Anesth Prog 37:82-87 1990
Psychophysiological
Assessment in Chronic
Orofacial Pain Thomas E. Rudy,
PhD Departments of Anesthesiology and Psychiatry and Pain Evaluation and Treatment Institute, University of Pittsburgh School of Medicine
attempt to provide a comprehensive overview of all psychophysiological aspects of TMD, but only highlights several key theoretical and methodological issues. The appropriate measurement of psychophysiological activity involved in TMD includes knowledge of electronics, anatomy, physiology, as well as familiarity with the psychological questions being asked and the responses being measured. The reader is referred to several excellent texts that provide this detailed information.2-5
Psychophysiological models of chronic pain
conditions have emerged in recent years due, in part, to the inadequacy of structural models to explain the etiology, maintenance, exacerbation, and/or remediation of these conditions. Psychophysiological theories of temporomandibular disorders (TMD) and related research evidence are reviewed. It is concluded that a number of methodological problems in previous psychophysiological studies of TMD preclude reaching firm conclusions that psychological stress causes masticatory hypermuscle arousal in TMD patients. Recommendations and guidelines for future psychophysiological research in TMD are presented.
PSYCHOPHYSIOLOGICAL MODELS OF TMD Over the past two decades, psychological factors increasingly have been recognik2d by many theorists dealing with the etiology and treatment of temporomandibular pain and dysfunction. Although other psychological factors have received some attention (e.g., personality, emotional characteristics), to date, psychophysiological models of TMD appear to be the most popular psychologicallybased explanations for the development and/or maintenance of TMD. There are at least three reasons for the popularity of psychophysiological models. First, if skeletal, traumatic, neoplastic, internal derangement, and infectious causes of TMD pain are eliminated, there still remain 70-80% of the patients presenting with typical TMD symptoms.6 Psychophysiological models attempt to provide a rationale for the majority of these TMD patients. Second, their emphasis on the association between stress and muscle hyperactivity has "face" validity to many dental practitioners. Pain and tenderness of the muscles of mastication as well as limitations of mandibular movements have become widely accepted diagnostic signs7 and highlight the central role of masticatory muscles in patients' reports of pain. Additionally, clinicians and researchers alike have suggested that TMD patients, at least those who seek treatment, are more anxious and appear to have more environmental stressors than other dental patients.8 In fact, some dental investigators9 have suggested that stress is the common denominator in TMD,
psychophysiological models of chronic pain conditions, particularly those believed to have a musculoskeletal component (e.g., low back pain, temporomandibular disorders), have emerged in recent years due, in part, to the inadequacy of structural models to explain the etiology, maintenance, exacerbation, and/or remediation of these conditions. Most psychophysiological models of chronic pain can be classified as a subset of myogenic models' and focus on the role that psychological and psychosocial stressors play in muscular pain and spasm. In this paper, temporomandibular disorders (TMD) will be used as an example of psychophysiological research and assessment approaches to chronic orofacial pain syndromes. It should also be noted that this paper does not
Address all correspondence to Dr. Thomas E. Rudy, Pain Evaluation and Treatment Institute, University of Pittsburgh School of Medicine, Baum Blvd. at Craig St., Pittsburgh, PA 15213. X 1990 by the American Dental Society of Anesthesiology
ISSN 0003-3006/90/$3.50
82
Rudy 83
Anesth Prog 37:82-87 1990
at least in those patients where a strong organic explanation for the pain cannot be found. Thus, bruxism and other parafunctional oral habits frequently seen in these patients are considered to be signs of psychological stress and patients' inability to cope effectively with life's stresses. A third primary reason for the acceptance of psychophysiological aspects of TMD is that this model was initially proposed by a dentist, Daniel Laskin.10 Based on the writings of Lacey and his colleagues,11'12 who proposed the "response specificity" notion that hypothesizes every individual has a characteristic physiological response to stress, as well as the concept of "symptom specificity" developed originally by Malmo and Shagass,13 which attempted to explain the association between psychological stress, heightened physiological arousal in specific body regions, and the development of specific somatic disorders, Laskin proposed that the myofascial pain-dysfunction syndrome could be conceptualized as a psychophysiologically-based disorder. He hypothesized that the development of TMD symptoms appears to be caused by a combination of a physiological predisposition on the part of the individual to develop dysfunction in the masticatory musculature, as well as individuals' current levels of psychological and physical stress and their inability to cope with these stresses. The basic assumption of this model of TMD, as well as other psychophysiological models that have been proposed to explain other types of chronic pain syndromes (e.g., back pain14), is that these chronic pain conditions result from the interaction of potentially stressful environmental events, inadequate coping abilities, and a predisposing organic or psychological condition, or diathesis. If the aversive stimulation to the individual is very intense or recurrent and the individual lacks adequate coping skills, a response stereotypy may develop in an unfavorably disposed body system. In TMD problems, this unfavorable disposition may be due to overutilization of masticatory muscles (e.g., nocturnal bruxism), a structural problem (e.g., internal derangement of the TMJ), observational learning (e.g., leamed oral behaviors from a parent, such as chewing on a pencil to find the answer to a problem), and so forth. In TMD, the individual response stereotypy is believed to manifest itself as a localized hyperreaction in the muscles of mastication. As the response becomes prolonged, the sympathetic nervous system becomes disregulated and the sustained hyperreactivity of these muscles may lead to local ischemia and reflex muscle spasm. Muscle hyperactivity may be mediated by the extrapyramidal gamma-motoric system, which is closely linked to the limbic system and thus very susceptible to emotional influences. With sustained muscular hyperactivity, pain develops as a consequence of local ischemic hypoxia and
pain-eliciting irritants from hypoxic cells (e.g., lactic acid). These irritants may cause nociceptive receptors to become increasingly sensitized. The resulting muscle pain then may act as a new stressor and thus perpetuate a vicious pain-tension cycle. The cycle, once started, tends to perpetuate itself. Additionally, once a muscle has been subjected to a myospastic episode it tends, for reasons not yet understood, to become more susceptible to future episodes. 15 Although the relationship between psychophysiological and structural factors in TMD remains unclear, several authors15"16 have suggested that just as articulating structural pathologies can aversely affect the neuromusculature, so too can long-standing neuromuscular problems produce organic changes in the arficulating elements of the TMJ. Moreover, secondary organic changes may become self-perpetuating because they result in altered oral patterns with attendant reinforcement of the initial spasm and pain. Thus, TMD may be conceptualized as a continuum, in that what initially may have been primarily a functional, psychophysiological disorder, may in time lead to structural changes in the TMJ. The reverse etiological order also may occur. 15 Experimentally, psychophysiological models of TMD predict that when presented with stressful stimuli, patients with masticatory pain should exhibit elevated and prolonged reactions in the muscles of mastication when compared to healthy controls. Additionally, from a symptom specificity perspective, muscular hyperreactivity to stress should occur only in masticatory muscles and not in distal muscles. Further, it has also been hypothesized17 that muscular reactions to stress only should occur in response to personally-relevant stressors and that the magnitude of these muscular reactions should be more closely associated with psychological variables (e.g., depression and anxiety levels) than physical variables (e.g., degree of TMJ abnormality).
