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Psychosomatic Medicine 67:957-963 (2005)
© 2005 American Psychosomatic Society

ORIGINAL ARTICLES

Abnormal Affective Modulation of Somatosensory Brain Processing Among Patients With Fibromyalgia

Pedro Montoya, PhD, Carolina Sitges, MS, Manuel García-Herrera, MD, PhD, Raúl Izquierdo, MD, Magdalena Truyols, MS, Nicole Blay, BS and Dolores Collado, MD

From the Department of Psychology and Research Institute of Health Sciences (IUNICS), University of the Balearic Islands, Palma, Spain (P.M., C.S., N.B.); the Medical Unit for Disability Assessment, Social Security Agency, Palma, Spain (M.G.-H., R.I., D.C.); and the Pain Clinic, General Hospital, Palma, Spain (M.T.).

Address correspondence and reprint requests to Pedro Montoya, PhD, Edificio Beatriu de Pinós, Department of Psychology, Cra. de Valldemossa km 7.5, 07122 Palma, Spain. E-mail: pedro.montoya{at}uib.es


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: It is well established that subjective pain perception can be modulated by negative mood states and that patients with chronic pain are characterized by high levels of depression and anxiety. Nevertheless, very little is known about the effects of negative mood induction on brain processing of somatosensory information in fibromyalgia. The objective of the present study was to examine the influence of two emotional states (pleasant and unpleasant) on brain activity of patients with fibromyalgia (FM; n = 27) and with musculoskeletal (MSK) pain resulting from identifiable somatic lesions (n = 16).

Methods: For this purpose, somatosensory-evoked potentials (SEPs) elicited by nonpainful pneumatic stimuli, delivered to the right and left hand following an oddball paradigm, were recorded when patients were viewing affective slides.

Results: As compared with patients with MSK pain, patients with FM displayed overall larger P50 amplitude to tactile stimuli. In addition, significantly larger P50 and smaller N80 amplitudes were found within patients with FM when they were viewing the unpleasant rather than the pleasant slides.

Conclusion: Our data suggest an abnormal processing of nonpainful somatosensory information in FM, especially when somatic signals are arising from the body within an aversive stimulus context. These findings provide further support for the use of biopsychosocial models for understanding FM and other chronic pain states.

Key Words: emotions • cognition • somatosensory processing • fibromyalgia • chronic pain • brain

Abbreviations: ACR = American College of Rheumatology; ANOVA = analysis of variance; BDI = Beck Depression Inventory; EEG = electroencephalogram; FM = fibromyalgia; fMRI=functional magnetic resonance imaging; IAPS = International Affective Picture System; MPI = West Haven–Yale Multidimensional Pain Inventory; MPQ = McGill Pain Questionnaire; MSK = musculoskeletal; SE = standard error of the mean; SEP = somatosensory-evoked potentials; STAI = State-Trait Anxiety Inventory.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
The diagnosis of fibromyalgia (FM) as defined by the American College of Rheumatology (ACR) (1) includes criteria such as chronic widespread musculoskeletal pain, hyperalgesia and/or allodynia, morning stiffness, insomnia, fatigue, cognitive problems, and often depression and headache. Although no pathophysiological process has yet been found to account for these symptoms, recent studies have demonstrated altered brain processing of nociceptive information in patients with FM (2–5), which might result from hyperexcitability of the central nervous system (6). In addition, previous studies have emphasized the role of emotions and psychological stressors in the origin and maintenance of FM, and suggested that these patients might be particularly vulnerable to the effects of negative mood (7–9). In this sense, there has been some evidence showing that negative affect is directly associated with increased pain perception in patients with FM (8,9). Thus, these studies do not only suggest that enhanced pain sensitivity and negative affect constitute relevant psychophysiological mechanisms in chronic pain, but also highlight their importance for FM pain.

Previous studies have also examined the influence of experimental mood induction on pain perception (10–12) and brain functioning (13) in healthy subjects. Basically, it has been found that subjective pain ratings can be enhanced by viewing unpleasant slides (10), negative emotional films (11), or reading negative emotional statements (12). Furthermore, a recent study using functional magnetic resonance imaging (fMRI) demonstrated that the induction of a negative mood state by presentation of fearful faces can also alter the brain processing of nonpainful visceral information within the anterior cingulate gyri and the insula (13). Thus, it seems that the emotional context in which the stimulation occurs could modulate the central processing of sensory information. However, little is known about the extent to which a negative emotional context can influence the brain processing of somatic information in chronic pain and, particularly, in FM.

