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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 electric stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels, to include TRPV, ASIC, TTX and P2X/Y. Electric 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 Ca2+ 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.
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Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals
Raymond Butts1*, James Dunning1, Thomas Perreault1,2, Firas Mourad1 and Matthew Grubb3
1American Academy of Manipulative Therapy, 1036 Old Breckenridge Ln Montgomery, AL 36117, USA
2Portsmouth Physical Therapy, 161 Corporate Drive Portsmouth, NH 03801, USA
3Palmetto Health Research Physical Therapy Specialists, 3010 Farrow Rd. Columbia, SC 29203, USA
*Corresponding author: Raymond Butts, American Academy of Manipulative Therapy, AAMT Fellowship in Orthopaedic Manual Physical Therapy Coordinator 1036
Old Breckenridge Ln Montgomery, AL 36117, USA, Tel: 803-422-3954; E-mail: buttsraymond@yahoo.com
Received date: February 4, 2016; Accepted date: March 17, 2016; Published date: March 21, 2016
Copyright: ©2016 Butts R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original author and source are credited.
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 fibers and N/OFQ to reverse C-fiber mediated central changes. Mechanotransduction of fibroblasts
and peripheral nerves via TRPV1 and P2X/Y-mediated intracellular Ca2+ 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.
Introduction
Over the last 20 years, the number of Americans seeking
acupuncture treatment has continued to rise. While less than 1% of the
U.S. population sought acupuncture treatment in the early 90’s, over 12
million Americans received acupuncture in 2010 [1]. Moreover, 2007
NHIS data suggests that the vast majority of Americans seeking
acupuncture do so for pain-related conditions, primarily arthritis, and
other types of musculoskeletal pain, headaches, and bromyalgia [1].
Another intervention that uses thin liform needles to penetrate the
skin is dry needling (DN). A procedure commonly used by Western-
based, health care professionals (i.e. physicians, osteopaths,
chiropractors, physical therapists, etc.), DN has also gained popularity
in the United States for the treatment of neuromusculoskeletal
conditions over the past 10 years. As Dunning et al. suggested, while
the terminology, philosophy, and theoretical constructs dier between
Western-based DN and traditional Chinese acupuncture, the
procedure of inserting monolaments into the body is essentially the
same [2]. erefore, manual DN and electrical DN (EDN) are used
synonymously with manual acupuncture and electroacupuncture,
respectively, throughout this narrative review to describe needling
procedures without medicine or injectate that penetrate the skin to
varying tissue depths. Furthermore, given the number of clinical trials
authored by acupuncturists not claiming to move “
qi
along channels
or meridians for the purpose of treating traditional Chinese medicine
(TCM) diagnoses such as blood stagnation and
bi
syndrome,
practitioners of DN should not ignore or abandon the acupuncture
literature [2]. On the contrary, evidence-based, health care
practitioners should pay attention to large-scale trials that describe
location, depth and stimulation of needles, and treatment duration
used to successfully treat neuromusculoskeletal conditions, regardless
of profession, while carefully considering the biochemical,
biomechanical, endocrinological, neurovascular, supraspinal and
segmental mechanisms underlying needling treatments without
injectate [2,3]. While the former is manageable, the latter is oen
overlooked. e purpose of this narrative review is to provide a
convenient, clinical resource tool for Western-based, health care
providers on the peripheral and spinal mechanisms responsible for
pain reduction following DN.
International Journal of Physical
Medicine & Rehabilitation Butts et al., Int J Phys Med Rehabil 2016, 4:2
http://dx.doi.org/10.4172/2329-9096.1000327
Review Open Access
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
e Physiology of Pain Related to Myofascial Trigger
Points
e “integrated hypothesis” of myofascial trigger point (MTrP)
formation was originally proposed by Travell and Simons in 1993 and
later expanded by Gerwin et al. [4]. e hypothesis suggests that
excessive acetylcholine (ACh) and subsequent Ca2+ release initiates a
continuous cycle of localized muscle contraction [4]. e increased
Ca2+ release from sarcoplasmic reticulum (SR) is likely the product of
muscle overuse or contracture, [5-7] while extracellular Ca2+ may
represent sarcolemma damage via muscle overload or trauma [8,9].
Importantly, a number of studies have recorded a signicant increase
of end plate noise in MTrP vs. non-MTrP locations, which seem to
correlate with patient irritability [8,10,11]. e localized hypertonicity
begins to block blood ow to the muscle, resulting in a shortage of
oxygen and nutrients and leading to ischemia and hypoxia [4,8].
Local ischemia and hypoxia lead to the release of a number of
chemicals responsible for propagating pain and inammation such as
bradykinin, prostaglandins, serotonin, calcitonin gene-related peptide
(CGRP) and substance P (SP) along with a number of inammatory
cytokines, such as tumor necrosis factor-α (TNF- α), interleukin-1β
(IL-1β, interleukin-6 (IL-6) and interleukin-8 (IL-8) [4,12]. ere is
also a signicant release of H+ ions and adenosine triphosphate (ATP)
[12]. e extracellular increase in H+ ions results in a drop in pH,
which directly aects the action of acetylcholinesterase, an enzyme
required to remove ACh from the neuromuscular junction. e acidic
environment exaggerates the release of CGRP, which inactivates
acetylcholinesterase, while the low pH directly inhibits it [4,12,13].
Gerwin et al. further reported that CGRP intensies the response of
muscle bers to ACh by increasing the sensitivity and synthesis of
receptors at the neuromuscular junction [4]. e increased metabolic
demand further depletes any remaining intracellular ATP, eectively
shutting down the Ca2+-ATPase pump’s ability to reuptake Ca2+ back
into the SR [14]. Inhibited acetylcholinesterase allows hypersensitive
ligand-gated receptors on the sarcolemma continuous access to ACh,
and improperly functioning Ca2+-ATPase pumps permit Ca2+ to
continuously bind with troponin, collectively resulting in hypertonicity
and propagating the metabolic crisis. Notably, Shah et al. found a
signicant increase in H+ ions, bradykinin, CGRP, SP, TNF-α, IL-1β,
serotonin and norepinephrine in patients with active trigger points
compared to patients with latent and no trigger points in their upper
trapezius muscles [12,15]. e continuous presence of factors of pain
and inammation sets the stage for peripheral hyperalgesia.