PSYCHOPHYSIOLOGICAL RESEARCH EVIDENCE IN TMD Adherents of the psychophysiological or neuromuscular models of TMD frequently use clinical evidence that almost any treatment that relaxes masticatory muscles alleviates pain as indirect support for these models. However, it is important to acknowledge that muscular hyperactivity is not isomorphic with reports of pain and that treatments designed to alter muscle hyperactivity have not demonstrated that the reduction in muscle activity is the actual mechanism of pain reduction. For example, studies that report the efficacy of biofeedback for TMD have not demonstrated that there is a co-occurrence of pain reduction
84 Psychophysiological Assessment
with reduction in masseter electromyographic (EMG) activity. 18 As direct evidence for the psychophysiological model of TMD, a wide variety of EMG-based studies are frequently cited as support for the importance of psychological stress on the muscles of mastication. For example, several studies have demonstrated a significant correlation between EMG-measured magnitudes of nocturnal bruxism and stressful daytime events19'20 and/or the anticipation of stressful events.21 While there is considerable evidence that the magnitude and duration of masticatory muscle contractions during bruxing and other parafunctional oral habits are sufficient to produce muscular pain and fatigue,22 the methodological design of these studies precludes reaching the conclusion that psychological stress causes increased masticatory muscle activity.23 To date, there are only a handful of studies24-28 that have directly addressed the question of whether TMD patients respond to psychological stress with increased masticatory muscle activity. Overall, the results of these studies are mixed. Several investigators25'26 have reported resting baseline EMG differences in masticatory muscles between TMD patients and healthy controls, while others24'27 have not found significant baseline differences between patients and controls. A similar state of affairs exists in terms of whether TMD patients, in comparison to control subjects, show significantly higher EMG increases in the muscles of mastication when presented with psychologically stressful stimuli. When baseline differences are controlled for, several studies have demonstrated no significant EMG increases in response to psychological stressors26'27 and other studies25'28 report TMD patients display significantly higher EMG levels during stressful stimuli when compared to the EMG level of control subjects. A number of methodological factors prevent reaching firm conclusions from psychophysiological studies of TMD. All of these studies have suffered from some of the following methodological flaws: (a) failure to match subjects on characteristics known to affect psychophysiological responses (e.g., gender, age, medication usage); (b) inadequate diagnostic information regarding the types of TMD patients used; (c) failure to include an adaptation period so that the physiological recordings could stabilize; (d) failure to control for movement artifacts before the analysis of EMG signals (e.g., swallowing); (e) failure to adjust for intergroup EMG baseline differences before computing EMG differences due to stressful stimuli; (f) inadequate description or inappropriate EMG measurement methodology (e.g., lack of standardized electrode placements, failure to measure electrode resistances prior to recording); (g) inappropriate data reduction and statistical procedures (e.g., multiple t-tests on correlated data); (h) failure to counterbalance the presentation of stimulus conditions to control for carry-over effects and to allow
Anesth
Prog 37:82-87 1990
sufficient time for physiological measures to return to prestimulus levels before the presentation of additional stimuli; (i) use of stress-induction tasks that have little ecological validity (e.g., white noise) and to measure subjects' subjective reactions to the stimuli to verify if they were perceived as psychologically stressful; (j) failure to assess the duration of elevated EMG activity in response to a stressor or the rate of recovery to baseline levels following termination of the stressor; and (k) failure to measure more than one muscle of mastication, to measure distal muscle sites to test for response specificity, or to include at least one other physiological measure (e.g., skin conductance level). Recently, at the University of Pittsburgh Pain Institute we29-31 have conducted a series of psychophysiological studies of TMD patients in an attempt to correct many of the methodological problems described above. In addition to addressing recording, statistical, and experimental design issues, we have been concerned with the concept of "stressful stimuli" and the ecological validity of many laboratory stress tasks. Psychological stress needs to be conceptualized as an interaction betweeen environmental stimulation and person variables. We have adopted this transactional view of stress and somatic adaptation,32'33 which emphasizes that an individual's appraisal of an environmental stimulus will determine if the environmental event is perceived as stressful. In other words, stress, much like pain, is ultimately a subjective phenomenon. Thus, it is possible that an environmental stimulus (e.g., threat of shock) can produce arousal and the activation of physiological responses, but this arousal is not perceived by the individual as stressful because it is largely an artificial stimulus that does not call into question the individual's leamed coping resources. In one of our psychophysiological experiments three experimental tasks were conducted, with counterbalanced presentation orders used across subjects to minimize potential carry-over effects between tasks. These tasks were: (1) a standardized neutral imagery task, presented to them by the experimenter, that placed subjects in their living rooms with the television on; (2) an experimenter-guided personally-relevant stressful image of a recent stressful experience that was elicited previously from the subject during the psychological intake interview; and (3) a general stress task, mental math, during which time subjects were instructed to keep their eyes closed and silently count backwards by 7s beginning from 543. During each task simultaneous EMG recordings were taken bilaterally from masseter and temporalis muscles as well as from several nonpain-specific muscle sites. Each task was also preceded by a baseline phase and followed by a retum-to-baseline phase. Subjects also rated their current stress, muscle tension, and pain levels following each task.