In the present study, we investigated whether sensory and cognitive processing of tactile stimuli could differ as a function of the context induced by external emotional stimulation in FM and patients with musculoskeletal pain as a result of identifiable somatic lesions (MSK), which served as an emotionally less disturbed comparison group. For this purpose, emotional context was manipulated using affective slides and asking patients to empathize with the mood state elicited by the pictures when they were simultaneously performing a somatosensory detection task at a nonpainful body location. By using such an experimental task, it was also possible to examine the influence of negative affect on cognitive processing in patients with chronic pain. In addition, brain activity was recorded from the electroencephalogram (EEG) using somatosensory-evoked potentials (SEPs). In accord with previous studies, SEP recordings have provided an easy, reliable, and robust tool for examining the central nervous hyperexcitability associated with chronic pain (3–5), as well as some cognitive variables involved in somatosensory information processing such as attention (14,15). In this sense, it has been suggested that early SEP components within the first 100 ms after stimulus onset (i.e., P50, N80) originate in primary sensory cortex and are related to sensory and attentional processing of somatosensory information, whereas SEP components at later latencies are linked to complex cognitive processes such as, for instance, shifting attention to deviant stimuli in an oddball task (i.e., P200). Based on previous evidence about central hyperexcitability and negative affect in FM, it was expected that the experimental induction of a negative mood state during the processing of nonpainful information would result in more increased pain perception and significant changes of brain activity within FM than patients with MSK pain. Particularly, we were interested in examining early and late SEP components to find out whether there are any group differences in the effects of mood induction on the early attentional and late cognitive processing of tactile information.


   PATIENTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Patients with a diagnosis of chronic musculoskeletal pain for at least 6 months who had normal hearing, corrected visual acuity, and no history of head trauma or drug abuse were recruited from the pain management unit of a tertiary care hospital and the Medical Unit for Disability Assessment of the Spanish Social Security Agency in Palma (Spain). Forty-three righthanded female patients aged between 40 and 65 years, from an initial sample of 84, agreed to participate in this study. At the time of the examination, 24 patients (19 patients with FM and 5 patients with MSK) were involved in a litigation process for financial compensation resulting from disability. Patients were classified according to the primary diagnosis recorded in their medical chart in two groups: FM (n = 27) and MSK pain disorders resulting from identifiable somatic lesions (n = 16). The diagnosis of fibromyalgia was further confirmed by an experienced and external rheumatologist. The MSK group was composed by patients with rheumatoid arthritis (n = 6) and patients diagnosed with radiculopathy with a herniated disk (n = 10). All patients, except in two cases, were taking regular pain medication, including antidepressants and myorelaxants; 48.8% of the patients were taking anxiolytic drugs.

At the time of recruitment, patients were verbally informed about the details of the study and noted that the participation in the study was not linked to their possible litigation process. A specifically designed patient information leaflet was also given, and after agreeing to participate, each patient provided written consent. The study was in accordance with the Declaration of Helsinki (1991) and was approved by the Ethics Committee of the University of Balearic Islands (Spain).

Clinical Pain Assessment
All patients underwent an extensive medical and psychological assessment, including examination of tender points and assessment of clinical pain characteristics through self-report questionnaires. The Spanish versions of the Beck Depression Inventory (BDI) (16), the State-Trait Anxiety Inventory (STAI) (17), the West Haven–Yale Multidimensional Pain Inventory (MPI) (18), and the McGill Pain Questionnaire (MPQ) (19) were completed.

Somatosensory Stimulation Task and Recording of Brain Activity
Somatosensory-evoked potentials elicited on tactile stimulation were recorded following a so-called oddball paradigm. During this experimental task, two types of stimuli are presented in a random series such that one of them occurs infrequently (oddball or deviant stimuli). In the present experiment, 480 stimuli were applied to the right hand (frequent stimuli) and 80 stimuli were applied to the left hand (deviant stimuli) in a random order. All stimuli were delivered using a pneumatic stimulator consisting of a small membrane attached to the second digit by a plastic clip and fixated with adhesive strips. Patients received two stimulation blocks; each consisted of 560 stimuli (480 frequent and 80 deviant stimuli) of 100-ms duration with a constant pressure of two bars and a variable interstimuli interval of 550 ms (±50 ms). None of the patients reported discomfort as a result of the tactile stimulation.

