Psychological and physiological parameters of masticatory muscle pain

Pain 76 (1998) 297–307

Psychological and physiological parameters of masticatory muscle pain Charles R. Carlson a ,*, Kevin I. Reid a, Shelly L. Curran a, Jamie Studts a, Jeffrey P. Okeson a, Donald Falace a, Arthur Nitz a, Peter M. Bertrand b a

Department of Psychology and Orofacial Pain Center, University of Kentucky, 112 Kastle Hall, University of Kentucky, Lexington, KY 40506-0044, USA b Naval Dental School, National Naval Medical Center, Lexington, KY 40506-0044, USA Received 14 July 1997; received in revised form 23 February 1998; accepted 2 March 1998

Abstract The objective of this research was to identify the psychological and physiological variables that differentiate persons reporting masticatory muscle pain (MMP) from normal controls (NC). This study examined the characteristics of 35 MMP patients in comparison to 35 age-, sex-, and weight-matched NCs. All subjects completed a series of standardized questionnaires prior to undergoing a laboratory evaluation consisting of a psychosocial stressor and pressure pain stimulation at multiple body sites. During the evaluation, subjects’ emotional and physiological responses (heart rate, blood pressure, respiration, skin temperature, and muscle activity) were monitored. Results indicated that persons with MMP reported greater fatigue, disturbed sleep, depression, anxiety, menstrual symptoms, and less selfdeception (P’s , 0.05) than matched controls. At rest, MMPs had lower end tidal carbon dioxide levels (P , 0.04) and lower diastolic blood pressures than the NCs (P , 0.02). During laboratory challenge, both groups responded to the standard stressor with significant physiological activity and emotional responding consistent with an acute stress response (P , 0.01), but there were no differences between the MMPs and NCs. Muscle pain patients reported lower pressure pain thresholds than did NCs at the right/left masseter and right temporalis sites (P’s , 0.05); there were no differences in pressure pain thresholds between MMPs and NCs for the left temporalis (P , 0.07) and right/left middle finger sites (P’s . 0.93). These results are discussed in terms of the psychological and physiological processes that may account for the development of muscle pain in the masticatory system.  1998 International Association for the Study of Pain. Published by Elsevier Science B.V. Keywords: Masticatory muscle pain; Pressure stimulation; Psychosocial stressor; Laboratory challenge

1. Introduction Temporomandibular (TM) disorders are a debilitating and often-refractory group of conditions affecting a significant sector of the population. Prevalence estimates for TM disorders indicate that 12% of the general population report experiencing these disorders (Von Korff et al., 1988). Despite extensive investigation dating back over five decades (Costen, 1937; Moulton, 1955), many questions regarding the etiology and effective treatment of this group of disorders remain unanswered. For example, there has recently been considerable discussion regarding the role of muscle activity in the development and maintenance of TM disorders (Lund and Widmer, 1989). Numerous studies

* Corresponding author. Tel.: +1 606 2574394; fax: +1 606 3231979.

(e.g. Mercuri et al., 1979; Gervais et al., 1989; Kapel et al., 1989; Flor et al., 1991) have reported the presence of elevated electromyographic (EMG) activity in the head and neck regions of persons with TM muscle pain. Some of the studies, however, contain methodological flaws involving subject selection criteria; failure to match age, sex, and weight; variants in body positioning during the evaluation; and movement artifacts. Lund and Widmer (1989) have pointed out that if postural hyperactivity of the masseter muscles is a causal factor in TM disorders, then greater activity in the orofacial muscles on the side of unilateral pain should be found as compared to activity on the contralateral side. Dolan and Keefe (1988) found among patients reporting right-sided muscle pain that greater EMG activity was observed for the left masseter as compared to the right masseter regions. For subjects experiencing left-sided muscle pain, no differences in EMG activ-

0304-3959/98/$19.00  1998 International Association for the Study of Pain. Published by Elsevier Science B.V. PII S0304-3959 (98 )0 0063-3