Anesth Prog 37:82-87 1990
Rudy 85
200
support for the psychological component of the psychophysiological model of TMD and identify potential differences between patients with and without structural abnormalities. The significant muscular increases observed in both patient groups appear to have led to differences in appraisals and perceptions of pain that were independent of their ratings of stress and muscle tension. Finally, and perhaps of most importance, these results indicate that even though EMG increases during the psychological stress tasks were quite small when compared to the EMG levels observed during physical stress tasks,22 at least a subset of TMD patients perceived these masticatory muscle increases as painful.
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CONSIDERATIONS FOR FUTURE RESEARCH Stress
Math
Experimental Task Figure 1. Mean EMG increases above baseline in percentages for masseter and temporalis muscles during 3 psychophysiology experimental tasks for healthy nonpain control subjects and
TMD patients with and without abnormal TMJ CT findings.
From a sample of 100 TMD patients, a subset of 40 patients were identified based on the presence of extreme positive (n = 20) or negative (n = 20) TMJ computed tomography (CT) results. Analysis of masseter and temporalis EMGs indicated no baseline EMG differences between TMD patients and healthy controls (n = 10) or differential responding to the neutral image, suggesting that TMD patients do not have higher resting muscle tension levels than normals. TMD patients, however, did display significant site-specific EMG elevations in response to the two stress tasks, in contrast to controls (Figure 1). EMG increases for the TMD patients were as high as 430% above baseline (M = 180%). Also, patients' EMG increases were significantly higher for the personally-relevant stress task when compared to the mental arithmetic task. Abnormalities of the TMJ based on CT were unrelated to muscular hyperarousal during baseline or stress tasks. Furthermore, during the stress tasks significant EMG changes for non site-specific muscles did not occur. Thus, although it is common to differentiate TMD patients based on joint abnormalities, these data demonstrate that hypermuscle arousal to stress can occur regardless of structural abnormalities. A striking pattem emerged from this psychophysiological experiment. Significantly different post-task pain ratings occurred, even though patients' levels of stress and muscle tension ratings were equivalent. The normal CT group reported significantly higher post-task pain levels for both stress tasks (Figure 2). These findings provide
Conceptual and methodological issues related to psychophysiological models and assessment of TMD patients have been raised throughout this paper. Although psychophysiologically-based research efforts show considerable promise and have the potential to make important and unique contributions to our understanding of the clinical phenomena of TMD, significant progress is unlikely to occur without investigators' attention to several key methodological problems. First, much of the discrepancy among psychophysiological studies of TMD lies in the fact that different laboratories use widely disparate physiological measurement techFigure 2. Mean pain intensity ratings following 3 psychophysiology experimental tasks for TMD patients with and without abnormal TMJ CT findings. 5
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* Normal CT * Abnormal CT
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Anesth Prog 37:82-87 1990
86 Psychophysiological Assessment
niques, stimulus paradigms, and subject samples. In terms of recording methodology, guidelines for EMG measurement,34 all of which are frequently used in TMD studies, are now available. Researchers whenever possible should adhere to these standards in order to facilitate the communication of findings between different laboratories. The standardization of electrode placements based on facial anatomical landmarks, electrode, size, passbands used for EMG detection, signal integration methods, and so forth, would result in improved measurement validity and reliability. For experimental stimuli, the definition and measurement of what stimuli are, in fact, psychologically stressful to subjects requires more careful inspection and clarification. The counterbalancing of stimulus orders as well as attention to both physiological and psychological habituation to experimental stimuli should be addressed in future research efforts. Finally, TMD patients cannot be considered to be a homogeneous population.8'37 Psychophysiological investigators should provide more complete descriptions of the types of TMD patients used in an experiment, including subject demographics, psychological assessment information, whether patients were in pain at the time of the experiment, dental examination findings, oral habits, and the results of laboratory tests. Second, to date, psychological stress experiments in TMD have, for the most part, been between-subjects designs that are summarized by univariate statistical approaches (e.g., t-tests, ANOVA). However, this type of statistical paradigm is not well suited to the study of psychophysiological aspects of TMD. Group designs obscure individual differences in response patterns which are known to exist in states of arousal and emotion.3 The emphasis on tests of statistical significance in group designs may not yield results that are interpretable or meaningful in terms of the association between psychological stress and neuromuscular responding in the individual TMD patient. Time series analyses of EMG waveforms, both in the time39 and frequency domain,40 as well as adaptive filtering techniques from engineering4' hold considerable promise for individualizing the analysis of psychophysiological assessment data. Just as TMD patients cannot be considered to be a homogeneous group of patients, neither can their physiological responses to psychological stressors be considered homogeneous. Single subject statistical methods may help to clarify patients' differential physiological response patterns to stressful stimuli. Finally, and perhaps of most importance, an increasing number of investigators are proposing that TMD should be conceptualized as being comprised of a set of multidimensional, multietiological disorders.816 From this perspective, the primary goal in the assessment of TMD patients is to understand and integrate a wide range of functional, structural, and psychological data. Psycho-