During each stimulation block (duration 8 minutes), patients were viewing a sequence of pictures selected from the International Affective Picture System (IAPS) (20). The IAPS constitutes a standardized and exhaustively investigated set of affective pictures containing more than 600 items. The content of the pictures ranges from explicit sexual material, to human injury and surgical slides, to pleasant pictures of children and wildlife. In the present experiment, patients were viewing 40 pictures with negative valence (unpleasant content) and 40 pictures with positive valence (pleasant content). The order of the two stimulation blocks was counterbalanced between the subjects within each group; for half of the participants (12 patients with FM, 8 patients with MSK), the unpleasant picture sequence was presented followed by the pleasant picture sequence, whereas the other half (15 patients with FM, 8 patients with MSK) viewed the affective pictures in the reverse order. Each picture was presented for 6 seconds and was followed by a 6-second blank screen. One deviant and six frequent tactile stimuli were delivered during each slide presentation, as well as during the blank screen. Patients were instructed to ignore tactile stimulation and to pay attention to the slides trying to imagine experiencing themselves in the situations described by the pictures. Subjects were seated in front of a computer screen in a sound-attenuated room, and instructed to keep eye movements and blinks to a minimum during the experiment.

SEPs were recorded from 32 electrodes placed in accordance with the international 10 to 20 system and with reference electrodes at ear mastoids. Nevertheless, for the purposes of the present experiment, only nine electrodes located over the midline (Fz, Cz, Pz), the left (F3, C3, P3), and the right hemisphere (F4, C4, P4) were analyzed. An electrooculogram channel was obtained by placing one electrode above and one below the left eye. Ground was placed anteriorly to the location of the Fpz electrode. Electrode impedance was measured to be less than 10 k{Omega}. The signals were amplified by a BrainAmp amplifier at a sampling rate of 1000 Hz with high and low pass filter setting at 0.10 Hz and 70 Hz, respectively. A 50-Hz notch filter was also applied. EEG was segmented in epochs of 700-ms duration (–100 ms to 600 ms relative to stimulus onset). Averaging was performed for frequent and deviant stimuli separately, and only SEPs elicited by tactile stimulation during the presentation of slides were used. All average waves were digitally filtered (30 Hz low pass) and baseline-corrected before statistical measures of component amplitude were computed.

Previous work has shown that nonpainful tactile stimuli evoke a typical SEP with readily identifiable components at several latencies between 20 and 400 ms (14,15,21). According with these studies and based on visual inspection of the mean waveforms, we calculated the maximal amplitudes (baseline-to-peak) of the following peaks from individual waveforms and for each condition: P50 (defined as the maximum positive amplitude in the time window 20–80 ms after stimulus onset at electrodes C3/C4), N80 (maximum negative amplitude in the time window 60–110 ms after stimulus onset at C3/C4), and P200 (maximum positive amplitude in the time window 135–260 ms after stimulus onset at Cz). Additionally, patients were asked to rate their current clinical pain using a 10-cm visual analog scale at three points during the experiment; at the beginning (after stimulation device was tested), after viewing the unpleasant and after viewing the pleasant slides.

Data Analysis
The study followed a randomized factorial mixed design with the within-subjects factors "type of stimulus" (frequent versus deviant), "emotional context" (viewing unpleasant versus pleasant slides), and "electrode locations" (9 electrodes), and the between-subjects factor "group" (patients with FM versus patients with MSK pain). The effects of these factors on SEP amplitudes were separately examined for each component (P50, N80, and P200) with multivariate repeated-measures analyses of variance (ANOVA). In addition, to further test the topographical effects on SEP amplitudes, subsequent multivariate repeated-measures ANOVAs were carried out separately for midline (Fz, Cz, Pz), and lateral electrode locations over the left (F3, C3, P3) and the right hemisphere (F4, C4, P4). Sociodemographic and questionnaire data were analyzed with two-sample t tests to examine differences between the two groups (patients with FM versus patients with MSK pain) on these variables. For pain ratings, an ANOVA for repeated measures was performed with the factors "emotional context" (baseline, viewing unpleasant versus pleasant slides), "presentation order" (pleasant first versus unpleasant first), and "group" (patients with FM versus patients with MSK pain). Only statistically significant results were reported.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Comparison of Sociodemographic and Pain Characteristics
Descriptive statistics of the self-report measures are shown in Table 1. Pairwise comparisons between patients with FM and patients with MSK pain revealed that both groups were comparable in all the clinical and sociodemographic variables, with the exception of pain duration in years (t[41] = 3.11, p < .01). Nevertheless, both groups did not differ on pain medication or clinical pain ratings.