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ity were noted between the left and right masseter regions. Based on data such as these, it is difficult to accept muscle tension alone as the causative factor for TM dysfunction. These data, however, do not omit the possible sequence that increases in muscle activity precede and produce the pain complaint, and that once a given group of motor units are fatigued or painful they are centrally inhibited from being recruited. Flor and colleagues (Flor et al., 1991, 1992) have developed an experimental paradigm whereby participants are asked to recall a personally stressful event while EMG activity is monitored. Using this approach, they reported that TM disorder patients displayed more EMG activity in the facial muscles than did controls, but the magnitudes of these differences were small (,10 mV). These data were interpreted as support for a hypothesis linking muscle pain to muscle overactivity. While TM disorder patients have been differentiated from controls with this paradigm, there are several interpretational problems created by this approach. First, the magnitudes of the muscle activity changes are relatively small; while small changes in resting muscle activity have been reported to be clinical indicators of dysfunction (Cram, 1988), it is controversial to what extent small differences in EMG activity may be a factor in the pathogenesis of the significant levels of muscle pain these patients report. Flor et al.’s data have also been used to suggest that TM disorder subjects may be more reactive to environmental challenges than normal controls when, in fact, they may be recalling more psychologically salient and stressful memories during the measurement trials than their normal counterparts. This possibility would be consistent with other literature (Curran et al., 1995; Fillingim et al., 1997), indicating that many TM disorder patients have experienced traumatic life events. In order to evaluate the responsivity of TM disorder patients to a standard stressor, Carlson and colleagues (Carlson et al., 1993; Curran et al., 1996) used a paradigm exposing participants to a mental arithmetic task where the nature of the stressor is more likely to be perceived consistently between patients and controls. Their results demonstrated that TM disorder patients were no more responsive with EMG activity to this form of stressor than matched controls; they did find that TM disorder patients displayed more cardiovascular and emotional reactivity to a laboratory stressor than matched controls. These studies were, however, conducted with relatively small sample sizes that could influence interpretations of results and point out the need for further examination of these issues. One area of investigation with persons reporting TM disorders that has consistently yielded reliable findings involves psychological assessment. There are numerous reports of greater levels of depression and anxiety in persons presenting with TM complaints as compared to normal controls (Molin et al., 1973; Marbach et al., 1988; Dworkin et al., 1989; Schnurr et al., 1990; McCreary et al., 1991; Carlson et al., 1993; Curran et al., 1996). It has also been shown

that TM disorder patients are more emotionally reactive to environmental challenge than normal controls (Curran et al., 1996). Kinney et al. (1992) reported that approximately 50% of the persons seeking treatment for TM disorders in a facial pain clinic were diagnosable with somatoform disorders according to DSM III-R criteria (American Psychiatric Association, 1987); they also found that more than one-third of the patients were experiencing depression. Overall, the available data indicate that significant psychological dysfunction is often present with many TM disorder patients. These psychological findings have led to the development of TM disorder treatment protocols addressing psychological dimensions (Rudy et al., 1995), as well as traditional dental management concerns. Several recent studies (Turk et al., 1993, 1996; Dworkin et al., 1994) have evaluated the potential contributions of adding cognitive-behavioral components (e.g. habit reversal, relaxation training, problemsolving/stress management, and brief cognitive restructuring) to the standard dental treatment regimen that typically involves education, fabrication of an oral appliance and provision of medication. The findings of these studies suggest that cognitive–behavioral interventions are an important adjunct to traditional dental therapies in the short term. After 6–12 months, the cognitive–behavioral programs provide a significant and measurable increment in pain and distress reduction as compared to traditional dental therapies for TM disorders. These very positive treatment outcomes for psychologically-oriented, cognitive–behavioral strategies can be interpreted as support for a psychosomatic component of TM disorders. It is not uncommon for TM disorder patients to express their frustration at being told ‘your pain is all in your head’ when standard dental treatment regimens have failed to manage symptoms. Since most of these patients have been treated initially by dentists, the primary focus has generally been on the reduction of pain complaints. This approach, and the specific strategies (e.g. occlusal adjustment, splint fabrication, and various surgical procedures) that are used, has often times proceeded without a clear understanding of what is causing the pain and why the treatment methods work. The recent consensus conference on TM disorders at the National Institutes of Health (NIH, 1996) forwarded the same conclusions and encouraged the development of comprehensive conceptual models based on available scientific literature for TM disorders. Whether or not there is a significant psychologic component underlying the development and maintenance of TM disorders is a matter for continued empirical research. In addition to the issues associated with the role of muscle activity and psychological dysfunction, several authors have recently provided data regarding the role of central nervous system modulation in TM disorders. Maixner et al. (1995) reported that TM disorder patients experiencing primarily muscle pain had lower thermal and ischemic pain thresholds and tolerance levels than did normal controls. Reid et al. (1994) also found that TM disorder patients with muscle

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pain have lower pressure pain thresholds in the temporalis and masseter regions than did normal controls. The findings from both of these studies were interpreted as supporting the role of central nervous system modulation of TM disorders. The use of pressure pain threshold determinations in the facial region has been shown to be a reliable and valid means for differentiating TM disorder patients from painfree controls (Ohrbach and Gale, 1989a,b; Reid et al., 1994). The pressure pain determinations are consistent with other studies of pain stimulation with TM disorder patients (Molin et al., 1973; Malow and Olson, 1981; Malow et al., 1989); however, several investigators (Hagberg et al., 1990; Curran et al., 1996) have not found differences in pain sensitivity between TM disorder patients and controls. Factors that may be influencing the discrepancies in results could include both mode and site of pressure stimulation. The Curran et al. (1996) study evaluated pressure pain tolerance in the non-dominant hand whereas, for example, Orhbach (Ohrbach and Gale, 1989a,b) and Reid (Reid et al., 1994) used sites within the trigeminal region. The findings from Curran et al. (1996) raise the possibility that peripheral pressure pain stimulation procedures may not be a sensitive index of generalized central nervous system dysfunction. The present investigation was conducted to further the conceptual framework for TM disorders by elaborating the psychological and physiological factors differentiating patients with a specific subclassification of TM disorders (Dworkin and LeResche, 1992), namely masticatory muscle pain (MMP), from healthy, matched controls under controlled, laboratory conditions. Based on previous research, we expected that chronic muscle pain patients would report more affective distress than their healthy counterparts. We also expected that MMP patients would display greater emotional and physiological responsivity to a standard laboratory stressor than normal controls. Finally, we hypothesized that chronic MMP patients would have lower pain thresholds when undergoing acute pressure pain stimulation as compared to normal controls.

