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Stretching psychophysiological models of TMD
Commentary
Stretching Psychophysiological Models ofTMD But Do the Muscles Respond? Thomas E. Rudy* and Carol M. Greco*t
sychophysiological models of chronic pain conditions, particularly those believed to have a musculoskeletal component (e.g., low back pain, temporomandibular disorders), have emerged over the past two decades due, in part, to the inadequacy of structural models to explain the etiology, maintenance, exacerbation, and/or remediation of these conditions." Psychological factors increasingly have been recognized by many theorists dealing with the etiology and treatment of temporomandibular disorders (TMDs). Although other psychological factors have received some attention, to date, psychophysiological models of TMDs appear to be the most popular psychologically based explanations for the development and/or maintenance of TMDs. Rudy6 suggests that one of the primary reasons for the acceptance of psychophysiological aspects of TMDs is that this model was initially proposed by a dentist, Daniel Laskin.s The focus article by Ohrbach and McCall suggests that all is not well with current psychophysiological conceptualizations of TMD, particularly from a research or empirical perspective. They highlight the numerous methodological, conceptual, and interpretational difficulties with previous psychophysiological studies. Their particular emphasis on the current lack of empirical support for the direct association between stressrelated electromyography (EMG) and pain severity levels is important and overdue. Ohrbach and McCall, however, do not abandon the psychophysiological model of TMD. Rather, they propose a revised theory of stress-hyperactivity and pain
P
From the 'Departments of Anesthesiology, Psychiatry, and Biostatistics, tDepartment of Anesthesiology, and 'Pain Evaluation and Treatment Institute, University of Pittsburgh, Pittsburgh, PA. Reprint requests: Thomas E. Rudy, PhD, Pain Evaluation and Treatment Institute, University of Pittsburgh Medical Center, 4601 Baum Boulevard, pittsburgh, PA 15213.
Pain Forum 5(1): 67-69, 1996
that draws on other theories of chronic myogenic pain, that is, myofascial pain and neuromatrix theories, as well as the general stress-hyperactivity model. Specifically, the authors suggest that a persistent pattern of frequent muscle activity (possibly of low magnitude) leads to shortened muscle length. Attempts at returning the muscle to normal length, including the muscle stretching associated with normal functioning (such as talking, mastication), are the proposed cause of pain. We will address this revised theory from a clinical perspective, followed by several methodological concerns.
CLINICALLY REASONABLE Our clinical experiences, derived from providing treatment to several hundred TMD patients who have participated in research protocols that consisted of education on oral habits, biofeedback for facial relaxation, stress management, and cognitive-behavioral therapy, suggest that many of the components of Ohrbach and McCall's revised theory are consistent with clinical observations and patients' reports. Nearly all patients readily provide personal experiences or beliefs that their "perceived increase" in masticatory muscle tension is associated with emotionally stressful events, which in turn are also associated with pain increases, either immediately or shortly after the stressful period. Many patients would agree that the stretching associated with functions such as talking, laughing, and eating leads to an increase in their pain perceptions. We also have found that a fairly substantial subset of patients report that their pain has increased rather than decreased following an initial biofeedback training session. These types of anecdotal reports, despite their scientific limitations, tend to support the revised stress-hyperactivity theory proposed by Ohrbach and McCall. However, most notable clinically, as well as from a research perceptive, is the heterogeneity of TMD patients.e?
67
68
COMMENTARY/Rudy and Greco
Considerable variability exists in these patients in terms of self-reported behaviors and coping patterns, patterns of pain increases and decreases, and responses to EMG biofeedback training, as well as other treatment interventions." Yet the psychophysiological literature on TMD has largely ignored response variability or patient heterogeneity, and Ohrbach and "McCall tend to gloss over this central issue as well.
UNRESOLVED METHODOLOGICAUSTATISTICAL ISSUES As noted by Ohrbach and McCall, the methodological quality of psychophysiological studies, at least from an experimental design perspective, has improved significantly in recent years. An area, however, that has not improved or kept pace with methodological advances has been the statistical models used to interpret the experimental findings.