Vessel compression resulting in an ischemic or hypoxic
environment could also be due to the formation of scar tissue in the
subacute and chronic patient [16]. Biomechanical deciencies such as
scoliosis, leg length discrepancy, pelvic torsion and facet joint
dysfunction could also serve as primary catalysts [17,18]. In the case of
facet joint dysfunction, the muscles that attach to or are associated
with the displaced or xated vertebrae would be tonically pulled,
stretched and/or irritated [19-21]. is would invariably activate
muscle spindles, located in the intrafusal aspect of the muscle. e
result is activation of type 1a and type II aerents, which stimulate
alpha and gamma motor neurons, respectively [22]. Alpha motor
neurons increase muscle tension to counter the stretch, while gamma
motor neurons maintain the sensitivity of the muscle spindles [22]. In
the case of an irritated facet, the continuous activation of α motor
neurons by muscle spindles could certainly propagate a cycle of
hypertonicity, catalyzing a metabolic crisis. Interestingly, however,
there is no evidence of persistent alpha motor neuron activity to
account for this hypertonicity [23]. Rather, the sustained muscle
contraction quickly fatigues, and the metabolic crisis results in factors
of pain and inammation, which stimulate chemo sensitive type III
and IV muscle spindle aerents [24,25]. Type III and IV aerents
inhibit alpha motor neurons [26] while stimulating beta and gamma
motor neurons in a positive-feedback loop [22]. While beta and
gamma motor neurons continue to sensitize muscle spindles,
propagating the cycle of pain and inammation, beta motor neurons
are able to directly stimulate extrafusal muscle bers, resulting in a
sustained, silent contraction more commonly referred to clinically as a
palpable taught band [22]. us, muscle spindles seem to play a
primary role in the formation of MTrPs.
Interestingly, Hubbard and Berkho originally hypothesized that
the electrical noise coming from active trigger points in the upper
trapezius was due to muscles spindles [11]. However, Simons found an
increase in motor endplates and not muscle spindles in the vicinity of
the trigger point [27]. Moreover the waveform of the noise in active
trigger points was consistent with motor endplate and not muscle
spindle activity [27]. Traditionally, electrophysiological recordings of
end plate noise consist of endplate potentials, caused by spontaneous
ACh release from neuromuscular junctions, and end plate spikes, the
result of needle irritation of the neuromuscular junction [22,28,29].
However, more recent studies suggest that the electrical noise is
produced by extrafusal neuromuscular junctions, while the
combination of noise and spikes demonstrates intrafusal activity in the
vicinity of the motor endplates [22]. Moreover the spikes may be
unique to intrafusal activity, representing the activation of gamma and
beta motor neurons by muscle spindles [22,30,31]. ese ndings
again strongly implicate the role of muscle spindles in trigger point
formation and maintenance.
e pain-spasm-pain model of hypertonicity also lends itself well to
the cycle of pain typically associated with trigger points. Originally
proposed by Travell et al. [6] and developed by Johansson and Sojka
[32], the model suggests that, regardless of the mechanism, hyperactive
muscle produces an increase in metabolic by-products such as lactic
and arachidonic acid, eventually resulting in vascularly compromised
tissue, which further drops the pH through the release of H+ ions.
Interestingly, Shah found that even in absence of muscle damage,
acidity was the primary driving force leading to mechanical
hyperalgesia [12,15]. e pain stimulates groups II, III and IV muscle
aerents, which provides continuous excitatory projections to γ motor
neurons in laminae-9 in the ventral horn of the spinal cord [22]. Since
γ motor neurons control the sensitivity of muscle spindles, their
stimulation increases the probability that muscle spindles will activate
α motor neurons, thereby propagating the cycle of hypertonicity [33].
Interestingly, Lund et al. recently conrmed the presence of pain
receptors within muscle spindles [34]. As the authors suggest,
activation of these nociceptors may allow spindles to auto-sensitize
and directly propagate the “γ-gain” cycle, further implicating their role
in the formation of MTrPs [34].
e model of “γ -gain” has been demonstrated in a number of
studies of joint pain. In particular, facet joint pain has been shown to
activate γ motor neurons and thereby increase the sensitivity of muscle
spindles [35-37]. In addition, numerous studies have demonstrated
that spinal manipulation increases the aerent discharge from
mechanoreceptors and subsequently quiets α motor neurons, resulting
in reduced EMG activity of paraspinal muscles [38]. Notably, one of
the most published and well-recognized researchers from the
acupuncture profession, Chang-Zern Hong, found that he could
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 2 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
reproduce trigger point pain in the rhomboid by adding pressure to the
C4-C5 facet joint, but he could not reproduce pain in the facet joint by
placing a needle in the trigger point [39]. As such, Hong concluded
that needling patients with paraspinal dysfunction is not justied until
they receive other non-invasive treatments such as spinal
manipulation, as the trigger point is likely the product of facet
dysfunction. erefore, and as Hong suggests, spinal manipulation and
needling techniques may work well additively to treat trigger point
related dysfunction [39].