2. Subjects and methods 2.1. Participants The participants in this study consisted of 35 facial pain patients with an average age of 30.17 years and an average weight of 137.79 pounds. They were sex (33 women), age (1–3 years), and weight (1–10 pounds) matched to a group of 35 normal controls who had an average age of 30.14 years and an average weight of 140.49 pounds, and were pain-free at the time of the study. Each facial pain patient was recruited and evaluated in the Orofacial Pain Center at the University of Kentucky for subjective and objective signs and symptoms of masticatory muscle pain (MMP) by a dentist trained in accord with the

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Research Diagnostic Criteria (Dworkin and LeResche, 1992). For this study, the primary diagnosis of masticatory muscle pain was made when the subject’s chief complaints originated from the masticatory muscles and were present for 6 months or longer. Pain report had to be greater than ‘2’ on a 10-point scale where ‘0’ represented no pain and ‘10’ represented the worst possible pain. The pain patients upon clinical examination by the dentist reported an average pain rating of ‘4.7’ on the 10-point scale. The average duration of the pain was 6.7 years. Patients with painful joint sounds; joint arthralgia or osteoarthritis; painful disc displacement; and pain upon digital palpation of the lateral pole of the right or left condyle were excluded from the study. During the period of the study, 81 patients presenting to the Orofacial Pain Center met the inclusion criteria and were approached for their participation. The most common reason reported for refusing to participate was travel distance to the clinic; other reasons included no convenient time available to participate and ongoing litigation that precluded research participation. Normal volunteers without pain in their masticatory or other body systems were recruited through announcements placed in community news media. Those pain-free volunteers selected for the study had not been seen previously for treatment at the Orofacial Pain Center. Additionally, all subjects had average resting blood pressures less than 140/90 mmHg, no previous injury to the hands/fingers, were not currently taking any centrally acting medications, and were in overall good health except for those with the masticatory muscle pain. If female subjects were not using oral contraception or were not post-menopausal, they were scheduled for the evaluation at a time other than during the ovulation phase of their menstrual cycle because of possible changes in pain sensitivity during that time (Goolkasian, 1980). Subjects were paid US $35 for their participation in the project. 2.2. Design The study design compared patients experiencing chronic facial muscle pain with a matched group of pain-free normal controls on responses to a set of standardized psychometric inventories and to a laboratory evaluation involving responsivity to a standard psychosocial stressor and pressure stimulation. Dentists experienced in the diagnosis and treatment of TM disorders conducted the initial screening. Subjects were then recruited for the study by research associates; the research was approved by the Institutional Review Board for the Protection of Human Subjects. The laboratory evaluation was conducted by personnel who were not told whether or not the subject was a MMP patient or a normal control. The research personnel included two men and three women. Data analyses from the laboratory evaluation were adjusted (ANCOVA) for the individual experimenters to insure that results were not systematically biased.

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2.3. Dependent measures Self-reports of pain were obtained using visual analog scales characterizing pain in the masseter, temporalis, and hand regions (Price et al., 1983). The Paulhus Balanced Inventory of Desirable Responses (PBIDR; Paulhus, 1984) was used to assess socially conforming responses with scales representing impression management and self-deception. The State Trait Personality Inventory (STPI; Spielberger et al., 1979) was used to assess trait anxiety, anger, and curiosity. Depression was measured with the CES-D selfreport scale (Radloff, 1977) that is well established as a screening instrument for use in the general population. The Piper Fatigue Scale (PFS; Piper, 1990) was used to assess perception of overall fatigue and the Pittsburgh Sleep Quality Index (PSQI; Buysse et al., 1989) was used to evaluate global sleep quality. Menstrual symptoms were assessed with the Menstrual Symptoms Questionnaire (MSQ; Chesney and Tasto, 1975). Finally, emotional reactivity of eight dimensions of emotional responding (happiness, surprise, fear, disgust, anger, guilt, anxiety, and sadness) was measured with the Emotional Assessment Scale (EAS; Carlson et al., 1989). Each of these instruments has established reliability and validity for the self-report assessment of the targeted domains. Physiological parameters involving musculoskeletal, cardiovascular, and respiratory functioning were evaluated during the laboratory phase of the study. Electromyographic (EMG) activity was recorded using silver/silver chloride miniature (0.5 cm2) surface electrodes. The electrodes were attached to the l/r masseter and l/r anterior temporalis muscle regions according to standard laboratory guidelines (Fridlund and Cacioppo, 1986). The EMG bandpass filter setting was at 25–1000 Hz. EMG measurements of interest in this study involved the relative changes from baseline levels of activity. Additionally, muscle pain subjects were matched according to age, sex, and weight in order to facilitate comparisons of these relative changes across subjects. EMG signals were recorded using a J + J I-330 computerized physiograph that integrated data over 1-s epochs and computed an average score for each experimental phase. Blood pressure (SBP, DBP, MAP) was recorded with a Paramed 9200 automated blood pressure cuff. The cuff was placed on the subject’s dominant arm. Heart rate was measured with a photoplethysmograph attached to the ring finger of the non-dominant hand; heart rate data were also recorded with a J + J I-330 physiograph. Both blood pressure and heart rate were averaged over 1-min periods. Skin temperature of the index finger of the non-dominant hand was recorded with a J + J thermistor probe. Respiration rate was recorded with a J + J I-330 respiration module using a strain gauge sensor attached across the upper abdomen. These latter data were also recorded over 1-s intervals and averaged over each experimental period. End-tidal carbon dioxide levels were monitored with an Ohmeda 4700 capnometer. A nasal cannula was affixed near