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  		TABLE 1. Clinical and Sociodemographic Characteristics of the Two Sample of Patients

 

Subjective Pain Ratings
The ANOVA for the subjective ratings of current clinical pain yielded a significant main effect of "emotional context" (F [2, 74] = 4.98, p < .05, Greenhouse-Geisser corrected), reflecting an overall increase in pain ratings after either positive or negative affective slides as compared with baseline ratings. Nevertheless, the primary result of interest was a significant "emotional context" x "group" interaction (F [2, 74] = 3.43, p < .05, Greenhouse-Geisser corrected), showing that patients with FM had higher ratings after viewing the unpleasant slides than after viewing pleasant slides or baseline (F [2, 48] = 6.68, p < .01, Greenhouse-Geisser corrected) (Figure 1). By contrast, no significant differences on current pain ratings were found in patients with MSK pain. In fact, only 4 of 16 patients with MSK pain reported increased subjective pain ratings after viewing unpleasant in comparison to pleasant slides. No significant effects were found resulting from the factor "presentation order" or its interaction with other factors, suggesting that the observed emotional modulation of pain ratings in FM was not influenced by the order of slides (unpleasant first versus pleasant first).



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  		Figure 1. Subjective ratings of ongoing pain for patients with musculoskeletal (MSK) and fibromyalgia (FM) at the beginning of the experiment and after viewing the pleasant and the unpleasant slides.

 

Somatosensory-Evoked Potentials
Figure 2 displays the averaged SEPs elicited by deviant and frequent tactile stimuli for the two patient groups during the presentation of unpleasant and pleasant slides. The scalp topography of the SEPs shows that within the first 150 ms after stimulus onset, the brain activity was more prominent over centroparietal regions on the hemisphere contralateral to the somatosensory stimulation than over the ipsilateral hemisphere, that is, at the left hemisphere for SEPs elicited by frequent stimuli and at the right hemisphere for those elicited by deviant stimuli.



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  		Figure 2. Scalp distribution of somatosensory-evoked potentials (SEPs) elicited by nonpainful tactile stimulation at the second digit of the left (deviant stimuli) or the right hand (frequent stimuli) when patients were viewing either unpleasant or pleasant slides. Waveforms correspond to the SEPs at electrodes C4 and C3 for deviant and frequent stimuli, respectively. Maps represent the scalp distribution at each peak (P50, N80, P200). Time is in milliseconds. MSK indicates musculoskeletal pain; FM = fibromyalgia.

 

The multivariate ANOVA on P50 amplitudes (20–80 ms after stimulus onset) revealed significant interaction effects of "group" x"electrode location" (F [8, 34] = 2.29, p < .05) and "emotional context" x"electrode location" (F [8, 34] = 2.67, p < .05), as well as significant main effects of "emotional context" (F [ 1, 41] = 4.26, p < .05). Basically, these effects indicated that there were significant differences on brain processing of the tactile stimuli depending on specific electrode locations. Therefore, additional ANOVAs were carried out separately for midline (Fz, Cz, Pz) and lateral electrode locations (F3, C3, P3, F4, C4, P4) for a detailed analysis of brain activity elicited by tactile stimulation. These analyses showed that FM showed more enhanced P50 amplitudes than patients with MSK pain at the lateral electrodes (F [6, 36] = 3.17, p < .05), but there were no significant group differences on P50 amplitudes at the midline electrodes (F [3, 39] = 0.32, not significant [NS]). Finally, a subsequent ANOVA conducted separately for each patient group at lateral electrodes showed that P50 amplitudes in patients with FM were greater when viewing unpleasant slides (mean = 1.04 µV, standard error [SE] = 0.16) than when viewing pleasant slides (mean = 0.65 µV, SE = 0.14) (F [6, 21] = 3.83, p < .05), but no differences resulting from "emotional context" were found for patients with MSK pain (unpleasant slides: mean = 0.63 µV, SE = 0.17; pleasant slides: mean = 0.44 µV, SE = 0.12) (F [6, 10] = 0.75, NS).