e Treatment of Myofascial Trigger Points with Dry
Needling
While the above explanation provides an excellent theoretical
construct for how MTrPs form and ultimately lead to pain, it does not
necessarily imply that trigger points are the primary target for DN
procedures [2]. Presently, there is a lack of robust, empirical evidence
validating the clinical diagnostic criteria for MTrPs [40] proposed by
Travell and Simons [41,42] and Fischer [43,44]. In a systematic review
by Myburgh et al., “tenderness” was the only criteria found to be
moderately reliable for trigger point identication and only in the
upper trapezius [45]. at is, examiners were able to agree that the
upper trapezius was tender because of a trigger point but not on the
actual location of the trigger point within the muscle. Moreover, while
the intra and inter-rater reliability of identifying a muscle with a MTrP
(not the location of the trigger point within the muscle) seems to
improve with clinical experience and knowledge of the impairment,
experts in myofascial pain syndrome and bromyalgia were unable to
reliably identify taught bands, active trigger points and localized
twitches when blinded to patient condition [46]. According to Sciotti
et al., the inter-examiner error associated with identifying the location
of trigger points in muscle ranges between 3.3 and 6.6 cm [47]. It is
therefore unlikely that clinicians are able to accurately target trigger
points in a reliable fashion with monolament needles between .025
mm and 0.35 mm wide [47].
e Physiology and Relevance of the Localized Twitch
Response
Based on the expanded integrated hypothesis, the primary objective
of needling MTrPs is to clear excessive ACh from neuromuscular
junctions and facilitate Ca2+ reuptake back into the SP [4]. By
repeatedly tapping a needle onto sensitive loci within MTrPs via a
technique commonly referred to as “pistoning, nociceptive aerent
information is thought to be sent to the spinal cord, resulting in the
activation of α motor neurons [48,49]. is results in a reexive
localized twitch response (LTR) that may be analogous to blowing up
the neuromuscular junction [49]. e LTR seems to be reproducible
until the excess ACh at the neuromuscular junction is depleted.
Moreover, a number of studies have demonstrated a reduction in
endplate noise following the LTR [48,50]. Shah et al. further reported a
reduction in CGRP and SP following a LTR in the upper trapezius and
a subsequent drop in pain and disability [12].
While clearing excessive ACh from neuromuscular junctions seems
advantageous, the results of controlled trials that aim to target trigger
points and elicit a LTR are inconsistent with respect to their ability to
reduce pain and disability. Two recent studies found no correlation
between LTR and treatment success rate aer needling the upper
trapezius [51] and brachialis muscle [52]. It is not presently known
whether the reduction of CGRP and SP is the product of the LTR or
simply a “wash-out” eect of an increase in blood ow secondary to
needling [53]. Also, while the LTR is able to produce immediate results
in pain and disability, the improvements are oen not long-term
[54,55]. Moreover, the repeated pistoning of the needle required to
elicit a LTR has been shown to be traumatic to muscle tissue, resulting
in added inammation and discomfort [56]. Interestingly, Qerama et
al. injected botulinum toxin into the vicinity of trigger points in the
infraspinatus, signicantly reducing the activity of the end plate
potentials. However, the injection did not inuence the patient’s pain
intensity and mechanical pain threshold, raising the question whether
the LTR is a clinically relevant phenomenon [57]. Aer injecting 312
painful sites throughout the body, Lewit found that needles, not the
injectate, resulted in immediate analgesia in 86.8% of his patients [58].
Notably, only 2 of the 14 most common treatment sites were muscle
tissue [58]. at is, 12 of the most common structures targeted by
Lewit did not have neuromuscular junctions required to cause a LTR.
Similarly, much of the work by Baldry further suggests that needling
the subcutaneous tissue overlaying a MTrP provides enough depth for
a successful outcome [59]. e fact that the needles never entered the
muscle tissue suggests that the LTR may not be a crucial component of
the treatment.
e Cellular Correlates of Peripheral Pain
Peripheral nerve endings contain a number of channels and
receptors that recognize various types of pain information [60]. ere
are a number of intra-cellular signal-transduction mechanisms that
process and integrate the information via protein kinase enzymes [60].
Interestingly, a number of studies have suggested that protein kinase C-
epsilon (PKC-ε) may be a commonality among the major cellular
mechanisms of peripheral hypersensitivity that provides a switch
separating acute conditions from central mediated chronic pain, a
concept more formally referred to as hyperalgesic priming [61,62-64].
Rats that were injected with carrageenan (low dose prostaglandin) had
an inammatory response, likely mediated by voltage gated
tetrodotoxin (TTX) currents via EP3 prostaglandin receptors, which
lasted 4-hours and then resolved [61]. However, if the rat was again
injected with carrageenan, the resulting inammation was more severe
and lasted for at least 24-hours [61]. During the initial injection, a PKA
inhibitor was enough to inhibit the hyperalgesia, but aer the second
injection, the PKA inhibitor was no longer sucient. Rather, the
hyperalgesia ended only aer treatment with a PKC-ε inhibitor.
Repeated painful stimuli have also been shown to result in the
conversion of previously insensitive, unresponsive, or silent sensory
aerents into active nociceptors [65]. It is therefore not surprising that
Hong found a signicant increase of sensitive loci in the area of MTrPs.
It is likely the increase in sensitive loci that Hong is referring to is not
the creation of new loci but the “awakening” of previously silent
nociceptors [66]. us, repeated pain stimuli likely activate cellular
cascades mediated by PKC-ε, leading to peripheral hypersensitivity.