the openings of the nostrils and attached to the capnometer. The instrument recorded carbon dioxide concentrations (% carbon dioxide) of the expired air on a breath by breath basis. These data were recorded and an average concentration of carbon dioxide level for each period was calculated. The average carbon dioxide level of expired air is directly proportional to the carbon dioxide concentration in the blood plasma (Fried, 1993). This equipment was not available at the beginning of the study, so degrees of freedom for this variable differ from the other physiological variables. 2.4. Laboratory evaluations Pain pressure thresholds were determined using a Somedic pressure algometer. The unit has a stimulation tip (0.5 cm2) at the end of a barrel connected to a pressure transducer. The pressure, measured in kilopascals (kPa), was applied at a rate of 30 kPa/s. When the pressure pain threshold was reached, the subject pushed a button which stopped the digital display of the pressure and the examiner discontinued the pressure application. The pressure pain threshold was recorded from the digital readout. Pain pressure thresholds were determined by repeating the procedure three times at each anatomical site with a 3-min interval between pressure application to the individual anatomical sites; this is the standard method used in previous research (Brennum et al., 1989). Six anatomical sites including the l/r second phalanx of the middle finger, l/r masseter muscle, and l/r temporalis muscle were evaluated in a randomly determined order. The mental arithmetic stressor consisted of a serial subtraction task (subtracting 13’s from a four-digit number) lasting 1 min for each trial. This standardized approach to a laboratory stressor task was chosen to insure similarity in task difficulty across participants and has been used successfully in numerous studies to activate physical and emotional parameters associated with the stress response (Williams et al., 1982; Hatch et al., 1986; Carlson et al., 1989). There were three consecutive trials of subtraction with 1-min rest periods between trials. Physiological data were collected throughout the trials and the rest periods and the EAS was given after the third trial to assess any emotional changes due to this stressor (Carlson et al., 1989). Mental arithmetic tasks of this nature have been used as an effective acute stressor in studies of stress-related disorders (e.g. Andrasik et al., 1982; Turner and Carroll, 1985; Matthews et al., 1986) and in previous research with TMD patients (Moss and Adams, 1984; Rudy, 1990; Carlson et al., 1993; Curran et al., 1996). 2.5. Procedure Prior to the experimental session, participants completed an informed consent and passed all screening criteria. Female subjects were not scheduled for a session during the ovulation phase of their menstrual cycles (days 15– 21), with the exception of any subjects using oral contra-

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ception. In addition, chronic pain subjects with the consent of the prescribing health professional discontinued any pain medication 12 h prior to the experimental session. Subjects were also asked to not smoke or drink caffeinated beverages for 2 h before the session. Following the completion of the consent form, subjects filled out the psychological assessment battery in a quiet environment free of distractions. Then the experimenter introduced the subject to the physiological laboratory and attached the physiological recording leads. After the recording leads were attached, the subject rested quietly for a 15-min adaption period followed by a 5min baseline recording period. After the baseline recording, the first EAS was given. Then either the mental arithmetic or the pain stressor was administered. The order of administration was randomized across subjects so that an equal number of subjects in the MMP and normal control condition received the math challenge or pressure stimulation first. After exposure to the initial stressor, subjects rested for 5 min, then the second laboratory stressor was given. Immediately after the math stressor, however, subjects completed the EAS. When both stressors were completed, subjects rested quietly for a 5-min post-baseline recording period. Following the post-baseline recording, subjects were administered the EAS again. Subjects were then debriefed and excused from the experimental session.