physiological assessment should be considered as only a component of the assessment process. The clinical utililty of psychophysiological assessment findings as well as how these findings relate to other functional, structural, and psychological findings awaits further research. In light of the scarcity of methodologically sound studies that demonstrate a significant association between psychological stress and masticatory hypermuscle activity or that the magnitude of muscular increases produced by psychological stressors is sufficient to lead to increased levels of pain, along with the expense and complexities involved in psychophysiological assessment, at the present time psychophysiological assessment of TMD patients cannot be recommended as a routine clinic assessment procedure. ACKNOWLEDGMENT
Support for the completion of this manuscript was provided in part by a National Institute of Dental Research Grant No. DE07514. REFERENCES 1. Dolce JJ, Raczynski JM: Neuromuscular activity and electromyography in painful backs: Psychological and biomechanical models in assessment and treatment. Psychol Bull 1985;97:502-520. 2. Coles MGH, Donchin E, Porges SW, eds.: Psychophysiology: Systems, processes, and applications, New York, Guilford Press, 1986. 3. Galbraith GC, Kietzman ML, Donchin E, eds.: Neurophysiology and psychophysiology, Hillsdale, NJ, Lawrence Erlbaum, 1988. 4. Martin I, Venables PH, eds.: Techniques in psychophysiology, New York, John Wiley, 1980. 5. Cacioppo JT, Petty RE, eds.: Social psychophysiology: A sourcebook, New York, Guilford Press, 1983. 6. Greene CS: The temporomandibular joint syndrome. J Am Med Assoc. 1973;224:622. 7. Check DK, chair: Report of the ad hoc committee on craniomandibular and temporomandibular joint disorders, Minnesota Dental Association, 1988. 8. Rugh JD: Psychological factors in the etiology of masticatory pain and dysfunction. In: Laskin D, Greenfield W, Gale E, Rugh J, Neff P, Alling C, and Ayer W, eds., The president's conference on the examination, diagnosis and management of temporomandibular disorders, Chicago, American Dental Association, 1983. 9. Fearon CG, Serwatka WJ: Stress: A common denominator for nonorganic TMJ pain-dysfunction. J Prosthet Dent 1983;49:805-808. 10. Laskin DM: Etiology of pain-dysfunction syndrome. J Amer Dent Assn 1969;79:147-153.
Anesth Prog 37:82-87 1990
11. Lacey JI, Bateman DE, Vanlehn R: Autonomic response specificity. Psychosom Med 1953;15:8-21. 12. Lacey JI, Lacey BC: Verification and extension of the principle of autonomic response sterotypy. Amer J Psychol 1958;71:50-73. 13. Malmo RB, Shagass C: Physiologic study of the symptom mechanisms in psychiatric patients under stress. Psychosom Med 1949; 11:25-29. 14. Flor H, Birbaumer N, Turk DC: A diathesis-stress model of chronic back pain: Empirical evidence and treatment applications. In: Miltner W, Gerber WD, and Mayer R, eds., Behavioral medicine: Results and perspectives of interdisciplinary research, Weinheim, West Germany, Edition Medizin, 1987, pp 37-54. 15. Buxbaum JD, Myslinski NR, Myers DE: Dental management of orofacial pain. In: Tollison CD, ed., Handbook of chronic pain management, Baltimore, Williams and Wilkins, 1989, pp 297-316. 16. Laskin DM: Myofascial pain-dysfunction syndrome: Etiology. In Samat B and Laskin D, eds., The temporomandibular joint: A biological basis for clinical practice, Springfield, Ill., Charles C Thomas, 1980, pp 289-299. 17. Flor H, Turk DC, Birbaumer N: Assessment of stressrelated psychophysiological reactions in chronic low back pain patients. J Consult Clin Psychol 1985;53:354-365. 18. Funch DP, Gale EN: Biofeedback and relaxation therapy for chronic temporomandibular joint pain: Predicting successful outcomes. J Consult Clin Psychol 1984;52:928-935. 19. Rugh JD, Solberg WK: Electromyographic studies of bruxist behavior before and after treatment. J Calif Dent Assn 1975;3:56-59. 20. Clark GT, Rugh JD, Handelman SL: Nocturnal masseter muscle activity and urinary catecholamine levels in bruxers. J Dent Res 1980;59:1571-1576. 21. Funch DP, Gale EN: Factors associated with nocturnal bruxism and its treatment. J Behav Med 1980;3:385-397. 22. Christensen LV: Jaw muscle fatigue and pains induced by experimental tooth clenching: A review. J Oral Rehabil 1981;8:27-36. 23. Katz JO, Rugh JD: Psychophysiological aspects of oral disorders. Ann Behav Med 1986;8:3-9. 24. Yemm R: Temporomandibular dysfunction and masseter muscle response to experimental stress. Brit Dent J 1969;127:508-510. 25. Thomas LJ, Tiber N, Schireson S: The effects of anxiety and frustration on muscular tension related to temporomandibular joint syndrome. Oral Surg Oral Med Oral Patho 1973;36:763-768. 26. Mercuri LG, Olson RE, Laskin DM: The specificity of response to experimental stress in patients with myofascial pain dysfunction syndrome. J Dent Res 1979;58:1866-1871.
