Referred muscle pain is primarily peripheral in origin: The “barrier-dam” theory

SummaryThe mechanisms leading to the frequent occurrence of referred muscle pain (RP) are largely unknown. It is possible that RP is caused by the increased sensitivity of local muscle nociceptors and/or by a central sensitisation. When deep pressure by palpation is used on a subject with smooth fibrotic lesions (myofibrosis) in a muscle, RP can originate as a hyperalgesic cutaneous area, adjacent to, or totally apart from the pressure pain locus. It is currently postulated that a chain reaction is activated implicating triggering of an ever-increasing number of afferent neurons and facilitation of the synaptic connection at the level of the spinal cord, causing more distally a distributed RP via convergent efferent pathways. The human interpretation of this phenomenon can be misleading when the tested person positions, after a few seconds, his RP distally from the site of pressure to the distally located RP area. As a result of what we have found in our experimentally induced RP probes, we hypothesize that deep pressure on a myofibrosis will, in the first place, within a few seconds, increase the nociceptive excitability of the afferent sensitive nerves from the RP area to the local spot of pressure on the muscle, which in return will, in the second place, excite the whole dependent RP area. The mechanism for referred muscle pain proposed in this article is linked to the “pre-local hyper-excitability theory” or “barrier-dam theory”. The afferent sensitive peripheral nerves might be entrapped in local muscle hardenings (barrier-dam) with the consequence of the hyper-excitation of pre-local nerves between the distally referred pain area and the local muscular zone of tenderness. The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa. Clinical and fundamental studies with experimentally induced RP are nevertheless needed to examine the hypothesis.