3. Results 3.1. Analytic strategy The baseline psychological data were first evaluated to determine whether or not differences between groups were present initially. Physiological data were evaluated with the multivariate general linear model using as covariates the experimenter and pre-existing baseline differences where appropriate on subsequent analyses. In order to control the familywise error rate associated with multiple dependent measures and multiple paired comparisons, a MANOVA was performed where appropriate such as in the conditions where multiple dependent variables might be expected to be correlated. All data analyses were conducted using the SAS or SPSS analysis program. Differences in degrees of freedom for physiological data reflect equipment unavailability or malfunction. 3.2. Baseline evaluation 3.2.1. Pain assessment Self-reports of pain were obtained from participants at the beginning of the laboratory evaluation as a means to insure that persons diagnosed with MMP were, in fact, experiencing ongoing muscle pain at the time of the evaluation. Masticatory muscle pain patients reported greater levels of pain overall [MMP = 27.77 mm vs. NC = 7.29 mm,

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F(1,68) = 19.69, P , 0.001] and in the temporalis [MMP = 24.00 mm vs. NC = 3.49 mm, F(1,68) = 18.65, P , 0.001] and masseter [MMP = 42.86 mm vs. NC = 4.26 mm, F(1,68) = 57.27, P , 0.001] regions than did the normal controls. Reports of masticatory muscle pain from the patient sample were very consistent with what was reported to the dentist in the clinic (average pain rating in the masticatory muscles of 4.7 on a 0–10 scale). There were no differences in self-reports of pain in the hands between the MMP (X = 2.54 mm) and the NC (X = 2.40 mm) groups, F(1,68) = 0.013, P , 0.91. Self-reports of present pain assessment confirmed the presence of significant masticatory muscle pain in the MMP group as compared to the NCs. 3.2.2. Psychological variables In order to control for the family-wise error rate, an overall MANOVA was performed on the psychological data collected at baseline indicating a significant difference between the MMPs and NCs, Wilks’ Lambda (9,51) = 3.18, P , 0.01. This analysis was followed up with univariate analyses that indicated on the Self-Deception scale of the PBIDR, MMPs (X = 64.37) scored significantly lower than the NCs (X = 67.91), F(1,59) = 6.63, P , 0.01. There were no differences between groups on the Impression Management scale of the PBIDR, MMP = 65.00 and NC = 64.29, F(1,59) = 0.44, P , 0.51. There was greater trait anxiety [MMP = 23.49 vs. NC = 21.83, F(1,59) = 9.10, P , 0.01], depression [CESD; MMP = 16.71 vs. NC = 10.63, F(1,59) = 5.30, P , 0.03], fatigue [PFS; MMP = 17.25 vs. NC = 9.37, F(1,59) = 16.37, P , 0.001], and sleep dysfunction [PSQI; MMP = 8.48 vs. NC = 4.57, F(1,59) = 15.65, P , 0.001] for MMP participants as compared to NCs. There were no differences between groups on trait anger scores for the STPI [MMP = 17.54 vs. NC = 18.06, F(1,59) = 1.35, P , 0.25] or on trait curiosity, MMP = 27.71 vs. NC = 30.23, F(1,59) = 2.63, P , 0.11. Finally, MMPs reported significantly more menstrual symptoms than did the matched controls [MMP = 27.50 vs. NC = 23.00, F(1,59) = 5.19, P , 0.03]. 3.2.3. Physiological variables Data for the physiological variables are presented in Table 1. There were two significant differences in physiological variables at the initial baseline evaluation. These differences were resting diastolic blood pressure [MMP = 63.54 mmHg vs. NC = 68.74 mmHg, F(1,66) = 5.77, P , 0.02] and end-tidal carbon dioxide concentration [MMP = 4.68% vs. NC = 5.03%, F(1,38) = 4.35, P , 0.04]. There were no other significant differences between groups for physiological variables at the baseline period. The reader is reminded that baseline comparisons on EMG activity were not conducted since the absolute level of EMG is a function of a variety of factors that include site placement, skin preparation, and distance from skin to muscle layer.

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Table 1 Physiological responses during the laboratory evaluation Baseline

Stressor

Post-baseline

Masticatory muscle pain patients R. masseter EMG (mV) R. temporalis EMG (mV) L. masseter EMG (mV) L. temporalis EMG (mV) SBP (mmHg) DBP (mmHg) HR (bpm) RR (rpm) End-tidal CO2 (%) Skin temp. (°F)

1.93 2.58 1.95 2.74 109.82 63.54 72.20 12.79 4.68 84.95

(0.83) (1.53) (0.74) (1.53) (9.49) (9.53)* (12.91) (3.67) (0.56)* (5.51)

5.56 5.84 5.84 5.97 118.92 69.71 80.88 11.06 4.57 83.27

(3.19)** (3.29)** (2.86)** (2.21)** (13.04)** (8.57)** (11.86)** (2.74)** (0.61)** (6.11)**

2.00 3.34 2.52 3.75 110.47 64.29 72.97 12.33 4.64 83.30

(0.82) (1.80) (1.21) (1.87) (10.53) (8.99) (11.74) (4.05) (0.59) (6.52)

