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Muscle pain syndromes: Hypersensitivity and treatment

Issue no 6 (vol. 7) of Current Pain and Headache Reports, to be published in December 2003, has several interesting articles on muscle pain syndromes such as fibromyalgia and myofascial pain syndrome.

K.G. Henriksson (at the Faculty of Health Sciences, Linkoping University, Sweden) has written a review, ”Hypersensitivity in muscle pain syndromes”, presenting research regarding the pathogenesis of hypersensitivity in these syndromes. From the abstract:

In a disorder such as fibromyalgia, decreased pain thresholds also are found at sites where there is no tenderness. Pathogenetic mechanisms for allodynia and hyperalgesia can be identified at several levels of the nociceptive system, from the nociceptors in the muscle to the cortex. Central sensitization of nociceptive neurons in the dorsal horn and a disturbed balance between inhibitory and facilitatory impulses in the descending tracts from the brain stem to the dorsal horn are the main mechanisms for pain hypersensitivity. Changes in function, biochemical make-up, and synaptic connections in the nociceptive neurons in the dorsal horn are considered to be caused by neuronal plasticity.

Nathan J. Rudin at the Department of Orthopedics and Rehabilitation, University of Wisconsin Medical School, writes in his ”Evaluation of treatments for myofascial pain syndrome and fibromyalgia” about ”available treatments for MPS and FM in the context of pathophysiology, clinical evidence, and experimental support” and hopes this information will be helpful in ”designing individualized treatment for patients with these complex syndromes”.

Thomas Graven-Nielsen and Lars Arendt-Nielsen at the Laboratory for Experimental Pain Research, Aalborg University in Denmark, write in ”Induction and assessment of muscle pain, referred pain, and muscular hyperalgesia” about several methods for this induction (from the abstract):

Ischemic and exercise-induced muscle pain are typical endogenous pain models; external stimulation with mechanical, electrical, and chemical modalities constitute the exogenous models. These models are a good basis to study the muscle sensitivity, muscle pain responses under normal and pathophysiologic conditions, and drug efficacy on specific muscle pain mechanisms. When evaluating muscle pain in clinical or experimental settings, it is important to assess parameters related to the pain intensity, pain quality, referred and local distribution, and the deep tissue sensitivity in local and referred areas. The experimental test paradigm must include different stimulation modalities (multimodal) to obtain sufficiently advanced and differentiated information about the human nociceptive system under normal and pathophysiologic conditions because the different stimuli activate different receptors, pathways, and mechanisms. This may be a useful approach in future mechanism-based classification and treatment of muscle pain. Similarly, the multimodal approach is important in clinical studies to provide evidence for which specific muscle pain modalities and mechanisms are affected and how they are modulated by pharmacologic approaches.

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