Rudy 87 27. Moss RA, Adams HE: Physiological reactions to stress in subjects with and without myofascial pain dysfunction symptoms. J Oral Rehabil 1984;11:219-232. 28. Dahlstrom L, Carlsson SG, Gale EN, Jansson TG: Stressinduced muscular activity in mandibular dysfunction: Effects of biofeedback training. J Behav Med 1985;8:191-200. 29. Rudy TE, Turk DC. Relationship between structural abnormalities and psychophysiological findings in TMJ patients. J Dent Res 1987;66:345. 30. Rudy TE, Turk DC, Flor H: Stress and chronic TMJ pain: A psychophysiological analysis. Paper presented at the Canadian and American Pain Societies Joint Meeting, Toronto, 1988. 31. Rudy TE, Turk DC: Structural abnormalities, muscular reactivity, and pain perception in TMJ patients. Paper presented at the Annual Scientific Sessions of the Society of Behavioral Medicine, San Francisco, 1989. 32. Lazarus RS, Launier R: Stress-related transactions between person and environment. In: Pervin LA and Lewis M, eds., Perspective in interactional psychology, New York, Plenum, 1978. 33. Holroyd KA, Lazarus RS: Stress, coping, and somatic adaptation, In: Goldberger L and Breznitz S, eds., Handbook of stress: Theoretical and clinical aspects, New York, Press Press, 1982, pp 21-35. 34. Fridlund AJ, Cacioppo JT: Guidelines for human electromyographic research. Psychophysiology 1986;23:567-589. 35. Fowles DC, Christie MJ, Edelberg R, Grings WW, Lykken DT, Venables PH: Publication recommendations for electrodermal measurements. Psychophysiology 1981;18:232-239. 36. Jennings JR, Berg WK, Hutcheson JS, Obrist P, Porges S, Turpin G: Publication guidelines for heart rate studies in man. Psychophysiology 1981;18:226-231. 37. Rudy TE, Turk DC, Zaki HS, Curtin HD: An empirical taxometric altemative to traditional classification of temporomandibular disorders. Pain, 1989;36:311-320. 38. Lacey JI: Somatic response patterning and stress: Some revisions of activation theory. In: Appley MH and Trumbull R, eds., Psychological stress, New York, Appleton-Century-Crofts, 1967. 39. McCleary R, Hay RA: Applied time series analysis for the social sciences. Beverly Hills, CA, Sage Publications, 1980. 40. VanBoxtel A, Goudswaard P, Van det Molen GM, Van den Bosch WEJ: Changes in electromyogram power spectra of facial and jaw-elevator muscles during fatigue. J Appl Physiol 1983;54:51-58. 41. Heath RA: Detection of change in physiological measures using an adaptive Kalman filter algorithm. Psychol Bull 1984;96:581-588.
Psychophysiological
Assessment in Chronic
Orofacial Pain Thomas E. Rudy,
PhD Departments of Anesthesiology and Psychiatry and Pain Evaluation and Treatment Institute, University of Pittsburgh School of Medicine
attempt to provide a comprehensive overview of all psychophysiological aspects of TMD, but only highlights several key theoretical and methodological issues. The appropriate measurement of psychophysiological activity involved in TMD includes knowledge of electronics, anatomy, physiology, as well as familiarity with the psychological questions being asked and the responses being measured. The reader is referred to several excellent texts that provide this detailed information.2-5
Psychophysiological models of chronic pain
conditions have emerged in recent years due, in part, to the inadequacy of structural models to explain the etiology, maintenance, exacerbation, and/or remediation of these conditions. Psychophysiological theories of temporomandibular disorders (TMD) and related research evidence are reviewed. It is concluded that a number of methodological problems in previous psychophysiological studies of TMD preclude reaching firm conclusions that psychological stress causes masticatory hypermuscle arousal in TMD patients. Recommendations and guidelines for future psychophysiological research in TMD are presented.
