the vicious cycle. This theory has become the basis of many treatments that attempt to break this proposed vicious cycle in pain conditions such as temporomandibular disorders (TMDs), fibromyalgia and tension-type headaches. For many years, the VCT seemed to provide a straightforward explanation of the cause of muscle pain. However, the supporting evidence for this theory is lacking. In most cases in which patients report jaw pain, their masticatory muscle activity actually is reduced rather than increased. Electromyographic recordings, which researchers use to measure the electrical activity (and consequently the work) of a contracting muscle, must be interpreted carefully. The surface electrodes often used in electromyography are placed on the skin overlying the masseter muscle to detect its activity, but they also may detect adjacent muscle activity (for example, grimacing activity from the nearby buccinator muscle). In addition, the degree of increase or decrease in a muscle’s electrical activity may not be significant from a clinical perspective. Pain-adaptation model. Lund and colleagues2 proposed the PAM in 1991 to counter the claims of the VCT. Unlike the VCT, it does not offer an explanation of the cause of pain, but it does explain the effects of the pain on muscle activity. The PAM proposes that pain leads to alterations in muscle activity that limit moveJADA, Vol. 140
http://jada.ada.org
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
December 2009
1505
CLINICAL PRACTICE PAIN UPDATE
ment and protect the skeletomotor system from further injury, thereby promoting healing. Advocates of this model propose that when masticatory muscles are in pain, agonist muscles (that is, those primarily responsible for the movement) will decrease their activity (for example, decreases in lateral pterygoid muscle activity during jaw opening) and antagonist muscles (that is, those resisting the movement) will increase their activity (for example, increases in masseter muscle activity during jaw opening). Pain, therefore, leads to movements that are slower and smaller, which reduces the chance of aggravating the injury and further increasing the pain. Conversely, jaw opening and the chewing rate are increased when the pain has been reduced. Much experimental evidence2-4 supports the PAM, and clinically it is common for a patient with a painful TMD to complain of reduced mouth opening and difficulty eating hard or chewy foods. In fact, it is this obvious correlation between jaw pain and movement that helps clinicians differentiate between TMD pain and pain from other orofacial disorders. The PAM is based on neural circuitry between the muscles and the brainstem, so that after a noxious stimulus happens, an automatic reflexlike change in muscle activity occurs with movement. However, it is likely that this circuitry also is modulated by higher brain activity.5 For example, motivation may override the PAM in certain circumstances (for example, the competitive athlete) so that a person can continue with normal or near-normal muscle activity despite experiencing pain. Conversely, when someone is quite fearful of pain and its consequences, the change in muscle activity, according to the PAM, may be much greater than that expected. These are only two examples of muscle responses to pain. CLINICAL IMPLICATIONS
When determining the relationship between pain and motor activity, clinicians need to consider the multiple dimensions of pain, including its location, duration and intensity and how much it bothers the affected person. Furthermore, clinicians must take into account a patient’s previous pain experiences, attention to pain, mood and
1506
JADA, Vol. 140
http://jada.ada.org
pain-related fear, as well as the expectations of significant others and society regarding how one “should” respond to pain. Such biological, psychological and social factors have important clinical implications when undertaking an assessment of a patient’s pain and movement and developing a treatment plan. The PAM has important implications for proper clinical management of musculoskeletal pain. For example, the clinician’s main focus should be on pain control, which will enable the patient to achieve better movement. Consequently, we would expect physical therapy to work best when the patient’s pain is suppressed. Depending on the patient’s pain experience, strategies to control pain include appropriate medication regimens and other approaches that focus on the multidimensional nature of pain. Clinicians also must be aware of the psychological and social aspects of pain, as outlined above. CONCLUSION
Although both the VCT and PAM explain the relationship between pain and jaw movement, the PAM is supported by much stronger evidence.2-4,6 Consequently, clinicians need to consider this model together with modulating factors such as a patient’s motivation, previous pain experiences and pain-related fear to help assess and treat the patient’s pain. ■ Dr. Peck is an associate professor, Faculty of Dentistry, The University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia, e-mail “[email protected]”. Address reprint requests to Dr. Peck. Disclosure. Dr. Peck did not report any disclosures. Pain Update is published in collaboration with the Neuroscience Group of the International Association for Dental Research. 1. Travell JG, Rinzler S, Herman M. Pain and disability of the shoulder and arm: treatment by intramuscular infiltration with procaine hydrochloride. JAMA 1942;120(6):417-422. 2. 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(5):683-694. 3. Svensson P, Graven-Nielsen T. Craniofacial muscle pain: review of mechanisms and clinical manifestations. J Orofac Pain 2001;15(2): 117-145. 4. Stohler CS. Craniofacial pain and motor function: pathogenesis, clinical correlates, and implications. Crit Rev Oral Biol Med 1999;10(4):504-518. 5. Murray GM, Peck CC. Orofacial pain and jaw muscle activity: a new model. J Orofac Pain 2007;21(4):263-278. 6. Lobbezoo F, van Selms MKA, Naeije M. Masticatory muscle pain and disordered jaw motor behaviour: literature review over the past decade. Arch Oral Biol 2006;51(9):713-720.