The multivariate ANOVA on N80 amplitudes (60–110 ms after stimulus onset) yielded significant effects of "emotional context" x "type of stimulus" x "group" (F [1, 41] = 4.63, p < .05), and "emotional context" x "type of stimulus" (F [1, 41] = 4.66, p < .05). Subsequent ANOVAs carried out separately for each group showed that deviant stimuli elicited more enhanced N80 amplitudes during pleasant slides (mean = –0.78 µV, SE = 0.39) as compared with unpleasant slides (mean = 0.15 µV, SE = 0.26) in patients with FM (F [1, 26] = 11.97, p < .01); but no differences were found in patients with MSK pain (unpleasant slides: mean = –0.63 µV, SE = 0.59; pleasant slides: mean = –0.47 µV, SE = 0.54) (F [1, 15] = 0.15, NS). By contrast, no differences resulting from "emotional context" were found on N80 amplitudes elicited by frequent stimuli, neither in the patients with FM (F [1, 26] = 0.37, NS) nor the patients with MSK pain (F [1, 15] = 0.64, NS).

The multivariate ANOVA on P200 amplitudes (135–260 ms after stimulus onset) yielded no significant effects involving the factors "emotional context" or "group."


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
In the present study, we investigated the affective modulation of somatosensory brain processing among patients with FM and patients with chronic MSK pain resulting from identifiable somatic lesions by using a laboratory-based mood induction task and the recording of SEPs elicited by nonpainful tactile stimulation. Patients were instructed to empathize with the mood state induced by pleasant and unpleasant slides, whereas frequent and infrequent target stimuli were simultaneously delivered in a randomized order to the hands. Based on previous studies, it was assumed that patients with FM would be more vulnerable to the influence of negative affect than other patients with chronic MSK pain with somatic lesions (7). Therefore, it was hypothesized that the experimental mood induction would elicit differential effects on brain correlates of somatosensory information processing and subjective pain ratings of patients with FM and patients with MSK pain.

Although we found an overall increase in pain ratings after either positive or negative affective slides, behavioral data provided evidence that current pain was differentially modulated by the emotional context in the two patient groups. Considering that the selected affective slides were clearly different on valence and quite similar on arousal ratings, the fact that current pain significantly increased in FM after viewing the unpleasant slides may suggest an abnormal vulnerability of these patients to the negative emotional context in which pain occurs. By contrast, we observed no influence of the negative emotional context on subjective pain ratings of patients with MSK pain. Thus, the main effect of emotional context on pain ratings remains puzzling and might suggest that the arousal level elicited by the affective slides could also play a relevant role by modulating pain experience. In any case, these results appear to be in line with extensive literature indicating that emotion and pain are strongly associated (22). Our findings are also in agreement with previous work suggesting that pain-related negative affect might contribute to clinical pain, particularly in FM (7,9), and that pain catastrophic thoughts might play an important role in increased pain perception of these patients (8).

Together with the lack of significant effects resulting from the presentation order of the slides and the comparable initial pain ratings of both groups, these results provide further support for the notion of an abnormal processing of body information associated with negative mood states in patients with FM. Recently, Philipps et al. (13) using nonpainful esophageal stimulation and the presentation of fearful versus neutral faces demonstrated a similar effect on a measure of perceived discomfort in healthy volunteers. The authors found that the intensity of the negative emotional context could modulate subjective responses and, more interestingly, modify the neural activity to esophageal stimulation within cerebral regions involved in the processing of visceral sensations.

The present study also demonstrated differential effects of experimental mood induction on brain correlates of somatosensory information processing in patients with FM and MSK pain. Specifically, it was observed that patients with FM displayed a significant enhancement of somatosensory P50, as well as a reduction of N80 amplitudes, when viewing unpleasant slides in comparison to viewing pleasant slides, whereas no differential effect was observed in patients with MSK pain at these latencies. In addition, nonpainful tactile stimulation elicited enhanced P50 amplitudes in patients with FM in comparison to patients with MSK. Earlier P50 and N80 brain responses analyzed in this experiment had a latency of 20 to 110 ms after stimulus onset, representing the primary evoked cortical response to somatic stimulation (23). Scalp topography also showed that the spatial distribution of both SEP components yielded its maximum over the contralateral hemisphere to stimulated body side within the primary somatosensory cortex (S1). These findings suggest the existence of a highly selective perceptual mechanism in FM, involved in the sensory processing of nonpainful tactile information in the central nervous system, which might be influenced by the affective characteristics of the stimulation context. This seems to be in agreement with some evidence showing that early brain activity can be modulated by psychological factors. Thus, for instance, it has been found that some laboratory stressors such as a cold-pressor test or a mental arithmetic task may attenuate the auditory P50 response (24,25). Recently, it has been also reported the existence of a visual-to-auditory crossmodal sensory gating phenomenon at very early processing stages during speech processing (26), as well as a negative correlation between social anhedonia and somatosensory P50 amplitude in a S1–S2 paradigm among patients with schizophrenia (27). Therefore, although it remains unclear what mechanisms may account for the P50 enhancement observed in FM during the unpleasant pictures, our data suggest that affective visual stimuli could differentially modulate the early processing of somatosensory information in these patients.