e Transition of Peripheral Pain to Central-mediated
Chronic Dysfunction
e cell bodies of rst-order nociceptive neurons are located in the
dorsal root ganglia (DRG). ese cells are pseudo-unipolar, as each
neuron has a single axon that branches into two parts. One part
extends to the periphery to become a nerve ending, while the second
part moves centrally to connect with second order nociceptive neurons
in the dorsal horn of the spinal cord. C-ber mediated pain is received
by the cell bodies of the DRG and subsequently results in release of
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 3 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
glutamate and SP from the presynaptic terminal in the dorsal horn of
the spinal cord [12,67]. e glutamate is initially received by ligand-
gated, NMDA and AMPA receptors. While the glutamate allows Na2+
and K+ to enter the postsynaptic terminal, it is not enough to open
NMDA channels secondary to an Mg2+ block [67]. However, when a
sustained amount of glutamate is present, enough Na2+ and K+ are able
to move through AMPA receptors to depolarize the postsynaptic
membrane and unblock the Mg2+ [67]. At the same time, substance-P
activates NK-1 receptors, further phosphorylating NMDA receptors
and facilitating the movement of Ca2+ through the NMDA channels
[67]. e inux of Ca2+ results in a number of metabolic and genetic
changes such as: 1. Production of Cox-2, an enzyme responsible for
speeding up the production of prostaglandin [12], 2. Greater sensitivity
of existing NMDA channels [67], 3. Synthesis of proteins required for
new channels [66] and 4. Activating previously dormant NMDA
channels [12,67,68]. rough this process, pain information is more
eciently relayed to the spinothalamic tract, a condition more
commonly referred to clinically as hypersensitivity or hyperalgesia.
e over activation and subsequent opening of AMPA and NMDA
channels leads to a toxic increase in Ca2+ activated enzymes in the
postsynaptic neuron, resulting in cell death [12,67]. As the cell
disintegrates, it causes a cytotoxic environment, which ultimately
results in interneuron apoptosis [12,67]. is is signicant, as
interneurons manage the receptive elds of dorsal horn neurons.
When disinhibited, dorsal horn neurons may therefore become
stimulated by previously silent, ineective or unused synapses from
rst order nociceptors [12,67]. For example, while both the
semitendinosus and the adductor magnus have the same proximal
attachment on the ischial tuberosity, nociceptors from the two muscles
correspond with their own unique dorsal horn neuron or group of
neurons. However, there are also likely a number of silent or unused
synapses from rst order semitendinosus nociceptors on adductor
magnus dorsal horn neurons and vice versa that are typically managed
by interneurons.
In the event of an injury resulting in chronic proximal inammation
of the adductor magnus whereby interneurons are lost, the previously
silent or unused synapses may become active, resulting in the
perception of pain over the adductor magnus and semitendinosus.
Given that dorsal horn neurons receive aerents from the skin, muscle
and viscera, these synapses are also susceptible to sensitization due to
interneuron apoptosis. Importantly, dis-inhibition of the dorsal horn
via interneuron apoptosis is a primary mechanism of peripheral
referred pain [12,67]. SP, glutamate, and ATP from apoptotic cells also
directly stimulate glial cells in the dorsal horn such as astrocytes and
microglia to produce cytokines, thereby propagating spinal
hyperalgesia [67] (Figures 1A-1C).
e resultant decrease in pain threshold and expansion of sensory
receptive elds is more formally referred to as central sensitization
[12]. In this case, the repeated C-ber stimuli, known as wind-up pain,
are thought to be the mechanism responsible for central sensitization
[69]. Previous studies have demonstrated increased sensitivity to
mechanical stimulation and receptive eld expansion in dorsal horn
neurons following injection of bradykinen into the lumbar multidus
[69,70]. By recording pain threshold following repeated stimuli to
peripheral C-bers, a number of studies have also reported wind-up
related, central sensitization in patients with low back pain [71-73]
TMJ pain [74] shoulder pain [75] and bromyalgia [76].
Figure 1A: Normal processing of acute pain in the spine.
Figure 1B: Subacute or chronic C-ber mediated pain increases the
release of glutamate and substance-P from sensory aerents in
spine, leading to hypersensitivity of second order, dorsal horn
neurons.
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 4 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
Figure 1C: Subacute or chronic C-ber mediated pain increases the
release of glutamate and substance-P from sensory aerents in the
spine, leading to disinhibition of second-order, dorsal horn neuron
receptive elds.
e Physiology and Relevance of Needle
Mechanotransduction
rough a series of elegant studies, Langevin et al. found that a
greater pullout force is required to remove a needle from tissue when
the needle is wound in one direction compared to when it is wound in
both directions [76,78]. Moreover, there was a greater pullout force
following uni- and bidirectional winding compared to needle insertion
without manipulation [77,78]. By using trichrome staining, Langevin
further demonstrated that pullout force is due to the mechanical
coupling of collagen bers to the needle [77]. e mechanical coupling
directly pulls on collagen bers, resulting in better alignment of
collagen bundles, and stimulates cells via mechanotranduction [79].
Importantly, Langevin noted that, “acupuncture needle rotation (either
uni- or bidirectional) may be important to initiate needle grasp, but
other types of needle manipulation such as pistoning may also
eectively transmit a mechanical signal to cells once needle grasp has
been initiated” [77]. at is, pistoning in the absence of winding is not
justied to elicit mechanotransduction. Consistent with this nding, a
recent study by Zhang et al. found that needle rotation resulted in
signicantly greater C-ber activation, distal supercial and deep
mechanoreceptors and stretch receptors compared to liing, thrusting,
scraping, shaking, and icking [80].
e Eect of Dry Needling Mechanotransduction on TRPv1
Receptors
Of the 4 primary channels/receptors that play a role in peripheral
hyperalgesia, TRP receptors are arguably the most intriguing given
their possible role in DN-mediated analgesia [81,82]. Interestingly,
TRPv1 receptors, TRPv4 receptors and ASIC3 channels are sensitive to
changes in PH and/or temperature, but these channels are also
responsive to mechanical stimulation [81,82]. e mechanical
stimulation provided by DN may therefore have the ability to inuence
the very same channels responsible for sensing pain and inammation
and mediating hypersensitivity. Wu et al. used immunouorescence to
demonstrate the presence of more TRPv1 receptors and ASIC3
channels at ST36 (proximal tibialis anterior) compared to a non-
acupoint location [82]. However, pharmaceutical stimulation revealed
that only the TRPv1 agonist reproduced the analgesic eects of DN at
ST36 [82].
