Muscle pain: mechanisms and clinical significance
original abstract†Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
INTRODUCTION: Muscle pain is common, but the understanding of its causes is still patchy. This article addresses the mechanisms of some important types of muscle pain.
METHODS: Selective literature review, predominantly of data derived from neuroanatomical and electrophysiological experiments on anesthetized rats.
RESULTS: Muscle pain is evoked by specialized nerve endings (nociceptors). Important stimuli for muscle pain are adenosintriphosphate (ATP) and a low tissue pH. Excitation of muscle nociceptors leads to hyperexcitability of spinal sensory neurones (central sensitization). Low frequency activity in muscle nociceptors is sufficient to induce central sensitization.
DISCUSSION: Central sensitization leads to increased excitation in the spinal cord and to referral of muscle pain. The motoneurones of a painful muscle are centrally inhibited. Muscular spasm is mostly secondary to a painful lesion in another muscle or joint. The pain of fibromyalgia is assumed to relate to a dysfunction of central nociceptive processing. Psychosocial factors also contribute to pain.
related content
- “Central sensitization: Implications for the diagnosis and treatment of pain,” an article in Pain, 2010.
These two articles on PainScience.com cite Mense 2008 as a source:
- PS Trigger Points & Myofascial Pain Syndrome — A guide to the unfinished science of muscle pain, with reviews of every theory and self-treatment and therapy option
- PS Central Sensitization in Chronic Pain — Pain itself can change how pain works, resulting in more pain with less provocation