PSYCHOPHYSIOLOGICAL MODELS OF TMD Over the past two decades, psychological factors increasingly have been recognik2d by many theorists dealing with the etiology and treatment of temporomandibular pain and dysfunction. Although other psychological factors have received some attention (e.g., personality, emotional characteristics), to date, psychophysiological models of TMD appear to be the most popular psychologicallybased explanations for the development and/or maintenance of TMD. There are at least three reasons for the popularity of psychophysiological models. First, if skeletal, traumatic, neoplastic, internal derangement, and infectious causes of TMD pain are eliminated, there still remain 70-80% of the patients presenting with typical TMD symptoms.6 Psychophysiological models attempt to provide a rationale for the majority of these TMD patients. Second, their emphasis on the association between stress and muscle hyperactivity has "face" validity to many dental practitioners. Pain and tenderness of the muscles of mastication as well as limitations of mandibular movements have become widely accepted diagnostic signs7 and highlight the central role of masticatory muscles in patients' reports of pain. Additionally, clinicians and researchers alike have suggested that TMD patients, at least those who seek treatment, are more anxious and appear to have more environmental stressors than other dental patients.8 In fact, some dental investigators9 have suggested that stress is the common denominator in TMD,
psychophysiological models of chronic pain conditions, particularly those believed to have a musculoskeletal component (e.g., low back pain, temporomandibular disorders), have emerged in recent years due, in part, to the inadequacy of structural models to explain the etiology, maintenance, exacerbation, and/or remediation of these conditions. Most psychophysiological models of chronic pain can be classified as a subset of myogenic models' and focus on the role that psychological and psychosocial stressors play in muscular pain and spasm. In this paper, temporomandibular disorders (TMD) will be used as an example of psychophysiological research and assessment approaches to chronic orofacial pain syndromes. It should also be noted that this paper does not
Address all correspondence to Dr. Thomas E. Rudy, Pain Evaluation and Treatment Institute, University of Pittsburgh School of Medicine, Baum Blvd. at Craig St., Pittsburgh, PA 15213. X 1990 by the American Dental Society of Anesthesiology
ISSN 0003-3006/90/$3.50
82
Rudy 83
Anesth Prog 37:82-87 1990
at least in those patients where a strong organic explanation for the pain cannot be found. Thus, bruxism and other parafunctional oral habits frequently seen in these patients are considered to be signs of psychological stress and patients' inability to cope effectively with life's stresses. A third primary reason for the acceptance of psychophysiological aspects of TMD is that this model was initially proposed by a dentist, Daniel Laskin.10 Based on the writings of Lacey and his colleagues,11'12 who proposed the "response specificity" notion that hypothesizes every individual has a characteristic physiological response to stress, as well as the concept of "symptom specificity" developed originally by Malmo and Shagass,13 which attempted to explain the association between psychological stress, heightened physiological arousal in specific body regions, and the development of specific somatic disorders, Laskin proposed that the myofascial pain-dysfunction syndrome could be conceptualized as a psychophysiologically-based disorder. He hypothesized that the development of TMD symptoms appears to be caused by a combination of a physiological predisposition on the part of the individual to develop dysfunction in the masticatory musculature, as well as individuals' current levels of psychological and physical stress and their inability to cope with these stresses. The basic assumption of this model of TMD, as well as other psychophysiological models that have been proposed to explain other types of chronic pain syndromes (e.g., back pain14), is that these chronic pain conditions result from the interaction of potentially stressful environmental events, inadequate coping abilities, and a predisposing organic or psychological condition, or diathesis. If the aversive stimulation to the individual is very intense or recurrent and the individual lacks adequate coping skills, a response stereotypy may develop in an unfavorably disposed body system. In TMD problems, this unfavorable disposition may be due to overutilization of masticatory muscles (e.g., nocturnal bruxism), a structural problem (e.g., internal derangement of the TMJ), observational learning (e.g., leamed oral behaviors from a parent, such as chewing on a pencil to find the answer to a problem), and so forth. In TMD, the individual response stereotypy is believed to manifest itself as a localized hyperreaction in the muscles of mastication. As the response becomes prolonged, the sympathetic nervous system becomes disregulated and the sustained hyperreactivity of these muscles may lead to local ischemia and reflex muscle spasm. Muscle hyperactivity may be mediated by the extrapyramidal gamma-motoric system, which is closely linked to the limbic system and thus very susceptible to emotional influences. With sustained muscular hyperactivity, pain develops as a consequence of local ischemic hypoxia and
pain-eliciting irritants from hypoxic cells (e.g., lactic acid). These irritants may cause nociceptive receptors to become increasingly sensitized. The resulting muscle pain then may act as a new stressor and thus perpetuate a vicious pain-tension cycle. The cycle, once started, tends to perpetuate itself. Additionally, once a muscle has been subjected to a myospastic episode it tends, for reasons not yet understood, to become more susceptible to future episodes. 15 Although the relationship between psychophysiological and structural factors in TMD remains unclear, several authors15"16 have suggested that just as articulating structural pathologies can aversely affect the neuromusculature, so too can long-standing neuromuscular problems produce organic changes in the arficulating elements of the TMJ. Moreover, secondary organic changes may become self-perpetuating because they result in altered oral patterns with attendant reinforcement of the initial spasm and pain. Thus, TMD may be conceptualized as a continuum, in that what initially may have been primarily a functional, psychophysiological disorder, may in time lead to structural changes in the TMJ. The reverse etiological order also may occur. 15 Experimentally, psychophysiological models of TMD predict that when presented with stressful stimuli, patients with masticatory pain should exhibit elevated and prolonged reactions in the muscles of mastication when compared to healthy controls. Additionally, from a symptom specificity perspective, muscular hyperreactivity to stress should occur only in masticatory muscles and not in distal muscles. Further, it has also been hypothesized17 that muscular reactions to stress only should occur in response to personally-relevant stressors and that the magnitude of these muscular reactions should be more closely associated with psychological variables (e.g., depression and anxiety levels) than physical variables (e.g., degree of TMJ abnormality).