The present findings are also consistent with previous evidence, supporting the hypothesis of an abnormal activation of pain-related brain regions in FM (2,28–32). For instance, some fMRI studies have shown that patients with FM, in comparison to healthy control subjects, reported more subjective pain and displayed more enhanced activation of pain-related brain regions (including somatosensory cortices, insular cortex, anterior and posterior cingulate) at similar levels of pressure (2,28,29). Plasticity in both the somatosensory and the motor system has been also observed in neuropathic and musculoskeletal pain such as phantom limb pain (33–35), low back pain (36), or complex regional pain syndrome (37). In these studies, a significant positive relationship was found between pain intensity and the amount of cortical reorganization of the somatosensory cortex, reflecting a process of central hyperexcitability that might be responsible for the maintenance of chronic pain in these patients. Similarly, in the present study, we found an abnormal brain processing of bodily information under an aversive context followed by an enhanced perception of clinical pain in FM. Recently, we have also provided a further demonstration that social support may reduce subjective pain ratings and early magnetic brain responses to nonpainful stimulation over the somatosensory cortex in FM (38). Thus, it is tempting to assume that the P50 might be reflecting some kind of plastic changes in brain functioning related to pain perception and the processing of nonpainful information in FM.

Basically, our results point to a disturbed cognitive processing of somatosensory nonpainful information in FM and provide further support for the notion that FM is characterized by an abnormal brain processing of nociceptive, as well as nonnociceptive information (39). Nevertheless, it remains unclear whether these abnormal mechanisms in the processing of somatosensory information within FM could also help to explain the enhanced pain sensitivity and the clinical pain reported by these patients. In this sense, some authors have proposed that attentional factors could also mediate the influence of emotions on pain in humans (40,41). Although our data do not provide direct support for an attentional bias on FM pain, it seems that emotional factors might alter brain processing of nonpainful body information in FM. Other possible shortcoming of the present study was the lack of a healthy control group to compare the effects of the mood induction on brain activity. Nevertheless, healthy control subjects are difficult to compare with clinical groups because they cannot be matched according to illness-related factors, particularly pain history, medication and treatment, social and personal restrictions, and many other factors. To clarify all these issues, further research should investigate whether brain correlates of pain processing can be also modulated by emotional factors in FM, as well as in other chronic pain diseases and healthy subjects.

Summarizing, our data reveal a significant influence of emotional context on pain processing among patients with FM and patients with MSK pain. It also indicates that affective mood states can modulate central nervous excitability thresholds without conscious cognitive processing in chronic pain states. These findings point toward the importance of considering a biopsychosocial model, integrating affective, cognitive, and social factors, to understand the brain mechanisms involved in the origin and maintenance of chronic pain.

The authors thank three anonymous reviewers and Dr. J. Richard Jennings for their helpful comments on a previous version of the manuscript.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 

Research was supported by the Spanish Ministerio de Ciencia y Tecnología, and European Funds (Fondos FEDER) (grant BSO2001-0693).