According to Wu et al. [82] the mechanotransduction of tissue
stimulates TRPv1 receptors on both neural and non-neural cells,
resulting in intracellular calcium wave propagation (CWP). e CWP
causes the release of ATP from pannexin-1 hemi-channels. As the ATP
catabolizes to ADP, it stimulates P2X and P2Y purinergic receptors,
respectively, on the same neuron or other neurons. Interestingly,
TRPv1 stimulation of non-neural cells [83,84] also results in CWP and
ATP release, likely amplifying the stimulation of P2X and P2Y
receptors on neurons, a process that has previously been demonstrated
in intestinal broblasts [85] and keratinocytes [86] following tissue
mechanotransduction.
Interestingly, the stimulation of neuronal P2X and P2Y receptors
results in brief pain and is therefore a possible correlate of
de qi
(subjective report of a deep pressure or spreading warmth upon needle
insertion and manipulation). In both cases, the intercellular CWP is
amplied, leading to alteration of C-ber aerents and, subsequently,
the release of glutamate from rst order sensory aerents [87].
According to Zhou et al. the altered C-ber excitation stimulates
glycinergic interneurons in laminae-2 of the spinal cord to release
glycine [87]. When glycine receptors on postsynaptic dorsal horn
neurons receive glycine, they attenuate pain transmission [87]. e
noxious stimulus-induced analgesia (NSIA) from DN also likely
stimulates the nucleus accumbens, resulting in opioid release. e
subsequent stimulation of μ and κ opioid receptors on interneurons in
the dorsal horn results in the release of GABA and glycine, further
inhibiting the transmission of pain information from sensory aerents
to second order dorsal horn neurons [82,88] us, the stimulation of
TRPv1 receptors via tissue mechanotransduction may help explain the
physiologic mechanism responsible for DN-mediated peripheral
analgesia. Given this mechanism, it is perhaps relevant to point out
that most acupuncturists consider
de qi
to be a crucial parameter in
eective needling treatments for pain [89,90]. Also, stimulation of the
“acupuncture responding channel” TRPv1 only achieved analgesia
when the needle was manipulated at ST-36. When the needle was
inserted but not manipulated, the treatment outcome was no better
than sham (Figure 2) [82].
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 5 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
Figure 2: DN-mediated analgesia secondary to TRPv1 activation,
ATP release, and the subsequent stimulation of PX/Y purinergic
receptors. e resulting CWP inhibits pain at the level of the spine
[91].
e Eect of Dry Needling Mechanotransduction on P1
Purinergic Receptors
Dry Needling has been shown to attenuate hyperalgesia via the P1
purinergic receptor family in models of both neuropathic and
inammatory pain [92]. Goldman et al. found a signicant release of
ATP, ADP and adenosine in the interstitial uid following 30-minutes
of manual DN at ST36, a phenomenon that is likely mediated via
stimulation of TRPv1 receptors and subsequent CWP [92]. e level of
ATP signicantly increased but returned to normal aer 30-minutes,
while the level of adenosine increased during the 30-minute period
24X and remained at 60-minutes post treatment [92]. Importantly,
mechanical stimulation of the needle via rotation every 5-minutes is
thought to initially stimulate TRPv1 receptors, facilitating ATP release
from sensory aerents via Pannexin-1 channels. e ATP is
catabolized to ADP and eventually adenosine, stimulating P2X, P2Y
and A1 receptors, respectively [92-95]. While genetically normal mice
suering from inammation or neuropathic pain experienced
signicant improvements in mechanical and heat analgesia secondary
to DN, A1 receptor knock-out mice did not [92]. Moreover, only
normal mice experienced signicantly less activation in the anterior
cingulate cortex, an area of the brain related to the experience or
emotional aspects of pain. In addition, Goldman et al. found that
administering deoxycoformycin [92] inhibited enzymes responsible for
extracellular adenosine breakdown, resulting in accumulation of
adenosine and prolonging the analgesic eect of the DN [92].
Takano et al. also performed DN at ST36 for 30-minutes, during
which the needle was rotated bilaterally to elicit
de qi
every 5-minutes
and found a signicant increase in interstitial adenosine [96]. Previous
studies have linked activation of A1 adenosine receptors located on
nerve endings [97], aerent nerves [98] and pre-synaptic DRG
terminals [99] with anti-nociception. As G-protein coupled receptors,
A1 receptor activation is thought to work by inhibiting adenylyl
cyclase, attenuating Camp and phospholipase C [96]. Since an increase
in Camp is associated with chronic pain, the inhibition of adenylyl
cyclase is noteworthy [96]. Given that opioids also inhibit adenylyl
cyclase, there may be a link between adenosine A1 receptors and
opioid receptors, suggesting that activation of one may result in
analgesia support from the other [100]. us, adenosine also seems to
play a key role in DN-mediated analgesia. However, consistent with
Wu et al., Takano et al. noted that ATP release secondary to DN is not
observed without needle manipulation. In the absence of ATP,
intracellular CWP and A1 adenosine receptor stimulation is not
possible, and the analgesic eects of DN are lost [96]. ese ndings
support the commonly held belief that needle insertion is not enough
to relieve pain (Figure 3) [96].
Figure 3: DN-mediated analgesia secondary to the stimulation of
TRPv1 receptors and subsequent release of ATP. e ATP
stimulates P2X/Y receptors, resulting in an intracellular CWP. e
ATP also catabolizes to adensosine, which activates A1 adenosine
receptors, inhibiting adenylyl cyclase and blocking pain [91].
e Eect of Dry Needling Mechanotransduction on Mast
Cells
e number of mast cells (MCs) located at acupoints, to include
ST36, SP6, GB34, LI4, LI11 and PC6 has been shown to be 50% higher
than at non-acupoint locations [101]. A number of studies have linked
the physical stimulation of needles with the activation of stretch-
sensitive chloride channels on MCs, resulting in degranulation
[83,102-104]. Some factors initially released during degranulation such
as cytokines, serotonin and SP result in discomfort and may add to the
perception of
de qi
[80,102]. However, given that MCs are primarily
located in loose connective tissue, the cells eectively connect sensory
aerents to blood and lymphatic vessels and therefore play a role in
vasodilation by releasing histamine, heparin, leukotrienes and NO
[80,102,105]. While MC degranulation also directly results in ATP
release [102,105], histamine further stimulates ATP release from
subcutaneous broblasts, amplifying P2X/P2Y and adenosine
mediated pain reduction [83].