PSYCHOPHYSIOLOGICAL RESEARCH EVIDENCE IN TMD Adherents of the psychophysiological or neuromuscular models of TMD frequently use clinical evidence that almost any treatment that relaxes masticatory muscles alleviates pain as indirect support for these models. However, it is important to acknowledge that muscular hyperactivity is not isomorphic with reports of pain and that treatments designed to alter muscle hyperactivity have not demonstrated that the reduction in muscle activity is the actual mechanism of pain reduction. For example, studies that report the efficacy of biofeedback for TMD have not demonstrated that there is a co-occurrence of pain reduction
84 Psychophysiological Assessment
with reduction in masseter electromyographic (EMG) activity. 18 As direct evidence for the psychophysiological model of TMD, a wide variety of EMG-based studies are frequently cited as support for the importance of psychological stress on the muscles of mastication. For example, several studies have demonstrated a significant correlation between EMG-measured magnitudes of nocturnal bruxism and stressful daytime events19'20 and/or the anticipation of stressful events.21 While there is considerable evidence that the magnitude and duration of masticatory muscle contractions during bruxing and other parafunctional oral habits are sufficient to produce muscular pain and fatigue,22 the methodological design of these studies precludes reaching the conclusion that psychological stress causes increased masticatory muscle activity.23 To date, there are only a handful of studies24-28 that have directly addressed the question of whether TMD patients respond to psychological stress with increased masticatory muscle activity. Overall, the results of these studies are mixed. Several investigators25'26 have reported resting baseline EMG differences in masticatory muscles between TMD patients and healthy controls, while others24'27 have not found significant baseline differences between patients and controls. A similar state of affairs exists in terms of whether TMD patients, in comparison to control subjects, show significantly higher EMG increases in the muscles of mastication when presented with psychologically stressful stimuli. When baseline differences are controlled for, several studies have demonstrated no significant EMG increases in response to psychological stressors26'27 and other studies25'28 report TMD patients display significantly higher EMG levels during stressful stimuli when compared to the EMG level of control subjects. A number of methodological factors prevent reaching firm conclusions from psychophysiological studies of TMD. All of these studies have suffered from some of the following methodological flaws: (a) failure to match subjects on characteristics known to affect psychophysiological responses (e.g., gender, age, medication usage); (b) inadequate diagnostic information regarding the types of TMD patients used; (c) failure to include an adaptation period so that the physiological recordings could stabilize; (d) failure to control for movement artifacts before the analysis of EMG signals (e.g., swallowing); (e) failure to adjust for intergroup EMG baseline differences before computing EMG differences due to stressful stimuli; (f) inadequate description or inappropriate EMG measurement methodology (e.g., lack of standardized electrode placements, failure to measure electrode resistances prior to recording); (g) inappropriate data reduction and statistical procedures (e.g., multiple t-tests on correlated data); (h) failure to counterbalance the presentation of stimulus conditions to control for carry-over effects and to allow
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sufficient time for physiological measures to return to prestimulus levels before the presentation of additional stimuli; (i) use of stress-induction tasks that have little ecological validity (e.g., white noise) and to measure subjects' subjective reactions to the stimuli to verify if they were perceived as psychologically stressful; (j) failure to assess the duration of elevated EMG activity in response to a stressor or the rate of recovery to baseline levels following termination of the stressor; and (k) failure to measure more than one muscle of mastication, to measure distal muscle sites to test for response specificity, or to include at least one other physiological measure (e.g., skin conductance level). Recently, at the University of Pittsburgh Pain Institute we29-31 have conducted a series of psychophysiological studies of TMD patients in an attempt to correct many of the methodological problems described above. In addition to addressing recording, statistical, and experimental design issues, we have been concerned with the concept of "stressful stimuli" and the ecological validity of many laboratory stress tasks. Psychological stress needs to be conceptualized as an interaction betweeen environmental stimulation and person variables. We have adopted this transactional view of stress and somatic adaptation,32'33 which emphasizes that an individual's appraisal of an environmental stimulus will determine if the environmental event is perceived as stressful. In other words, stress, much like pain, is ultimately a subjective phenomenon. Thus, it is possible that an environmental stimulus (e.g., threat of shock) can produce arousal and the activation of physiological responses, but this arousal is not perceived by the individual as stressful because it is largely an artificial stimulus that does not call into question the individual's leamed coping resources. In one of our psychophysiological experiments three experimental tasks were conducted, with counterbalanced presentation orders used across subjects to minimize potential carry-over effects between tasks. These tasks were: (1) a standardized neutral imagery task, presented to them by the experimenter, that placed subjects in their living rooms with the television on; (2) an experimenter-guided personally-relevant stressful image of a recent stressful experience that was elicited previously from the subject during the psychological intake interview; and (3) a general stress task, mental math, during which time subjects were instructed to keep their eyes closed and silently count backwards by 7s beginning from 543. During each task simultaneous EMG recordings were taken bilaterally from masseter and temporalis muscles as well as from several nonpain-specific muscle sites. Each task was also preceded by a baseline phase and followed by a retum-to-baseline phase. Subjects also rated their current stress, muscle tension, and pain levels following each task.
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support for the psychological component of the psychophysiological model of TMD and identify potential differences between patients with and without structural abnormalities. The significant muscular increases observed in both patient groups appear to have led to differences in appraisals and perceptions of pain that were independent of their ratings of stress and muscle tension. Finally, and perhaps of most importance, these results indicate that even though EMG increases during the psychological stress tasks were quite small when compared to the EMG levels observed during physical stress tasks,22 at least a subset of TMD patients perceived these masticatory muscle increases as painful.
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TMD patients with and without abnormal TMJ CT findings.