DOI:10.1097/01.psy.0000188401.55394.18


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

  1. Wolfe FW, Smythe HA, Yunas MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Ables M, Clark P, Fam AG, Farber SJ, Fiechtner JJ, Franklin CM, Gatter RA, Hamty D, Lessard J, Lichtbronn AS, Masi AT, McCain GA, Reynolds WJ, Romano TJ, Russell IJ, Sheon RP. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Arthritis Rheum 1990;33:160–72.[Medline]
  2. Gracely RH, Petzke F, Wolf JM, Clauw DJ. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum 2002;46:1333–43.[CrossRef][Medline]
  3. Lorenz J, Grasedyck K, Bromm B. Middle and long latency somatosensory evoked potentials after painful laser stimulation in patients with fibromyalgia syndrome. Electroencephalogr Clin Neurophysiol 1996;100:165–8.[CrossRef][Medline]
  4. Gibson SJ, Littlejohn GO, Gorman MM, Helme RD, Granges G. Altered heat pain thresholds and cerebral event related potentials following painful CO2 laser stimulation in subjects with fibromyalgia syndrome. Pain 1994;58:185–93.[CrossRef][Medline]
  5. Granot M, Buskila D, Granovsky Y, Sprecher E, Neumann L, Yarnitsky D. Simultaneous recording of late and ultra-late pain evoked potentials in fibromyalgia. Clin Neurophysiol 2001;112:1881–7.[CrossRef][Medline]
  6. Desmeules JA, Cedraschi C, Rapiti E, Baumgartner E, Finckh A, Cohen P, Dayer P, Vischer TL. Neurophysiologic evidence for a central sensitization in patients with fibromyalgia. Arthritis Rheum 2003;48:1420–9.[Medline]
  7. Davis MC, Zautra AJ, Reich JW. Vulnerability to stress among women in chronic pain from fibromyalgia and osteoarthritis. Ann Behav Med 2001;23:215–26.[CrossRef][Medline]
  8. Geisser ME, Casey KL, Brucksch CB, Ribbens CM, Appleton BB, Crofford LJ. Perception of noxious and innocuous heat stimulation among healthy women and women with fibromyalgia: association with mood, somatic focus, and catastrophizing. Pain 2003;102:243–50.[CrossRef][Medline]
  9. Staud R, Robinson ME, Vierck CJ Jr, Cannon RC, Mauderli AP, Price DD. Ratings of experimental pain and pain-related negative affect predict clinical pain in patients with fibromyalgia syndrome. Pain 2003;105:215–22.[CrossRef][Medline]
  10. Meagher MW, Arnau RC, Rhudy JL. Pain and emotion: effects of affective picture modulation. Psychosom Med 2001;63:79–90.[Abstract/Free Full Text]
  11. Weisenberg M, Raz T, Hener T. The influence of film-induced mood on pain perception. Pain 1998;76:365–75.[CrossRef][Medline]
  12. Zelman DC, Howland EW, Nichols SN, Cleeland CS. The effects of induced mood on laboratory pain. Pain 1991;46:105–11.[CrossRef][Medline]
  13. Phillips ML, Gregory LJ, Cullen S, Coen S, Ng V, Andrew C, Giampietro V, Bullmore E, Zelaya F, Amaro E, Thompson DG, Hobson AR, Williams SC, Brammer M, Aziz Q. The effect of negative emotional context on neural and behavioural responses to oesophageal stimulation. Brain 2003;126:669–84.[Abstract/Free Full Text]
  14. Eimer M, Forster B. Modulations of early somatosensory ERP components by transient and sustained spatial attention. Exp Brain Res 2003;151:24–31.[CrossRef][Medline]
  15. Kida T, Nishihira Y, Wasaka T, Nakata H, Sakamoto M. Passive enhancement of the somatosensory P100 and N140 in an active attention task using deviant alone condition. Clin Neurophysiol 2004;115:871–9.[CrossRef][Medline]
  16. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Arch Gen Psychiatry 1961;56:561–71.
  17. Spielberger CD, Gorsuch RL, Lushene RE. The State-Trait Anxiety Inventory (STAI): Test Manual. Palo Alto, CA: Consulting Psychologists Press; 1970.
  18. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale Multidimensional Pain Inventory (WHYMPI). Pain 1985;23:345–56.[CrossRef][Medline]
  19. Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain 1975;1:277–99.[CrossRef][Medline]
  20. Lang PJ, Bradley MM, Cuthbert BN. International Affective Picture System (IAPS): Technical Manual and Affective Ratings. Gainesville: The Center for Research in Psychophysiology, University of Florida; 1997.
  21. Zopf R, Giabbiconi CM, Gruber T, Muller MM. Attentional modulation of the human somatosensory evoked potential in a trial-by-trial spatial cueing and sustained spatial attention task measured with high density 128 channels EEG. Brain Res Cogn Brain Res 2004;20:491–509.[Medline]