The Mean Is Meaningless To date, psychophysiological studies of EMG levels have averaged across time and subjects and only report inferential statistics based on EMG means. This practice makes several unwarranted assumptions that lead to serious interpretational difficulties and limitations. First, computing averaged EMG levels across experimental conditions (e.g., baseline and a stressinduced task) and across subjects, in particular, assumes that EMG values represent a ratio scale, that is, possess a common absolute zero point. However, surface EMG values represent relative muscle tension and are, at best, interval measures with an unknown constant or lntercept.s The amplitude of the muscle action potentials recorded in EMG studies is dependent on many complex physiological and electronic factors that contribute to the "baseline noise" or unknown constant of the EMG signal. 1,2 For example, individual differences in tissue conductivity, the distance between the active muscle fiber and the detection site, the diameter of the muscle fiber, electrode size and distance between electrodes, the accuracy of electrode placement across subjects, and the amount and type of signal amplification used, all contribute to the relativeness of EMG values and, therefore, the inappropriateness of directly comparing absolute EMG levels across subjects. Although the need for EMG normalization procedures to permit comparison among subjects, muscles, or activities has been widely recognized in other areas of EMG research,s it has been virtually ignored in psychophysiological research. Second, given the amount and complexities of the time series data collected during psychophysiological experiments with TMD patients that are designed to
evoke stress responses in the muscles of mastication, all EMG studies by necessity use some form of data reduction. However, the typical strategy of averaging EMG levels across time and subjects results in considerable loss of information. Additionally, traditional data analytic approaches (e.g., ANOVA, t-tests) are insensitive to rapid fluctuations that often occur in physiological measures during an experiment. They cannot detect transient effects, the duration of a significant response to an experimental procedure, or the length of time it takes an individual to return to pre-response baseline levels. Thus, current analytic approaches obscure important individual differences in response profiles, that is, subjects' idiosyncratic reactions to the experimental manipulations. The two methodological problems outlined above may well explain some of the contradictory findings in the psychophysiological literature on TMD. Close inspection of the standard deviations for mean EMG levels reported in the literature indicates very wide distributions, particularly when patients' responses are compared to control subjects. This is apparent for resting baseline as well as mean levels computed for stress induction trials. Thus, some of the statistically significant, or for that matter nonsignificant, findings reported in the literature may well be spurious and unreliable, because the assumptions of the statistical models used were significantly violated.
CONCLUSION Although we concur with Ohrbach and McCall that the significance of musculoskeletal nociception for chronic TMD conditions cannot be overestimated, we believe that psychophysiological models probably are only relevant for a subset of patients. lntersubject response variability is generally the "rule-of-thumb" in psychophysiological experiments and these differences are due to both physiological differences among subjects as well as differences in the psychological impact of the experimental stimuli and setting. Until more appropriate analytic tools are developed to test and validate what types of patients respond to psychologically stressful stimuli with increased hyperactivity in the muscles of mastication, under what conditions, and with what level and duration of response, we believe that the amount of support for psychophysiological models of TMD is not nearly as strong as Ohrbach and McCall suggest. The wide variances in EMG changes in response to psychological stressors suggest that only a subset of patients display hypermuscle activity. Thus, alternative analyses at the individual subject level, rather than group-oriented analyses, are necessary to identify those individuals fitting psychophysiological models. Once these
COMMENTARY/Rudy and Greco
patients are identified, additional research, in line with some of the theoretical extensions proposed by Ohrbach and McCall, may help to delineate the seemingly weak association between muscle hyperactivity and nociception. Finally, we believe that it is important to distinguish between the etiological and pain exacerbation or maintenance significance of masticatory hyperactivity to psychological stress. Based on the available evidence, it seems more reasonable to hypothesize that, in at least some patients, the small but persistent increases in muscle activity may facilitate the maintenance or intensification of the pain experience. We believe that the low levels of EMG increases, relative to the contractile forces that can be generated by the muscles in question, observed in psychophysiological experiments in and of themselves are insufficient to explain the development of TMD or other orofacial pain conditions. Ohrbach and McCall's revised stress-hyperactivity-pain theory of myogenic pain may be a clinically plausible model that may explain the maintenance of pain in a subset of TMD patients. However, implying that this model can explain the etiology of TMD is stretching the available empirical evidence for muscular responses to stressful conditions beyond a point we find comfortable.
