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Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise?

Jo Nijs, Eva Kosek, Jessica Van Oosterwijck UGent and Mira Meeus UGent (2012) PAIN PHYSICIAN. 15(3S). p.ES205-ES213
abstract
Background: Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established (i.e. evidence based), it is currently unclear whether exercise has positive effects on the processes involved in chronic pain (e.g. central pain modulation). Objectives: Reviewing the available evidence addressing the effects of exercise on central pain modulation in patients with chronic pain. Methods: Narrative review. Results: Exercise activates endogenous analgesia in healthy individuals. The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain. Exercise triggers the release of β-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively. The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms. However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain. Muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients. In patients having local muscular pain (e.g. shoulder myalgia), exercising non-painful muscles activates generalized endogenous analgesia. However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations. Limitations: The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy. Conclusions: A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
PNEUMOCEPHALUS, BRADYCARDIA, COMPLICATIONS, ANESTHESIA, CARDIAC-ARREST, STEROID INJECTIONS, chronic neck pain, vasovagal, cardiac accelerator, pneumocephalus, Cardiopulmonary arrest, cervical epidural steroid injection, ASYSTOLE
journal title
PAIN PHYSICIAN
Pain Physician
volume
15
issue
3S
issue title
Opioids
pages
ES205 - ES213
Web of Science type
Review
Web of Science id
000314461300015
ISSN
1533-3159
language
English
UGent publication?
no
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
2964153
handle
http://hdl.handle.net/1854/LU-2964153
alternative location
http://www.painphysicianjournal.com/2012/july/2012;15;ES205-ES213.pdf
date created
2012-07-25 09:11:29
date last changed
2013-07-10 14:22:11
@article{2964153,
  abstract     = {Background: Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established (i.e. evidence based), it is currently unclear whether exercise has positive effects on the processes involved in chronic pain (e.g. central pain modulation).
Objectives: Reviewing the available evidence addressing the effects of exercise on central pain modulation in patients with chronic pain.
Methods: Narrative review.
Results: Exercise activates endogenous analgesia in healthy individuals. The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain. Exercise triggers the release of \ensuremath{\beta}-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating \ensuremath{\mu}-opioid receptors peripherally and centrally, respectively. The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms. However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain. Muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients. In patients having local muscular pain (e.g. shoulder myalgia), exercising non-painful muscles activates generalized endogenous analgesia. However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations.
Limitations: The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy.
Conclusions: A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues.},
  author       = {Nijs, Jo and Kosek, Eva and Van Oosterwijck, Jessica and Meeus, Mira},
  issn         = {1533-3159},
  journal      = {PAIN PHYSICIAN},
  keyword      = {PNEUMOCEPHALUS,BRADYCARDIA,COMPLICATIONS,ANESTHESIA,CARDIAC-ARREST,STEROID INJECTIONS,chronic neck pain,vasovagal,cardiac accelerator,pneumocephalus,Cardiopulmonary arrest,cervical epidural steroid injection,ASYSTOLE},
  language     = {eng},
  number       = {3S},
  pages        = {ES205--ES213},
  title        = {Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise?},
  url          = {http://www.painphysicianjournal.com/2012/july/2012;15;ES205-ES213.pdf},
  volume       = {15},
  year         = {2012},
}

Chicago
Nijs, Jo, Eva Kosek, Jessica Van Oosterwijck, and Mira Meeus. 2012. “Dysfunctional Endogenous Analgesia During Exercise in Patients with Chronic Pain: To Exercise or Not to Exercise?” Pain Physician 15 (3S): ES205–ES213.
APA
Nijs, J., Kosek, E., Van Oosterwijck, J., & Meeus, M. (2012). Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise? PAIN PHYSICIAN, 15(3S), ES205–ES213.
Vancouver
1.
Nijs J, Kosek E, Van Oosterwijck J, Meeus M. Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise? PAIN PHYSICIAN. 2012;15(3S):ES205–ES213.
MLA
Nijs, Jo, Eva Kosek, Jessica Van Oosterwijck, et al. “Dysfunctional Endogenous Analgesia During Exercise in Patients with Chronic Pain: To Exercise or Not to Exercise?” PAIN PHYSICIAN 15.3S (2012): ES205–ES213. Print.