  22. Keefe FJ, Lumley M, Anderson T, Lynch T, Studts JL, Carson KL. Pain and emotion: new research directions. J Clin Psychol 2001;57:587–607.[CrossRef][Medline]
  23. Hari R, Reinikainen K, Kaukoranta E, Hamalainen M, Ilmoniemi R, Penttinen A, Salminen J, Teszner D. Somatosensory evoked cerebral magnetic fields from SI and SII in man. Electroencephalogr Clin Neurophysiol 1984;57:254–63.[CrossRef][Medline]
  24. Johnson MR, Adler LE. Transient impairment in P50 auditory sensory gating induced by a cold-pressor test. Biol Psychiatry 1993;33:380–7.[Medline]
  25. Yee CM, White PM. Experimental modification of P50 suppression. Psychophysiology 2001;38:531–9.[CrossRef][Medline]
  26. Lebib R, Papo D, de Bode S, Baudonniere PM. Evidence of a visual-to-auditory cross-modal sensory gating phenomenon as reflected by the human P50 event-related brain potential modulation. Neurosci Lett 2003;341:185–8.[Medline]
  27. Arnfred SM, Chen AC. Exploration of somatosensory P50 gating in schizophrenia spectrum patients: reduced P50 amplitude correlates to social anhedonia. Psychiatry Res 2004;125:147–60.[CrossRef][Medline]
  28. Cook DB, Lange G, Ciccone DS, Liu WC, Steffener J, Natelson BH. Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol 2004;31:364–78.[Medline]
  29. Giesecke T, Gracely RH, Grant MA, Nachemson A, Petzke F, Williams DA, Clauw DJ. Evidence of augmented central pain processing in idiopathic chronic low back pain. Arthritis Rheum 2004;50:613–23.[CrossRef][Medline]
  30. Gracely RH, Geisser ME, Giesecke T, Grant MA, Petzke F, Williams DA, Clauw DJ. Pain catastrophizing and neural responses to pain among persons with fibromyalgia. Brain 2004;127:835–43.[Abstract/Free Full Text]
  31. Chang L, Berman S, Mayer EA, Suyenobu B, Derbyshire S, Naliboff B, Vogt B, FitzGerald L, Mandelkern MA. Brain responses to visceral and somatic stimuli in patients with irritable bowel syndrome with and without fibromyalgia. Am J Gastroenterol 2003;98:1354–61.[CrossRef][Medline]
  32. Wik G, Fischer H, Bragee B, Kristianson M, Fredrikson M. Retrosplenial cortical activation in the fibromyalgia syndrome. Neuroreport 2003;14:619–21.[Medline]
  33. Montoya P, Ritter K, Huse E, Larbig W, Braun C, Topfner S, Lutzenberger W, Grodd W, Flor H, Birbaumer N. The cortical somatotopic map and phantom phenomena in subjects with congenital limb atrophy and traumatic amputees with phantom limb pain. Eur J Neurosci 1998;10:1095–102.[CrossRef][Medline]
  34. Birbaumer N, Lutzenberger W, Montoya P, Larbig W, Unertl K, Topfner S, Grodd W, Taub E, Flor H. Effects of regional anesthesia on phantom limb pain are mirrored in changes in cortical reorganization. J Neurosci 1997;17:5503–8.[Abstract/Free Full Text]
  35. Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N, Larbig W, Taub E. Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation. Nature 1995;375:482–4.[CrossRef][Medline]
  36. Flor H, Braun C, Elbert T, Birbaumer N. Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neurosci Lett 1997;224:5–8.[CrossRef][Medline]
  37. Pleger B, Tegenthoff M, Schwenkreis P, Janssen F, Ragert P, Dinse HR, Volker B, Zenz M, Maier C. Mean sustained pain levels are linked to hemispherical side-to-side differences of primary somatosensory cortex in the complex regional pain syndrome I. Exp Brain Res 2004;155:115–9.[Medline]
  38. Montoya P, Larbig W, Braun C, Preissl H, Birbaumer N. Influence of social support and emotional context on pain processing and magnetic brain responses in fibromyalgia. Arthritis Rheum 2004;50:4035–44.[Medline]
  39. Montoya P, Pauli P, Batra A, Wiedemann G. Altered processing of pain-related information in patients with fibromyalgia. Eur J Pain 2005;9:293–303.[Medline]
  40. Dehghani M, Sharpe L, Nicholas MK. Selective attention to pain-related information in chronic musculoskeletal pain patients. Pain 2003;105:37–46.[Medline]
  41. Keogh E, Ellery D, Hunt C, Hannent I. Selective attentional bias for pain-related stimuli amongst pain fearful individuals. Pain 2001;91:91–100.[CrossRef][Medline]




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