Matched control participants R. masseter EMG (mV) R. temporalis EMG (mV) L. masseter EMG (mV) L. temporalis EMG (mV) SBP (mmHg) DBP (mmHg) HR (bpm) RR (rpm) End-tidal CO2 (%) Skin temp. (°F)

1.84 2.22 1.95 2.64 113.31 68.74 67.11 12.83 5.03 84.75

(0.71) (0.93) (0.74) (1.27) (10.93) (9.17)* (11.60) (3.32) (0.47)* (6.03)

5.51 4.99 5.76 5.04 123.97 73.74 77.69 11.98 4.87 83.83

(3.05)** (2.23)** (2.91)** (1.91)** (12.57)** (8.41)** (13.51)** (3.01)** (0.60)** (5.45)**

2.16 2.86 2.26 3.16 112.97 65.50 67.50 12.39 4.95 84.03

(1.11) (1.51) (1.21) (1.80) (9.88) (10.75) (11.47) (3.77) (0.50) (5.85)

*P , 0.01–0.05, between-groups comparison. **P , 0.01, within-groups comparison.

3.3. Reactivity to psychosocial stressor Participants in both groups displayed significant physiological and emotional reactivity to the psychosocial challenge (all P’s , 0.01) that indicated the task was perceived as stressful and produced levels of activation consistent with previous studies. These physiological results are also presented in Table 1 and the results for the emotional data are

presented in Table 2. The self-report data also revealed this task was perceived as producing a significant increase in anxiety and dysphoria (sadness, guilt, anger, fear, and disgust) as would be expected from a stressful task. Together with the physiological data, there is strong evidence that the task was perceived as stressful by the participants. There were, however, no physiological or emotional data differentiating experimental groups from each other during the

Table 2 Emotional self-ratings during the laboratory session Baseline

Stressor

Post-baseline

Masticatory muscle patients Surprise Fear Anger Disgust Guilt Anxiety Sadness Happiness

3.82 2.13 1.15 1.12 1.07 5.35 2.89 6.90

(4.78) (3.22) (1.48) (1.81) (2.07) (5.09) (4.74) (5.86)

5.47 4.77 4.94 4.39 6.41 10.69 5.29 3.45

(4.72)* (5.44)* (5.17)* (5.85)* (5.57)* (7.17)* (5.19)* (3.88)*

1.41 1.26 1.06 0.87 1.17 3.26 1.97 4.49

(1.70) (2.28) (1.49) (1.28) (1.86) (3.89) (2.93) (4.760

Matched control participants Surprise Fear Anger Disgust Guilt Anxiety Sadness Happiness

2.71 1.42 0.92 0.73 0.95 3.60 1.38 8.33

(3.50) (1.72) (1.34) (0.99) (1.19) (3.93) (1.57) (5.40)

5.70 3.39 3.44 3.31 5.41 8.84 3.76 4.29

(5.79)* (4.11)* (4.13)* (4.08)* (5.49)* (6.71)* (4.10)* (5.41)*

1.23 0.62 0.84 0.56 0.65 1.89 0.94 5.93

(2.68) (0.77) (1.12) (0.68) (0.83) (2.30) (1.08) (5.73)

**P , 0.01, within-groups comparison.

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math challenge or at the post-challenge recovery periods. Both experimental groups responded in a similar manner to the laboratory challenge and returned to pre-stressor baseline levels during the post-challenge period. 3.4. Sensitivity to pressure stimulation Sensitivities to pressure stimulation were evaluated at six different anatomic sites. There were differences in r. temporalis [MMP = 119.29 kPa vs. NC = 140.17 kPa, F(1,66) = 5.88, P , 0.02], r. masseter [MMP = 110.17 kPa vs. NC = 140.20 kPa, F(1,66) = 4.15, P , 0.05], and l. masseter [MMP = 105.37 kPa vs. NC = 150.14 kPa, F(1,66) = 9.49, P , 0.01] sensitivities to pressure stimulation between MMPs and NCs. There was a nearly significant difference for the l. temporalis region, MMP = 113.94 kPa vs. NC = 136.17 kPa, F(1,66) = 3.32, P , 0.07. There were no significant differences between groups for pressure sensitivity at either the r. finger [MMP = 300.57 kPa vs. NC = 304.12 kPa, F(1,66) = 0.00, P , 0.96] or l. finger [MMP = 276.40 kPa vs. NC = 278.68 kPa, F(1,66) = 0.01, P , 0.94] sites.