Notably, blocking MC degranulation by disodium chromoglycate
abolished the analgesic eects of DN [106]. Also, the degranulation of
MCs further emphasizes the importance of needle manipulation. By
comparing 3 types of needle manipulation, a deep needling group, a
supercial needling group and a group in which the needle was
bilaterally rotated, Choi et al. found that rotation lead to greater
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 6 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
improvement in pressure pain threshold compared to the two groups
in which the needle was simply inserted, regardless of depth [107].
Moreover, there was a signicant correlation of needle sensation (
de
qi
) secondary to needle rotation and improvement in pain pressure
threshold [107].
Dry Needling Mechanotransduction and Tissue
Restructuring
e mechanical stimulation via winding or twirling of needles and
application of electricity leads to mechanotransduction of broblasts
secondary to their adhesion to collagen bers, resulting in a signicant
increase in the elongation, cell perimeter, and cross sectional area
along with increased lamilapodia formation and upregulation of
mechanical signaling markers such as Rho and Rac kinases [79,108].
Importantly, these structural and genetic changes have been shown to
occur in the vicinity of and distal to the needle insertion site [108]. In
addition, mechanotransduction has been shown to cause ATP release
from keratinocytes [93] broblasts [93] MCs [109] and other tissue
types [93]. e extracellular ATP is quickly broken down into
adenosine, mediating the reduction in pain and inammation typically
associated with DN. Before doing so, however, the ATP is recognized
by purinergic P2X/P2Y receptors on broblasts, resulting in an inux
of cytosolic Ca2+ [110]. e CWP leads to the transient disassembly of
polymerized actin and the subsequent decrease in broblast stress
bers [110]. Simply put, a reduction of broblast stress bers changes
the viscoelastic properties of the cells, allowing them to be more easily
remodeled. Interestingly, this process requires mechanotransduction,
as using cyclopiazonic acid to increase intracellular Ca2+ was not
enough to alter the actin cytoskeleton in the absence of P2X/P2Y
receptor activation [110]. Moreover, the inhibition of rho kinase, a
product of DN-mediated mechanotransduction, prevented viscoelastic
changes in broblasts [110,111].
Langevin et al. found that broblasts actively contribute to
viscoelastic nature of the entire tissue in which they are found via a
rho-dependent mechanism [112]. Scar tissue and brotic tissue are
typically painful, structurally thicker and less elastic than healthy tissue
[112]. However, DN mediated mechanotransduction of broblasts may
be able to help remodel painful tissue by dampening tissue tension via
actin polymerization [110]. A number of studies have demonstrated
the use of DN to reduce pain associated with scar [58,113] and brotic
tissue [114] further supporting this possibility.
Dry Needling Mechanotransduction and Tissue Healing
DN is thought to improve tendon healing via a three-pronged
approach. Inammation typically reduces type 1 collagen synthesis,
but DN has been shown to decrease cytokines responsible for
inammation via activation of toll-like receptors on broblasts
[115,116]. is action sets an appropriate environment for collagen
remodeling and production. DN-mediated mechanotransduction
stimulates rho/rac kinases, disrupting the actin cytoskeleton, and
allowing the tissue to be reorganized [108,115]. Finally, mechanical
stimulation of broblasts results in collagen synthesis via activation of
mitogen activated protein kinases (MAPK). MAPK, the most
prominent kinase activated by mechanotransduction, initiates the
extracellular signal regulated-kinase ½ (ERK½) pathway [117]. ERK
stimulates the production of Type-1 collagen bers via transcription
factors such as activator protein-1 [115,117]. Interestingly, a recent
study by Park et al. found that DN at GB34 turned on 236 genes
secondary to the ERK cascade [118]. Moreover, blocking the ERK
pathway inhibited the anti-nociceptive eects of DN, suggesting that
ERK may be the biochemical hallmark of DN analgesia [118].
e Physiology and Relevance of Electrical Dry
Needling
A number of studies have also demonstrated a direct eect of
electrical dry needling (EDN) on P2X2 and P2X3 purinergic receptors
[119,120]. Despite their role in peripheral hyperalgesia following
inammation and neuropathic pain, the literature has only reported
on the use of EDN to aect P2X2 and P2X3 receptors exclusively in
neuropathic pain models [119,120]. Following a chronic constriction
injury to rat hind legs, the number of P2X3 receptors in the L4-L5
DRG increased, corresponding with mechanical and thermal
hyperalgesia. Aer 7 days of ipsilateral or contralateral EDN to GB34
and ST-36 X30 minutes, however, there was a signicant reduction in
P2X3 expression [119], attenuation of ATP stimuli [119] and an
improvement in thermal and mechanical pain thresholds [120].
Calcitonin Gene Regulated Peptide and Substance-P
Evidence from the acupuncture literature suggests that EDN results
in a signicant increase in peripheral CGRP and SP [80,121], a nding
that is counterintuitive given that the primary function of SP and
CGRP is to propagate pain and inammation [67,122]. While the
discomfort associated with DN likely leads to the release of SP and
CGRP-β from peripheral nerve terminals, the mechanical stimulation
also causes release from non-neural sources. Previous studies have
shown that more than 50% of SP may be released in peripheral tissue
from monocytes, macrophages, keratinocytes, broblasts, lymphocytes
and platelets, especially in pathologic conditions [80]. ere are two
primary theories for the early increase in SP and CGRP following DN.