References 1. Basmajian JV, Deluca CJ: Muscles alive: their functions revealed by electromyography. 5th ed. Williams & Wilkins, Baltimore, 1985
69
2. Gerleman DG, Cook TM: Instrumentation. pp. 44-67. In Soderberg Gl (ed): Selected topics in surface electromyography for use in the occupational setting: expert perspectives. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, No. 91-100, Washington, DC, 1992 3. Laskin DM: Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 79:147-153,1969 4. leVeau B, Andersson G: Interpretation of the electromyographic signal. pp. 70-102. In Soderberg Gl (ed): Selected topics in surface electromyography for use in the occupational setting: expert perspectives. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, No. 91-100, Washington, DC, 1992 5. Marras W: Applications of electromyography in ergonomics. pp. 122-143. In Soderberg Gl (ed): Selected topics in surface electromyography for use in the occupational setting: expert perspectives. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, No. 91-100, Washington, DC, 1992 6. Rudy TE: Psychophysiological assessment in chronic orofacial pain. Anesth Prog 37:1-6,1990 7. Rudy TE, Turk DC, Kubinski JA, Zaki HS: Differential treatment responses of TMD patients as a function of psychological characteristics. Pain 61:103-112, 1995 8. Rudy TE, Turk DC, Zaki HS, Curtin HD: An empirical taxometric alternative to traditional classification of temporomandibular disorders. Pain 36:311-320,1989 9. Von Korff M, Dworkin SF, leResche l, Kruger A: An epidemiologic comparison of pain complaints. Pain 32: 173-183, 1988
Stretching Psychophysiological Models ofTMD But Do the Muscles Respond? Thomas E. Rudy* and Carol M. Greco*t
sychophysiological models of chronic pain conditions, particularly those believed to have a musculoskeletal component (e.g., low back pain, temporomandibular disorders), have emerged over the past two decades due, in part, to the inadequacy of structural models to explain the etiology, maintenance, exacerbation, and/or remediation of these conditions." Psychological factors increasingly have been recognized by many theorists dealing with the etiology and treatment of temporomandibular disorders (TMDs). Although other psychological factors have received some attention, to date, psychophysiological models of TMDs appear to be the most popular psychologically based explanations for the development and/or maintenance of TMDs. Rudy6 suggests that one of the primary reasons for the acceptance of psychophysiological aspects of TMDs is that this model was initially proposed by a dentist, Daniel Laskin.s The focus article by Ohrbach and McCall suggests that all is not well with current psychophysiological conceptualizations of TMD, particularly from a research or empirical perspective. They highlight the numerous methodological, conceptual, and interpretational difficulties with previous psychophysiological studies. Their particular emphasis on the current lack of empirical support for the direct association between stressrelated electromyography (EMG) and pain severity levels is important and overdue. Ohrbach and McCall, however, do not abandon the psychophysiological model of TMD. Rather, they propose a revised theory of stress-hyperactivity and pain
P
From the 'Departments of Anesthesiology, Psychiatry, and Biostatistics, tDepartment of Anesthesiology, and 'Pain Evaluation and Treatment Institute, University of Pittsburgh, Pittsburgh, PA. Reprint requests: Thomas E. Rudy, PhD, Pain Evaluation and Treatment Institute, University of Pittsburgh Medical Center, 4601 Baum Boulevard, pittsburgh, PA 15213.