From a sample of 100 TMD patients, a subset of 40 patients were identified based on the presence of extreme positive (n = 20) or negative (n = 20) TMJ computed tomography (CT) results. Analysis of masseter and temporalis EMGs indicated no baseline EMG differences between TMD patients and healthy controls (n = 10) or differential responding to the neutral image, suggesting that TMD patients do not have higher resting muscle tension levels than normals. TMD patients, however, did display significant site-specific EMG elevations in response to the two stress tasks, in contrast to controls (Figure 1). EMG increases for the TMD patients were as high as 430% above baseline (M = 180%). Also, patients' EMG increases were significantly higher for the personally-relevant stress task when compared to the mental arithmetic task. Abnormalities of the TMJ based on CT were unrelated to muscular hyperarousal during baseline or stress tasks. Furthermore, during the stress tasks significant EMG changes for non site-specific muscles did not occur. Thus, although it is common to differentiate TMD patients based on joint abnormalities, these data demonstrate that hypermuscle arousal to stress can occur regardless of structural abnormalities. A striking pattem emerged from this psychophysiological experiment. Significantly different post-task pain ratings occurred, even though patients' levels of stress and muscle tension ratings were equivalent. The normal CT group reported significantly higher post-task pain levels for both stress tasks (Figure 2). These findings provide
Conceptual and methodological issues related to psychophysiological models and assessment of TMD patients have been raised throughout this paper. Although psychophysiologically-based research efforts show considerable promise and have the potential to make important and unique contributions to our understanding of the clinical phenomena of TMD, significant progress is unlikely to occur without investigators' attention to several key methodological problems. First, much of the discrepancy among psychophysiological studies of TMD lies in the fact that different laboratories use widely disparate physiological measurement techFigure 2. Mean pain intensity ratings following 3 psychophysiology experimental tasks for TMD patients with and without abnormal TMJ CT findings. 5
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86 Psychophysiological Assessment
niques, stimulus paradigms, and subject samples. In terms of recording methodology, guidelines for EMG measurement,34 all of which are frequently used in TMD studies, are now available. Researchers whenever possible should adhere to these standards in order to facilitate the communication of findings between different laboratories. The standardization of electrode placements based on facial anatomical landmarks, electrode, size, passbands used for EMG detection, signal integration methods, and so forth, would result in improved measurement validity and reliability. For experimental stimuli, the definition and measurement of what stimuli are, in fact, psychologically stressful to subjects requires more careful inspection and clarification. The counterbalancing of stimulus orders as well as attention to both physiological and psychological habituation to experimental stimuli should be addressed in future research efforts. Finally, TMD patients cannot be considered to be a homogeneous population.8'37 Psychophysiological investigators should provide more complete descriptions of the types of TMD patients used in an experiment, including subject demographics, psychological assessment information, whether patients were in pain at the time of the experiment, dental examination findings, oral habits, and the results of laboratory tests. Second, to date, psychological stress experiments in TMD have, for the most part, been between-subjects designs that are summarized by univariate statistical approaches (e.g., t-tests, ANOVA). However, this type of statistical paradigm is not well suited to the study of psychophysiological aspects of TMD. Group designs obscure individual differences in response patterns which are known to exist in states of arousal and emotion.3 The emphasis on tests of statistical significance in group designs may not yield results that are interpretable or meaningful in terms of the association between psychological stress and neuromuscular responding in the individual TMD patient. Time series analyses of EMG waveforms, both in the time39 and frequency domain,40 as well as adaptive filtering techniques from engineering4' hold considerable promise for individualizing the analysis of psychophysiological assessment data. Just as TMD patients cannot be considered to be a homogeneous group of patients, neither can their physiological responses to psychological stressors be considered homogeneous. Single subject statistical methods may help to clarify patients' differential physiological response patterns to stressful stimuli. Finally, and perhaps of most importance, an increasing number of investigators are proposing that TMD should be conceptualized as being comprised of a set of multidimensional, multietiological disorders.816 From this perspective, the primary goal in the assessment of TMD patients is to understand and integrate a wide range of functional, structural, and psychological data. Psycho-
physiological assessment should be considered as only a component of the assessment process. The clinical utililty of psychophysiological assessment findings as well as how these findings relate to other functional, structural, and psychological findings awaits further research. In light of the scarcity of methodologically sound studies that demonstrate a significant association between psychological stress and masticatory hypermuscle activity or that the magnitude of muscular increases produced by psychological stressors is sufficient to lead to increased levels of pain, along with the expense and complexities involved in psychophysiological assessment, at the present time psychophysiological assessment of TMD patients cannot be recommended as a routine clinic assessment procedure. ACKNOWLEDGMENT
Support for the completion of this manuscript was provided in part by a National Institute of Dental Research Grant No. DE07514. REFERENCES 1. Dolce JJ, Raczynski JM: Neuromuscular activity and electromyography in painful backs: Psychological and biomechanical models in assessment and treatment. Psychol Bull 1985;97:502-520. 2. Coles MGH, Donchin E, Porges SW, eds.: Psychophysiology: Systems, processes, and applications, New York, Guilford Press, 1986. 3. Galbraith GC, Kietzman ML, Donchin E, eds.: Neurophysiology and psychophysiology, Hillsdale, NJ, Lawrence Erlbaum, 1988. 4. Martin I, Venables PH, eds.: Techniques in psychophysiology, New York, John Wiley, 1980. 5. Cacioppo JT, Petty RE, eds.: Social psychophysiology: A sourcebook, New York, Guilford Press, 1983. 6. Greene CS: The temporomandibular joint syndrome. J Am Med Assoc. 1973;224:622. 7. Check DK, chair: Report of the ad hoc committee on craniomandibular and temporomandibular joint disorders, Minnesota Dental Association, 1988. 8. Rugh JD: Psychological factors in the etiology of masticatory pain and dysfunction. In: Laskin D, Greenfield W, Gale E, Rugh J, Neff P, Alling C, and Ayer W, eds., The president's conference on the examination, diagnosis and management of temporomandibular disorders, Chicago, American Dental Association, 1983. 9. Fearon CG, Serwatka WJ: Stress: A common denominator for nonorganic TMJ pain-dysfunction. J Prosthet Dent 1983;49:805-808. 10. Laskin DM: Etiology of pain-dysfunction syndrome. J Amer Dent Assn 1969;79:147-153.
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