First, the additional neuropeptides provided by non-neurologic
sources could provide negative feedback onto auto receptors located on
nerve endings [80]. Second, the increase in SP may function to regulate
peripheral levels of CGRP [123]. e latter is particularly intriguing,
given that CGRP has been shown to propagate inammation in high
quantities but provides potent [123-125] anti-inammatory actions in
low concentrations via TTX channel inhibition.
Consistent with the proposed mechanism of hyperalgesia priming,
the eect that CGRP has on TTX channels is PKA and PKC dependent
[126] and repeated or sustained exposure to CGRP could tip the
balance toward PKC-ε and ip the cellular switch from an acute to a
chronic pain response [127,128]. It is also interesting to note that while
a series of high-dose injections of CGRP are required to stimulate
PKC-ε, a sustained low-dose CGRP managed by SP and stimulated by
EDN may be able to ip the switch in the opposite direction [124].
erefore, the analgesic eects of EDN may be due to partial depletion
of peripheral CGRP stores followed by a low-level, sustained release of
CGRP. As for SP, EDN eventually results in reduction of SP release
from the dorsal horn and peripheral nerve endings [129-131].
us, while manual stimulation of acupuncture needles initially
increases peripheral levels of CGRP and SP, the addition of electricity
may allow clinicians to maintain appropriate levels of SP and CGRP to
block cellular correlates of hyperalgesia, thereby inhibiting pain and
breaking the cycle of chronicity. It is perhaps worth pointing out that
RCTs from the acupuncture literature achieve better analgesia by
adding electricity than by brief or intermittent manual stimulation
alone [132]. While only one systematic review has directly compared
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 7 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
the outcomes of EDN to manual DN, the use of EDN for joint
osteoarthritis was superior (Figure 4) [133].
Figure 4A: EDN-mediated analgesia secondary to potentiation of
TTX channels. A. Needle manipulation plus EDN facilitates a
sustained release of low-dose CGRP, leading to analgesia.
Figure 4B: A sustained exposure to CGRP activates PKC-ε to
sensitize TTX, ASIC and TRPv1 receptors, leading to hyperalgesia.
C. A brief exposure to CGRP activates PKA to sensitize TTX
channels, leading to the perception of brief pain [91].
Electro-Dry Needling for Joint Osteoarthritis: Underlying
Mechanisms
e fact that CGRP promotes inammation acutely is somewhat of
a paradox, as the ability of CGRP to increase blood ow through
vasodilation has been shown to contribute to tissue healing [134]. A
recent study demonstrated that DN is able to promote tendon healing
via angiogenesis and broblast migration via CGRP release from
sensory nerve endings and mechanical stimulation of collagen bers,
respectively [135,136]. In general, CGRP causes vasodilation by
binding to CGRP1 receptors on vascular smooth muscle, resulting in
the increase of PKA. e subsequent opening of K channels and
reduction of Ca2+ results in smooth muscle relaxation and vasodilation
[134]. e increase in PKA also stimulates nitric oxide (NO) synthase,
an enzyme responsible for producing NO, thereby enhancing the
response [134]. Zhang et al. further hypothesized that DN may directly
stimulate the sympathetic nervous system to release NO by creating an
“axon reex” within densely innervated tissue [80].
e role of CGRP in joint OA is particularly counterintuitive, as the
pain associated with joint OA has been linked to an upregulation of
vascular and neural tissue (with CGRP and substance P) in the vicinity
of joint structures that are typically aneural [137,138]. However, given
that DN has been shown to improve pain in osteoarthritic joints using
traditional acupoint and non-acupoint locations, [139] most
researchers believe that the general eect of DN may be due to
improved blood ow. Following EDN to the vastus medialis, Lazaro et
al. measured a signicant increase in arteriolar diameter and a
persistent increase in mean arterial pressure of arterioles supporting
the knee joint [140]. Since the vasodilation disappeared upon
application of L-name, a NO synthase inhibitor, the resulting change in
vasodilation was likely due to an increase in NO. Whether CGRP also
plays a role has yet to be determined, but given the numerous studies
that report an increase of CGRP post DN and the potential for CGRP
to mediate NO release from endothelial cells, [124,134] it is also a
likely player in the vasodilation. Importantly, blocking neuromuscular
junctions with succinylcholine, a nicotinic Ach receptor blocker, also
inhibited vasodilation, suggesting that muscle contraction via EDN
may be required for CGRP and NO-mediated vasodilation [140].
e increased blood ow likely has three primary eects on joints
with OA. First, while the role of microvascular restriction is unclear, a
recent study by Hussain et al. found that patients with retinal arteriole
narrowing are twice as likely to develop knee OA and require a knee
replacement [141]. is nding suggests that reduced microcirculation
of the knee is likely a factor in the development of OA, to include the
muscles that surround the joint [141,142]. Similarly, Biberthaler et al.
noted less microcirculation in degenerative rotator cu lesions [143].
In this regard, EDN may be able to improve vascularity of the joint via
CGRP and NO, thereby stopping and/or reversing symptoms
associated with osteoarthritis. Second, a number of studies have shown
a signicant reduction of inammatory cytokines in the synovial uid
of osteoarthritic joints post DN [144,145]. e increased blood ow
likely facilitates the recruitment of opioid producing immune cells
required to reduce the level of inammatory cytokines. Ahsin et al.
reported a signicant increase in plasma β-endorphin levels aer EDN
to local points at the knee that correlated with reductions in pain,
stiness and disability, which is likely due to vasodilation [144]. EDN
further blocks the local release of IL-1 β and TNF-α in the synovia of
osteoarthritic joints [145] and the systemic release of IL-1 β and TNF-
α by inhibiting melanocortin-4 in the periaqueductal gray of the brain
stem [146]. ird, there is limited evidence suggesting that DN may
stimulate an increase in hyaluronic acid, allowing the synovial uid to
better lubricate the joint [147].