Pain Forum 5(1): 67-69, 1996
that draws on other theories of chronic myogenic pain, that is, myofascial pain and neuromatrix theories, as well as the general stress-hyperactivity model. Specifically, the authors suggest that a persistent pattern of frequent muscle activity (possibly of low magnitude) leads to shortened muscle length. Attempts at returning the muscle to normal length, including the muscle stretching associated with normal functioning (such as talking, mastication), are the proposed cause of pain. We will address this revised theory from a clinical perspective, followed by several methodological concerns.
CLINICALLY REASONABLE Our clinical experiences, derived from providing treatment to several hundred TMD patients who have participated in research protocols that consisted of education on oral habits, biofeedback for facial relaxation, stress management, and cognitive-behavioral therapy, suggest that many of the components of Ohrbach and McCall's revised theory are consistent with clinical observations and patients' reports. Nearly all patients readily provide personal experiences or beliefs that their "perceived increase" in masticatory muscle tension is associated with emotionally stressful events, which in turn are also associated with pain increases, either immediately or shortly after the stressful period. Many patients would agree that the stretching associated with functions such as talking, laughing, and eating leads to an increase in their pain perceptions. We also have found that a fairly substantial subset of patients report that their pain has increased rather than decreased following an initial biofeedback training session. These types of anecdotal reports, despite their scientific limitations, tend to support the revised stress-hyperactivity theory proposed by Ohrbach and McCall. However, most notable clinically, as well as from a research perceptive, is the heterogeneity of TMD patients.e?
67
68
COMMENTARY/Rudy and Greco
Considerable variability exists in these patients in terms of self-reported behaviors and coping patterns, patterns of pain increases and decreases, and responses to EMG biofeedback training, as well as other treatment interventions." Yet the psychophysiological literature on TMD has largely ignored response variability or patient heterogeneity, and Ohrbach and "McCall tend to gloss over this central issue as well.
UNRESOLVED METHODOLOGICAUSTATISTICAL ISSUES As noted by Ohrbach and McCall, the methodological quality of psychophysiological studies, at least from an experimental design perspective, has improved significantly in recent years. An area, however, that has not improved or kept pace with methodological advances has been the statistical models used to interpret the experimental findings.
The Mean Is Meaningless To date, psychophysiological studies of EMG levels have averaged across time and subjects and only report inferential statistics based on EMG means. This practice makes several unwarranted assumptions that lead to serious interpretational difficulties and limitations. First, computing averaged EMG levels across experimental conditions (e.g., baseline and a stressinduced task) and across subjects, in particular, assumes that EMG values represent a ratio scale, that is, possess a common absolute zero point. However, surface EMG values represent relative muscle tension and are, at best, interval measures with an unknown constant or lntercept.s The amplitude of the muscle action potentials recorded in EMG studies is dependent on many complex physiological and electronic factors that contribute to the "baseline noise" or unknown constant of the EMG signal. 1,2 For example, individual differences in tissue conductivity, the distance between the active muscle fiber and the detection site, the diameter of the muscle fiber, electrode size and distance between electrodes, the accuracy of electrode placement across subjects, and the amount and type of signal amplification used, all contribute to the relativeness of EMG values and, therefore, the inappropriateness of directly comparing absolute EMG levels across subjects. Although the need for EMG normalization procedures to permit comparison among subjects, muscles, or activities has been widely recognized in other areas of EMG research,s it has been virtually ignored in psychophysiological research. Second, given the amount and complexities of the time series data collected during psychophysiological experiments with TMD patients that are designed to
evoke stress responses in the muscles of mastication, all EMG studies by necessity use some form of data reduction. However, the typical strategy of averaging EMG levels across time and subjects results in considerable loss of information. Additionally, traditional data analytic approaches (e.g., ANOVA, t-tests) are insensitive to rapid fluctuations that often occur in physiological measures during an experiment. They cannot detect transient effects, the duration of a significant response to an experimental procedure, or the length of time it takes an individual to return to pre-response baseline levels. Thus, current analytic approaches obscure important individual differences in response profiles, that is, subjects' idiosyncratic reactions to the experimental manipulations. The two methodological problems outlined above may well explain some of the contradictory findings in the psychophysiological literature on TMD. Close inspection of the standard deviations for mean EMG levels reported in the literature indicates very wide distributions, particularly when patients' responses are compared to control subjects. This is apparent for resting baseline as well as mean levels computed for stress induction trials. Thus, some of the statistically significant, or for that matter nonsignificant, findings reported in the literature may well be spurious and unreliable, because the assumptions of the statistical models used were significantly violated.
