Anneleen Malfliet1, Roselien Pas2, Raf Brouns3, Joris De Win4, Samar M Hatem5, Mira Meeus6, Kelly Ickmans7, Robbert-Jan van Hooff3, Jo Nijs8. 1. Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium; Department of Physiotherapy, Physiology and Anatomy, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium; "Pain in Motion" international research group, www.paininmotion.be. 2. Pain in Motion International Research Group, www.paininmotion.be; Department of Physiotherapy, Human Physiology and Anatomy (KIMA), Vrije Universiteit Brussel, Belgium. 3. Department of Neurology, Universitair Ziekenhuis Brussel, Belgium; Center for Neurosciences (C4N), Vrije Universiteit Brussel, Belgium. 4. Department of Physical Medicine and Rehabilitation, University Hospital Gent, Ghent University, Belgium. 5. Department of Physiotherapy, Human Physiology and Anatomy (KIMA), Vrije Universiteit Brussel, Belgium; Clinic of Physical Medicine and Rehabilitation, Brugmann University Hospital, Belgium; Physical Medicine and Rehabilitation, Vrije Universiteit Brussel, Belgium; Systems & Cognition division (COSY), Institute of Neuroscience, Université catholique de Louvain, Belgium. 6. Department of Rehabilitation Sciences and Physiotherapy, Ghent University, Belgium; Pain in Motion international research group, www.paininmotion.be; Department of Rehabilitation Sciences and Physiotherapy, University of Antwerp, Belgium. 7. Pain in Motion Research Group (www.paininmotion.be); Department of Physiotherapy, Human Physiology and Anatomy (KIMA), Vrije Universiteit Brussel, Belgium; Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Belgium. 8. Pain in Motion Research Group (www.paininmotion.be); Department of Human Physiology and Physiotherapy, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium; Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Brussels, Belgium.
Abstract
BACKGROUND:Pain, fatigue, and concentration difficulties are typical features of chronic fatigue syndrome (CFS). The exact underlying mechanisms of these symptoms are still unknown, but available evidence suggests an important role for impaired pain modulation. As evidence also suggests that pain modulation is related to cardiovascular mechanisms, it seems logical to investigate whether cerebral blood flow (CBF) and heart rate variability (HRV) are altered in these patients. OBJECTIVES: We aimed to investigate the role of the cardiovascular system in pain modulation and symptoms of CFS; the response of CBF and HRV to physical stress and their relation to the change in temporal summation (TS) of pressure pain and self-reported symptoms was evaluated. STUDY DESIGN: A controlled, randomized cross-over trial. SETTING: University Hospital Brussels. METHODS:Twenty CFS patients and 20 sedentary healthy controls were included in this study. In both of the groups, the change in TS of pressure pain, CBF (using transcranial Doppler), and HRV (using finger plethysmography) was examined during physical and emotional stress (to control for potential bias), as well as their association mutually and with self-reported symptoms of pain, fatigue, and concentrations difficulties. RESULTS: There was no significant interaction or group (F-values ranging from .100 to 1.862, P-values ranging from .754 to .181) effect in CBF or HRV parameters. HRV and CBF did change during physical exercise, but the changes did not differ between patients and controls. While pain scores during TS at the trapezius site reduced in the control group after the physical exercise protocol (P = .037), they did not change in the CFS group (P = .108), suggesting impaired pain modulation. There were no significant correlations between CBF, HRV, TS, and self-reported symptoms (all P-values of correlation analyses > .01). LIMITATIONS: Although effect sizes were medium to large, the study sample was relatively low. Also, the mild nature of the exercise bout is discussable. Nonetheless, this mild exercise was able to provoke endogenous pain modulation in the control group, which endorsed a proper execution of the cycling exercise. Moreover, mild exercises are more applicable to daily physical activities in CFS patients than vigorous exercises. CONCLUSION: These results seem to refute the previously suggested alterations of CBF/HRV in CFS patients. These cardiovascular parameters appear not to explain pain before, during, and following exercise. KEY WORDS: Chronic pain, physical exercise, emotional stress, pain modulation, cardiovascular systems, temporal summation, pain pressure thresholds, transcranial Doppler, plethysmography.
RCT Entities:
BACKGROUND:Pain, fatigue, and concentration difficulties are typical features of chronic fatigue syndrome (CFS). The exact underlying mechanisms of these symptoms are still unknown, but available evidence suggests an important role for impaired pain modulation. As evidence also suggests that pain modulation is related to cardiovascular mechanisms, it seems logical to investigate whether cerebral blood flow (CBF) and heart rate variability (HRV) are altered in these patients. OBJECTIVES: We aimed to investigate the role of the cardiovascular system in pain modulation and symptoms of CFS; the response of CBF and HRV to physical stress and their relation to the change in temporal summation (TS) of pressure pain and self-reported symptoms was evaluated. STUDY DESIGN: A controlled, randomized cross-over trial. SETTING: University Hospital Brussels. METHODS: Twenty CFS patients and 20 sedentary healthy controls were included in this study. In both of the groups, the change in TS of pressure pain, CBF (using transcranial Doppler), and HRV (using finger plethysmography) was examined during physical and emotional stress (to control for potential bias), as well as their association mutually and with self-reported symptoms of pain, fatigue, and concentrations difficulties. RESULTS: There was no significant interaction or group (F-values ranging from .100 to 1.862, P-values ranging from .754 to .181) effect in CBF or HRV parameters. HRV and CBF did change during physical exercise, but the changes did not differ between patients and controls. While pain scores during TS at the trapezius site reduced in the control group after the physical exercise protocol (P = .037), they did not change in the CFS group (P = .108), suggesting impaired pain modulation. There were no significant correlations between CBF, HRV, TS, and self-reported symptoms (all P-values of correlation analyses > .01). LIMITATIONS: Although effect sizes were medium to large, the study sample was relatively low. Also, the mild nature of the exercise bout is discussable. Nonetheless, this mild exercise was able to provoke endogenous pain modulation in the control group, which endorsed a proper execution of the cycling exercise. Moreover, mild exercises are more applicable to daily physical activities in CFS patients than vigorous exercises. CONCLUSION: These results seem to refute the previously suggested alterations of CBF/HRV in CFS patients. These cardiovascular parameters appear not to explain pain before, during, and following exercise. KEY WORDS: Chronic pain, physical exercise, emotional stress, pain modulation, cardiovascular systems, temporal summation, pain pressure thresholds, transcranial Doppler, plethysmography.