December 2009
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
PA I N U P D AT E
The relationship between pain and movement Christopher C. Peck, PhD, MScDent, BDS
CLINICAL PROBLEM
patient underwent a lengthy crown preparation five days ago and returned to the dentist’s office the day after the procedure complaining of limited mouth opening and difficulty eating and speaking. The right masseter muscle was severely tender to palpation, and the dentist prescribed analgesics. The patient returns today having experienced a vast improvement in the pain, but with similar limited opening and eating and speaking difficulties. A clinical assessment revealed no pathology causing this functional impairment. How does pain affect the jaw muscles and consequently jaw movement?
A
EXPLANATION
It is not unusual for pain to affect movement; for example, consider an episode of low back pain, which often transforms a person from walking tall to being a slow shuffler whose every step is taken with caution. Similarly, people with jaw pain arising, for example, from a needle injury of the medial pterygoid muscle or as a result of pericoronitis commonly eat more slowly and complain of reduced jaw opening and limitations in other jaw movements. However, slower and smaller movements are not always seen in patients with pain; this is demonstrated by competitive athletes who continue to perform with seemingly no problems, although they may have undergone extreme tissue trauma and are experiencing severe pain. This paradoxical observation is explained below. Vicious-cycle theory. Researchers have proposed two key theories to explain how musculoskeletal pain affects movement: the vicious-cycle
theory (VCT)1 and the pain-adaptation model (PAM).2 Adherents of the VCT propose that an initiating factor (such as an abnormality in posture or structure, stress or excessive movement) produces pain that leads to excessive muscle activity (muscle hyperactivity) and fatigue. This results in further muscle pain, which perpetuates the vicious cycle. This theory has become the basis of many treatments that attempt to break this proposed vicious cycle in pain conditions such as temporomandibular disorders (TMDs), fibromyalgia and tension-type headaches. For many years, the VCT seemed to provide a straightforward explanation of the cause of muscle pain. However, the supporting evidence for this theory is lacking. In most cases in which patients report jaw pain, their masticatory muscle activity actually is reduced rather than increased. Electromyographic recordings, which researchers use to measure the electrical activity (and consequently the work) of a contracting muscle, must be interpreted carefully. The surface electrodes often used in electromyography are placed on the skin overlying the masseter muscle to detect its activity, but they also may detect adjacent muscle activity (for example, grimacing activity from the nearby buccinator muscle). In addition, the degree of increase or decrease in a muscle’s electrical activity may not be significant from a clinical perspective. Pain-adaptation model. Lund and colleagues2 proposed the PAM in 1991 to counter the claims of the VCT. Unlike the VCT, it does not offer an explanation of the cause of pain, but it does explain the effects of the pain on muscle activity. The PAM proposes that pain leads to alterations in muscle activity that limit moveJADA, Vol. 140
http://jada.ada.org
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
December 2009
1505
CLINICAL PRACTICE PAIN UPDATE