CONCLUSION Although we concur with Ohrbach and McCall that the significance of musculoskeletal nociception for chronic TMD conditions cannot be overestimated, we believe that psychophysiological models probably are only relevant for a subset of patients. lntersubject response variability is generally the "rule-of-thumb" in psychophysiological experiments and these differences are due to both physiological differences among subjects as well as differences in the psychological impact of the experimental stimuli and setting. Until more appropriate analytic tools are developed to test and validate what types of patients respond to psychologically stressful stimuli with increased hyperactivity in the muscles of mastication, under what conditions, and with what level and duration of response, we believe that the amount of support for psychophysiological models of TMD is not nearly as strong as Ohrbach and McCall suggest. The wide variances in EMG changes in response to psychological stressors suggest that only a subset of patients display hypermuscle activity. Thus, alternative analyses at the individual subject level, rather than group-oriented analyses, are necessary to identify those individuals fitting psychophysiological models. Once these
COMMENTARY/Rudy and Greco
patients are identified, additional research, in line with some of the theoretical extensions proposed by Ohrbach and McCall, may help to delineate the seemingly weak association between muscle hyperactivity and nociception. Finally, we believe that it is important to distinguish between the etiological and pain exacerbation or maintenance significance of masticatory hyperactivity to psychological stress. Based on the available evidence, it seems more reasonable to hypothesize that, in at least some patients, the small but persistent increases in muscle activity may facilitate the maintenance or intensification of the pain experience. We believe that the low levels of EMG increases, relative to the contractile forces that can be generated by the muscles in question, observed in psychophysiological experiments in and of themselves are insufficient to explain the development of TMD or other orofacial pain conditions. Ohrbach and McCall's revised stress-hyperactivity-pain theory of myogenic pain may be a clinically plausible model that may explain the maintenance of pain in a subset of TMD patients. However, implying that this model can explain the etiology of TMD is stretching the available empirical evidence for muscular responses to stressful conditions beyond a point we find comfortable.
References 1. Basmajian JV, Deluca CJ: Muscles alive: their functions revealed by electromyography. 5th ed. Williams & Wilkins, Baltimore, 1985
69
2. Gerleman DG, Cook TM: Instrumentation. pp. 44-67. In Soderberg Gl (ed): Selected topics in surface electromyography for use in the occupational setting: expert perspectives. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, No. 91-100, Washington, DC, 1992 3. Laskin DM: Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 79:147-153,1969 4. leVeau B, Andersson G: Interpretation of the electromyographic signal. pp. 70-102. In Soderberg Gl (ed): Selected topics in surface electromyography for use in the occupational setting: expert perspectives. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, No. 91-100, Washington, DC, 1992 5. Marras W: Applications of electromyography in ergonomics. pp. 122-143. In Soderberg Gl (ed): Selected topics in surface electromyography for use in the occupational setting: expert perspectives. U.S. Department of Health and Human Services, National Institute for Occupational Safety and Health, No. 91-100, Washington, DC, 1992 6. Rudy TE: Psychophysiological assessment in chronic orofacial pain. Anesth Prog 37:1-6,1990 7. Rudy TE, Turk DC, Kubinski JA, Zaki HS: Differential treatment responses of TMD patients as a function of psychological characteristics. Pain 61:103-112, 1995 8. Rudy TE, Turk DC, Zaki HS, Curtin HD: An empirical taxometric alternative to traditional classification of temporomandibular disorders. Pain 36:311-320,1989 9. Von Korff M, Dworkin SF, leResche l, Kruger A: An epidemiologic comparison of pain complaints. Pain 32: 173-183, 1988