4. Discussion The present results confirmed previous findings regarding the psychological status of MMP patients (Molin et al., 1973; Marbach et al., 1988;Dworkin et al., 1989; Schnurr et al., 1990; McCreary et al., 1991; Kinney et al., 1992; Carlson et al., 1993; Curran et al., 1996). The MMP patients reported greater levels of depressive and anxiety symptoms than did matched controls, although the differences in anxiety level may not be clinically significant in this sample. The level of depression measured in this study for the MMP patients, however, generally is considered clinically significant (Radloff, 1977) rather than just statistically significant. The MMP patients also reported more fatigue and sleep dysfunction than did normal controls. These latter findings could be seen as originating from the negative affect states already present in these patients. On the other hand, the data for self-report bias (PBIDR) where MMP patients are likely to be less self-deceiving than the NCs suggests that these patients are likely to be more objective in their self assessments as compared to the NCs. The level of depression reported by these patients suggests the presence of significant psychopathology, regardless of origin. With this in mind, it is not surprising that treatments known to address depressed mood (e.g. cognitive–behavioral therapy) have been shown to be effective with this patient group (Dworkin et al., 1994). While it is not possible with the present data set to determine whether or not the dysphoric mood represents a causal component or is a consequence of a chronic pain condition, the data do support continued efforts towards alleviating the ongoing symptoms of depression itself.

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One way to interpret the psychological data distinguishing MMP patients is that these patients may be more prone to report symptomatology (Wilson et al., 1991), and thus may be more likely to report various aches and pains as compared to normal controls. The general tendency to report a greater number of non-specific physical symptoms could be interpreted to suggest that pain patients are likely to be more sensitive, in general, to painful stimuli. Our current data, however, argue against the general interpretation that pain patients are more sensitive to painful stimuli. Even though the MMP patients displayed increased sensitivity to pressure stimulation at the masseter and temporalis muscle sites as compared to normal controls, there were no differences in pressure sensitivity at peripheral, non-painful finger sites. A generalized sensitivity model (Reid et al., 1994) would predict, as we had anticipated, that enhanced sensitivity to peripheral stimulation at any body site would characterize the MMP patients, but we did not find this to be the case. The present data for pressure stimulation at peripheral sites and previous findings (Curran et al., 1996) do not support the hypothesis that MMP patients are generally more sensitive to peripheral pressure stimulation than normal controls, but they are consistent with reports of central nervous system sensitization within the area of injury (Baumann et al., 1991). This interpretation, however, is not inconsistent with the hypothesis that chronic pain patients report more symptoms than normal controls because that particular hypothesis was not tested in this study. The heightened perception of pain for the trigeminal region as compared to spinal thalamic input may be due to how the trigeminal system modulates motor behavior as it processes input from its extensive receptive fields throughout the head and neck. Other researchers (Maixner et al., 1995; Reid et al., 1994) have reported that TM disorder patients have altered sensory pain reports consistent with a general central nervous system (CNS) dysfunction. At the present time, the distinction between our findings and the reports of others may represent differences in experimental paradigms and assessment modalities (e.g. vibratory stimulation) from the present study, or they may indicate that increased CNS sensitivity is created by certain forms of painful stimuli from specific receptive fields. Maixner’s ischemic pain procedure, for example, mimics perceived central muscle fatigue and is likely to increase central levels of norepinephrine (NE). This would contribute to general CNS sensitivity as opposed to the procedures employed in this study which would not likely result in a significant change in ischemic metabolic activity that would alter CNS activity in a manner likely to influence peripheral pain sensitivity. Recent laboratory studies have elaborated the neuroanatomical and neurophysiological circuitry of the trigeminal system for proprioception, pain, and fatigue (Olsson et al., 1986; Groenewegen et al., 1990; Berendse and Groenewegen, 1991; Sessle and Hu, 1991; Grunwerg and Krauthamer, 1992; Westberg et al., 1995; Winhorst and Boorman, 1995).

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Perceived fatigue, sleep dysfunction, anxiety, and pain are also associated with increased norepinephrine (NE) and acetylcholine (ACh) (Newsholme and Blomstrand, 1995; Sieck and Prakash, 1995). Fatigue and pain are both stressors that can severely tax reserves of adaptation energy and lead to eventual dysfunction. Interestingly, the same nerve fibers convey both metabolic fatigue and nociception centrally. When efforts to manage prolonged pain are not successful, physiologic control becomes disturbed and anxiety can be heightened. Anxiety has been defined as the inability to perform because of physiologic overactivation (Gift, 1991). Chronic anxiety and stress, along with a loss of control, can also lead to depression (Jefferson and Greist, 1994). The appearance of depression among chronic MMP patients is a reasonable expectation when fatigue and pain inhibit efficient responses to gain positive reinforcement from the environment. If non-restorative rest, associated with sleep dysfunctions, becomes a chronic problem due to changes in brain neurochemistry induced by fatigue and pain, depression may also become chronic since MMP patients will have a reduced capacity to recover physiologically. Electromyogram data from this study do not support the use of integrated surface EMG as a means to differentiate pain patients from normal controls using standard stressors. It is important to emphasize that the standard stressors used in this study resulted in a significant level of physiological and emotional activation that is a necessary characteristic of a laboratory stressor. We found no differences in muscular response to a math stressor between MMP patients and matched controls. These findings were consistent for EMG activity during the math computations and during the silent periods that served as a control for the influence of movement artifacts. Based on these data and findings from previous studies (Carlson et al., 1993; Curran et al., 1996), it is reasonable to conclude that EMG monitoring with the paradigm for this study is not useful for distinguishing MMP patients from normal controls. The stressful serial subtraction task used in this study did not involve the recollection of a personally-relevant stressor that has been shown by Flor and colleagues (Flor et al., 1991, 1992) to be critical in differentiating TM disorder patients from normal controls. Flor and colleagues have reported small differences in EMG activity between TM disorder patients and normal controls when recalling personally stressful life events. Their findings support the role of emotional memories in generating muscle activity that may differentiate pain patients from controls even though the intensity of the stress response can vary between patients and controls. We believe the role of emotional factors in generating parafunction cannot be overlooked, especially if fatigue is induced. Future studies, however, need to demonstrate the mechanisms by which personally-relevant stressors generate the magnitude of physiological activity necessary to elicit fatigue and pain in the trigeminal system. Recently it has been shown that masticatory muscles in TM disorder patients fatigue more rapidly than in normal con-

