In the recent blog post some may feel it is remiss of Fernández-de-las-Peñas not to have at least considered the possibility that the clinical phenomena attributed to the so-called latent TrP (trigger point) could also be explained as arising from sensitised peripheral neural tissue. This concept was suggested nearly 25 years ago  and again more recently . Both historical clinical evidence from the medical literature  and relevant animal experimental studies [4,5] support this proposition.
Moreover, there is increasing recognition that in response to danger the peripheral nervous system directly communicates with the immune system, forming an integrated protective mechanism via neurogenic inflammation . This mechanism provides a plausible explanation for the biochemical findings reported by Shah et al. [7,8] in their studies of the tissue milieu of putative trigger points.
The error in logical argument repeatedly made by proponents of the “myofascial pain/trigger point” explanatory hypothesis is known as “begging the question”. Their argument as to the tissue or tissues wherein the pathology lies can persuade only those who have faith in their conclusion. Proponents of the theory remain locked in a circular argument – that is, because muscles contain them, “myofascial pain” must arise from “myofascial trigger points”.
But as Robert Gerwin , a prominent proponent of myofascial pain syndrome (MPS) recently conceded: “To say that MPS always requires a TrP in order to make the diagnosis is a tautology in the absence of credible evidence because then no diagnosis of MPS could be made in the absence of a TrP.”
In his book Café Chats (1920), Spanish neuroscientist Santiago Ramón y Cajal [1852-1934] penned a relevant aphorism: “That which enters the mind through reason can be corrected. That which is admitted through faith, hardly ever.” Such is the nature of faith!
About John Quintner
John Quintner is a retired physician in Rheumatology and Pain Medicine who is currently a volunteer with Arthritis and Osteoporosis WA. He is now interested in contributing to pain education for health professionals and consumers. John has long been active as an iconoclast in the field of pain theory and practice. The prime targets have been myofascial pain theory and the North American fibromyalgia construct. His skeptical approach has been well balanced by Milton Cohen’s critical analytical skills, and Geoffrey Bove’s inspired experimental approaches. Most of John’s useful ideas have come to him whilst “in the zone” atop his long-cherished bicycle.
 Quintner JL, Cohen ML. Referred pain of peripheral neural origin: an alternative to the “Myofascial Pain” construct. Clin J Pain 1994; 10: 243-251.
 Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatol 2015; 54: 392-9.
 Quintner JL, Bove GM. From neuralgia to peripheral neuropathic pain: evolution of a concept. RAPM 2001; 26(4): 368-372.
 Govea RM, Barbe MF, Bove GM. Group IV nociceptors develop axonal chemical sensitivity during neuritis and following treatment of the sciatic nerve with vinblastine. J Neurophysiol 2017; 118: 2103-2109.
 Satkeviciute I, Goodwin G, Bove GN, Dilley A. Time course of ongoing activity during neuritis and following axonal transport disruption. Neurophysiol 2018; 119(5): 1993-2000. doi: 10.1152/jn.00882.2017
 Chiu IM, von Hehn CA, Woolf CJ. Neurogenic inflammation and the peripheral nervous system in host defense and immunopathology. Nature Neuroscience 2012; 15(8): 1063-1067. doi:10.1038/nn.3144
 Shah JP, Phillips TM, Danoff JV, et al. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol 2005; 99:1977-84.
 Shah J, Danoff J, Desai M, et al. Biochemicals Associated With Pain and Inflammation are Elevated in Sites Near to and Remote From Active Myofascial Trigger Points. Arch Phys Med Rehab 2008; 89:16-23.
 Gerwin R. Trigger point diagnosis: at last, the first word on consensus. Pain Med 2018; 19(1): 1-2. doi: 10.1093/pm/pnx219