Dysfunctional Endogenous Analgesia During Exercise in Patients with Chronic Pain: To Exercise or Not

[Dolphin]

Free full text: http://www.painphysicianjournal.com/2012/july/2012;15;ES205-ES213.pdf

Pain Physician 2012; 15:ES205-ES213 • ISSN 2150-1149

Dysfunctional Endogenous Analgesia During Exercise in Patients with Chronic Pain: To Exercise or Not to Exercise?

Narrative Review
Jo Nijs, PhD, Eva Kosek, MD, PhD, Jessica VanOosterwijck, PhD, and Mira Meeus, PhD

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 beta-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.

Key words: Whiplash, fibromyalgia, chronic pain, low back pain, exercise, rehabilitation,
chronic fatigue syndrome, osteoarthritis, rheumatoid arthritis, sensitization, shoulder

 

[biophile]

The studies showing dysfunctional EA during exercise in some chronic pain conditions do not contradict the clinical evidence favoring the use of exercise as an intervention for chronic pain. Exercise is an effective treatment for chronic whiplash associated disorders (10,11), fibromyalgia (13,14), chronic fatigue syndrome (61,62), osteoarthritis (48), and rheumatoid arthritis (49). Hence, its clinical use and benefits should not be questioned. To exercise or not to exercise patients with chronic pain, is no longer the question. On the other hand, the dysfunctional EA during exercise in patients with chronic pain should not be ignored.

61. Wallman KE, Morton AR, Goodman C, Grove R, Guilfoyle AM. Randomised controlled trial of graded exercise in chronic fatigue syndrome. Med J Austral 2004; 180:444-448.

62. Edmonds M, McGuire H, Price J. Exercise therapy for chronic fatigue syndrome. Cochrane Database Syst Rev 2004 ;3:CD003200.pub2. DOI: 10.1002/14651858.CD003200.pub2.

"But how?" Of course, GET and cognitive restructuring are presented as the answer.

Clinically cognitive-emotional sensitization is typically addressed in comprehensive pain management programs that include pain physiology education to address illness perceptions and maladaptive pain cognitions, stress management, time-contingent activity management (i.e. graded activity), and time-contingent exercise therapy (i.e. graded exercise therapy) (Table 1).

 

[mellster]

I think one could try to combine anti inflammatories, lactic acid reducers with a general opiod stimulating therapy such as LDN to increase exercise tolerance.

 

[Battery Muncher]

Interesting thoughts, mellster. What works as a lactic acid reducer? Is it available over the counter? And what is LDN?

 

[Sam Carter]

Interesting thoughts, mellster. What works as a lactic acid reducer? Is it available over the counter? And what is LDN?

LDN = low dose naltrexone (an opioid antagonist).

 

[Simon]

I've only read the absract, but some of the findings are interesting:

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.

So, for example, while exercise leads to pain killing effects in healthy individuals, it leads to the reverse in fibromyalgia. I think that's important. And the conclusion about avoiding exacerbating sypmptoms is certainly at odds with the PACE GET cavalier advice for dealing with setbacks ("Carry on!").

 

[biophile]

If "exercise therapy should be individually tailored with emphasis on prevention of symptom flares", then many patients won't be doing any additional exercise at all then.