Exercise, Not to Exercise, or How to Exercise in Patients With Chronic Pain? Applying Science to Practice

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Abstract

Exercise is an effective treatment strategy in various chronic musculoskeletal pain disorders, including chronic neck pain, osteoarthritis, headache, fibromyalgia and chronic low back pain. Although exercise can benefit those with chronic pain (CP), some patients (eg, those with fibromyalgia, myalgic encephalomyelitis/chronic fatigue syndrome and chronic whiplash associated disorders) encounter exercise as a pain inducing stimulus and report symptom flares due to exercise. This paper focuses on the clinical benefits and detrimental effects of exercise in patients with CP. It summarizes the positive and negative effects of exercise therapy in migraine and tension-type headache and provides an overview of the scientific evidence of dysfunctional endogenous analgesia during exercise in patients with certain types of CP. Further, the paper explains the relationship between exercise and recovery highlighting the need to address recovery strategies as well as exercise regimes in the rehabilitation of these patients. The characteristics, demands and strategies of adequate recovery to compensate stress from exercise and return to homeostatic balance will be described. narrative review. Exercise is shown to be effective in the treatment of chronic tension-type headache and migraine. Aerobic exercise is the best option in migraine prophylaxis, whereas specific neck and shoulder exercises is a better choice in treating chronic tension-type headache. Besides the consensus that exercise therapy is beneficial in the treatment of CP, the lack of endogenous analgesia in some CP disorders should not be ignored. Clinicians should account for this when treating CP patients. Furthermore, optimizing the balance between exercise and recovery is of crucial merit in order to avoid stress-related detrimental effects and achieve optimal functioning in patients with CP. Exercise therapy has found to be beneficial in CP, but it should be appropriately and individually tailored with emphasis on prevention of symptom flares and applying adequate recovery strategies.

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Mark J Millan (2002)

Upon receipt in the dorsal horn (DH) of the spinal cord, nociceptive (pain-signalling) information from the viscera, skin and other organs is subject to extensive processing by a diversity of mechanisms, certain of which enhance, and certain of which inhibit, its transfer to higher centres. In this regard, a network of descending pathways projecting from cerebral structures to the DH plays a complex and crucial role. Specific centrifugal pathways either suppress (descending inhibition) or potentiate (descending facilitation) passage of nociceptive messages to the brain. Engagement of descending inhibition by the opioid analgesic, morphine, fulfils an important role in its pain-relieving properties, while induction of analgesia by the adrenergic agonist, clonidine, reflects actions at alpha(2)-adrenoceptors (alpha(2)-ARs) in the DH normally recruited by descending pathways. However, opioids and adrenergic agents exploit but a tiny fraction of the vast panoply of mechanisms now known to be involved in the induction and/or expression of descending controls. For example, no drug interfering with descending facilitation is currently available for clinical use. The present review focuses on: (1) the organisation of descending pathways and their pathophysiological significance; (2) the role of individual transmitters and specific receptor types in the modulation and expression of mechanisms of descending inhibition and facilitation and (3) the advantages and limitations of established and innovative analgesic strategies which act by manipulation of descending controls. Knowledge of descending pathways has increased exponentially in recent years, so this is an opportune moment to survey their operation and therapeutic relevance to the improved management of pain.

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L. Kelman (2007)

The aim of this study was to evaluate and define the triggers of the acute migraine attack. Patients rated triggers on a 0-3 scale for the average headache. Demographics, prodrome, aura, headache characteristics, postdrome, medication responsiveness, acute and chronic disability, sleep characteristics and social and personal characteristics were also recorded. One thousand two hundred and seven International Classification of Headache Disorders-2 (1.1-1.2, and 1.5.1) patients were evaluated, of whom 75.9% reported triggers (40.4% infrequently, 26.7% frequently and 8.8% very frequently). The trigger frequencies were stress (79.7%), hormones in women (65.1%), not eating (57.3%), weather (53.2%), sleep disturbance (49.8%), perfume or odour (43.7%), neck pain (38.4%), light(s) (38.1%), alcohol (37.8%), smoke (35.7%), sleeping late (32.0%), heat (30.3%), food (26.9%), exercise (22.1%) and sexual activity (5.2%). Triggers were more likely to be associated with a more florid acute migraine attack. Differences were seen between women and men, aura and no aura, episodic and chronic migraine, and between migraine and probable migraine.