Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Abstract

There are a number of biochemical, biomechanical, endocrinological and neurovascular mechanisms underpinning the anti-nociceptive and anti-inflammatory effects of dry needling (DN). While myofascial trigger points likely play a role in peripheral pain, a diagnostic tool for localizing them has not been validated, and DN studies that have targeted trigger points to elicit localized twitch responses have reported mixed results. Therefore, the mechanism responsible for DN-mediated analgesia may be more complicated. DN activates opioid-based pain reduction, mediated by endogenous cannabinoids and the sympathetic nervous system, and non-opioid pain relief via serotonin and norepinephrine from the brain stem. DN also triggers the hypothalamic-pituitary-adrenal axis centrally and the corticotropin releasing hormone-proopiomelanocortin-corticosteroid axis locally to inhibit cox-2, reducing inflammatory cytokines. Recent studies demonstrate that DN combined with mechanical and/or electrical stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels, to include TRPV, ASIC, TTX and P2X/Y. Electrical DN (EDN) stimulates immune cells, fibroblasts and keratinocytes to release CGRP and substance-P, altering the stimulation of TTX receptors to reverse hyperalgesia. It also encourages the supraoptic nucleus to release oxytocin to quiet ASIC receptors peripherally and stimulate opioid interneurons spinally. Moreover, EDN inhibits ERK1/2 kinase pathways of inflammation in the spinal cord and stimulates Aδ fibers and N/OFQ to reverse C-fiber mediated central changes. Mechanotransduction of fibroblasts and peripheral nerves via TRPV1 and P2X/Y-mediated intracellular Ca 2+ wave propagation and subsequent activation of the nucleus accumbens inhibits spinal pain transmission via glycinergic and opioidergic interneurons. The increased ATP is metabolized to adenosine, which activates P1 purinergic receptors, events considered key to DN analgesia and rho kinase-based tissue remodeling. Mechanotransduction-mediated release of histamine further explains analgesia secondary to needling points distal to pain. DN-mediated analgesia is dependent on a number of synergistic physiologic events involving biochemical and mechanical processes in neural, connective and muscle tissue.

The local twitch response during trigger point dry needling: Is it necessary for successful outcomes?

“…Interestingly, studies from the acupuncture literature report an initial increase of CGRP and SP after needling in the absence of a LTR (Butts et al, 2016;Wu et al, 2015). The added CGRP may initiate a cascade of vasodilators, to include nitric oxide, which may lead to a washout effect (Shinbara et al, 2013(Shinbara et al, , 2015.…”

“…The latter explanation is particularly interesting, as CGRP has been shown to propagate inflammation in high quantities but provide potent anti-inflammatory actions in low quantities (Zijlstra et al, 2003). In this case, leaving needles in situ with intermittent stimulation via winding or electric stimulation may be more advantageous than TrPDN with a LTR, as it may facilitate continuous low levels of SP and CGRP over time, thereby leading to lasting reduction of peripheral pain (Butts et al, 2016).…”

“…The accumulation of adenosine activates A1 adenosine receptors and provides a strong anti nociceptive effect via inhibition of adenylate cyclase (Takano et al, 2012). The intracellular Ca2þ propagation also helps initiate rho kinase mediated tissue remodeling and blocks pain at the level of the spine by stimulating glycinergic and GABAergic interneurons (Butts et al, 2016;Goldman et al, 2013;Langevin et al, 2011;Zhou et al, 2008). Importantly, insertion (and likely repeated insertion) of the needle was shown to not be enough to activate TRPv1 receptors and initiate the analgesic cascade.…”

Platelet-Rich Plasma in Treatment of Plantar Fasciitis: Randomized Double-Blinded Placebo Controlled Study

“…In the present study, the percent change reflecting a reduction in the plantar fascia thickness was significantly higher in the PRP group than in the saline group. Ultrasound has proven to be a useful tool to assess plantar fasciitis through the production of high-quality spatial resolution sonograms [28].…”

“…It has been suggested that the beneficial effect of needling results from improved muscle activation pattern, increased joint range of motion, and alleviation of pain [35]. In the context of plantar fasciitis, needling may be responsible for the central release of opioid peptides, increased regional blood flow and anti-inflammatory effects presumably through inhibition of production of tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 [28,36]. Rastegar et al [36] compared the effect of needling and steroid injection in the treatment of plantar fasciitis.…”