ment and protect the skeletomotor system from further injury, thereby promoting healing. Advocates of this model propose that when masticatory muscles are in pain, agonist muscles (that is, those primarily responsible for the movement) will decrease their activity (for example, decreases in lateral pterygoid muscle activity during jaw opening) and antagonist muscles (that is, those resisting the movement) will increase their activity (for example, increases in masseter muscle activity during jaw opening). Pain, therefore, leads to movements that are slower and smaller, which reduces the chance of aggravating the injury and further increasing the pain. Conversely, jaw opening and the chewing rate are increased when the pain has been reduced. Much experimental evidence2-4 supports the PAM, and clinically it is common for a patient with a painful TMD to complain of reduced mouth opening and difficulty eating hard or chewy foods. In fact, it is this obvious correlation between jaw pain and movement that helps clinicians differentiate between TMD pain and pain from other orofacial disorders. The PAM is based on neural circuitry between the muscles and the brainstem, so that after a noxious stimulus happens, an automatic reflexlike change in muscle activity occurs with movement. However, it is likely that this circuitry also is modulated by higher brain activity.5 For example, motivation may override the PAM in certain circumstances (for example, the competitive athlete) so that a person can continue with normal or near-normal muscle activity despite experiencing pain. Conversely, when someone is quite fearful of pain and its consequences, the change in muscle activity, according to the PAM, may be much greater than that expected. These are only two examples of muscle responses to pain. CLINICAL IMPLICATIONS
When determining the relationship between pain and motor activity, clinicians need to consider the multiple dimensions of pain, including its location, duration and intensity and how much it bothers the affected person. Furthermore, clinicians must take into account a patient’s previous pain experiences, attention to pain, mood and
1506
JADA, Vol. 140
http://jada.ada.org
pain-related fear, as well as the expectations of significant others and society regarding how one “should” respond to pain. Such biological, psychological and social factors have important clinical implications when undertaking an assessment of a patient’s pain and movement and developing a treatment plan. The PAM has important implications for proper clinical management of musculoskeletal pain. For example, the clinician’s main focus should be on pain control, which will enable the patient to achieve better movement. Consequently, we would expect physical therapy to work best when the patient’s pain is suppressed. Depending on the patient’s pain experience, strategies to control pain include appropriate medication regimens and other approaches that focus on the multidimensional nature of pain. Clinicians also must be aware of the psychological and social aspects of pain, as outlined above. CONCLUSION
Although both the VCT and PAM explain the relationship between pain and jaw movement, the PAM is supported by much stronger evidence.2-4,6 Consequently, clinicians need to consider this model together with modulating factors such as a patient’s motivation, previous pain experiences and pain-related fear to help assess and treat the patient’s pain. ■ Dr. Peck is an associate professor, Faculty of Dentistry, The University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia, e-mail “[email protected]”. Address reprint requests to Dr. Peck. Disclosure. Dr. Peck did not report any disclosures. Pain Update is published in collaboration with the Neuroscience Group of the International Association for Dental Research. 1. Travell JG, Rinzler S, Herman M. Pain and disability of the shoulder and arm: treatment by intramuscular infiltration with procaine hydrochloride. JAMA 1942;120(6):417-422. 2. 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(5):683-694. 3. Svensson P, Graven-Nielsen T. Craniofacial muscle pain: review of mechanisms and clinical manifestations. J Orofac Pain 2001;15(2): 117-145. 4. Stohler CS. Craniofacial pain and motor function: pathogenesis, clinical correlates, and implications. Crit Rev Oral Biol Med 1999;10(4):504-518. 5. Murray GM, Peck CC. Orofacial pain and jaw muscle activity: a new model. J Orofac Pain 2007;21(4):263-278. 6. Lobbezoo F, van Selms MKA, Naeije M. Masticatory muscle pain and disordered jaw motor behaviour: literature review over the past decade. Arch Oral Biol 2006;51(9):713-720.
December 2009
Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.