trols (Kroon and Naeije, 1992; Gay et al., 1994). It has also been shown that power spectra from Fourier analysis of the EMG signal are a reliable EMG index differentiating muscle activity in painful and non-painful states (Buxbaum et al., 1996). These findings suggest that further exploration of muscle activity in TM disorder patients is warranted. In addition, since cervical C-fibers and A-d fibers synapse in the trigeminal system, evaluation of cervical musculature as well as the classic facial muscles of mastication for functional and parafunctional movement may provide data to further our understanding of muscle dysfunction in the trigeminal region. The lower diastolic blood pressure findings for MMP subjects as compared to controls in this study are consistent with the relationships between fatigue and pain described above. Elevated brainstem levels of NE, 5-HT, and epinephrine occur with perceived fatigue (Newsholme and Blomstrand, 1995). With stressors, increased sympathetic tone redistributes a finite vascular supply to sites of need within the body, but local metabolic tissue demand determines microcirculation characteristics. With perceived fatigue, local peripheral vasodilation develops as tissues demand oxygen and glucose; venous congestion evolves due to the accumulation of metabolites (Guyton, 1996). With an increase in peripheral fluid volume retained at vasodilated sites of prolonged fatigue, and no increase in overall body fluid level, a lowered diastolic pressure, due to small decreases in venous return, would be reasonable. The slightly decreased end-tidal carbon dioxide levels for MMP subjects as compared to normal controls indicate that there is the possibility that alkaline pH levels may contribute to dysfunction (Fried, 1993) among the MMP patients in the present sample. It may be tempting to dismiss this finding because of the relatively small mean differences in the percentages of end-tidal carbon dioxide concentrations. Such differences, however, may underlie even greater physiological variability in the natural environment. The finding for end-tidal carbon dioxide level, especially since we did not find respiration rates differing between MMP patients and controls, indicates that further exploration of respiratory parameters is needed. The relaxation and diaphragmatic breathing strategies that are common to many of the reported self-regulation therapies for MMP may be based on restoring normal pH and reducing neuronal activity (Fried, 1993). The widespread usage of such procedures warrants improved understanding of their mechanisms of action in MMP. The finding for perceived fatigue in the present sample, although partially linked to sleep disturbances [r(70) = 0.61, P , 0.001], suggests that it could be a primary treatment target for these patients. It remains to be determined how and to what extent depression and perceived fatigue are linked together. Correlational data from the present sample indicate there is some shared variance [r(70) = 0.66, P , 0.001], but each construct also has its unique features. If perceived fatigue, pain, and sleep dys-

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functions are identified as primary management targets for MMP patients, then obtaining restorative rest, establishing oxygen–carbon dioxide balance, and maintaining glucose availability would be reasonable first line interventions. Normal function of the tissues of the trigeminal system would be difficult to obtain if these fundamental components are not available. Despite many decades of research, the development of an integrated model accounting for and explaining the symptoms of MMP has been elusive. Clinical observations have focused research efforts on muscle activity and the role of muscle overactivation in recent years. While research has not confirmed this hypothesis, widespread clinical practices focus rehabilitative efforts in this direction. The perceived fatigue–pain linkage may offer new avenues for research exploration. What is ultimately needed in this area are research based treatment interventions derived from databased theories. The treatment of TM disorders results in initial success in the majority of cases regardless of the intervention selected (Rugh and Dahlstrom, 1994). It should be no surprise that treatment procedures are currently applied without strong evidence for efficacy from randomized, controlled clinical trials when almost any intervention works to some degree initially. The role of oral appliances is a case in point where under controlled conditions there were no differences in outcomes between those who had been given a ‘muscle relaxation appliance’ from those who had not (Dao et al., 1994). The science and practice communities responsible for orofacial pains must continue to do the difficult work of sorting myths from facts in understanding the pathogenesis and treatment of TM disorders.

Acknowledgements This research was supported by NIDR Grant #R03 DE10534-02.

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