Bajaj et al. also reported a signicant increase in the number of
latent MTrPs in the muscles surrounding osteoarthritic joints [148].
Moreover, the number of latent trigger points corresponded to positive
ndings of osteoarthritis on radiographs. However, EDN-mediated
vasodilation may help combat the physiology associated with MTrPs
by reversing the hypoxic environment mediating the energy crisis.
Given that Cagnie et al. reported an immediate improvement in blood
ow and oxygen saturation following DN in the upper trapezius, DN
may also have therapeutic value for muscles associated with joint OA
[149].
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 8 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
Stimulation of the Neuroendocrine System via Dry
Needling
EDN may also help to reduce and/or normalize systemic
inammation via activation of the hypothalamic-pituitary-adrenal
(HPA) axis. Li et al. measured a signicant increase in corticotrophin
releasing hormone (CRH) from the paraventricular nucleus,
adrenocorticotropic hormone (ACTH) from the anterior pituitary and
corticosterone (cortisol in humans) from the adrenal cortex in
response to inammation via complete Freund’s adjuvant (CFA) [150].
Interestingly, EDN exaggerated the response of the HPA axis in
inamed rats but not in healthy controls, suggesting a unique role of
EDN in the presence of inammation [150]. While ACTH was found
to play no role in EDN mediated analgesia, CRH stimulated beta-
endorphins from the paraventricular nucleus [150]. Corticosterone
also prevents the production of inammatory cytokines by inhibiting
TNF-α and cox-2 [151]. Following an injection of CFA, EDN was able
to control the resulting edema by stimulating a 10-fold increase in
corticosterone. When corticosterone receptors were chemically
blocked, however, the anti-inammatory eects of DN were lost [152].
Corticotrophin Releasing Hormone Proopiomelanocortin
Corticosteroid Axis
Much like the HPA axis, human dermal broblasts have a CRH-
POMC-corticosteroid axis that responds to local stressors such as solar,
thermal and mechanical stress [153] to include EDN [154]. Human
dermal broblasts have the ability to produce CRH and express CRH
receptors. When the CRH receptor is activated, it stimulates
proopiomelanocortin (POMC) gene and protein expression via the
second messenger cAMP, leading to the production and release of
ACTH [155]. Unlike the HPA axis, in the CRH-POMC-corticosteroid
axis, both CRH and ACTH stimulate the production of corticosterone
from broblasts [155]. Importantly, CRH has also been shown to
directly stimulate opioids release from immune cells, and CRH
antagonists have been shown to block EDN’s ability to inhibit pain in
inammatory tissue [156]. Corticosterone locally inhibits
inammatory cytokines, prostaglandin and cox-2, thereby optimizing
opioid-based pain reduction [146,151,154]. e CRH-POMC-
corticosteroid axis provides another mechanism by which EDN may be
able to have an eect peripherally via non-neural cells and may further
explain the positive eects of supercial DN.
ASIC Channels
A number of studies have linked ASIC3 to mechanical but not heat
hyperalgesia following carrageenan-induced inammation and a series
of acid injections [157,158]. Chen et al. further noted an up regulation
of ASIC3 channels in DRG neurons following carrageenan and CFA
models of inammation in mice, a phenomenon stopped and reversed
by DN at ST36 [158]. At rst glance, these ndings suggest that DN
may exploit the mechanical aspects of the receptor to reverse
hyperalgesia. Unlike TRPv1 receptors, however, there is little evidence
to support that down regulation of ASIC channels is a result of tissue
mechanotransduction [82]. Rather, in the case of ASIC channels, the
down regulation seems to be mediated by oxytocin. According to Yang
et al., DN results in elevated oxytocin in the supraoptic nucleus but,
surprisingly, not the paraventricular nucleus of the thalamus [159].
Yang et al. further demonstrated a dose-dependent, enhanced analgesic
eect of DN with stimulation of the supraoptic nucleus and a minimal
analgesic eect when the nucleus was ablated [160]. According to Qiu
et al. the activation of vasopressin (V1A) receptors by oxytocin
released form the posterior pituitary is thought to trigger calcineurin-
dependent phosphorylation of ASIC channels, decreasing the
amplitude of ASIC currents, acid-evoked membrane excitability, and
the depolarization amplitude secondary to acid stimuli [161]. In
addition, oxytocin has been shown to inhibit pain directly by binding
to oxytocin receptors (OXTR) on rst order sensory aerents, second
order neurons and GABAergic interneurons in the spinal cord,
inhibiting the transmission of pain [162]. us, the stimulation of
oxytocin from the supraoptic nucleus may help account for the
physiologic mechanism responsible for DN mediated peripheral
analgesia (Figure 5).
Figure 5: DN-mediated analgesia secondary to potentiation of ASIC
channels. Needling stimulates oxytocin release from the posterior
pituitary. e oxytocin inhibits ASIC channels peripherally by
activating vasopressin receptors. Oxytocin also activates GABAergic
interneurons, rst order sensory aerents, and second order dorsal
horn neurons to block pain at the level of the spine [91,163].
e Physiology of Aβ bre Stimulation Secondary to Dry
Needling
e interneurons of the dorsal horn also play a primary role in
managing pain information being relayed from the peripheral to the
central nervous system in the spinal cord. According to Melzack and
Wall, inhibitory interneurons reside primarily in lamina II and III of
the dorsal horn, a region more commonly referred to as the substantia
gelatinosa (SG) [164]. Aerents provided by small myelinated Aδ and
unmyelintated C-bers synapse with second order dorsal horn neurons
in lamina V, inhibiting interneurons in the SG and relaying pain
information to the CNS. When large-diameter Aβ bers are activated
via non-nociceptive stimuli, interneurons of the SG release GABA. e
GABA was originally thought to inhibit presynaptic pain bers, but it
is now thought that GABA may also block pain post-synaptically
[165]. is should explain why it is oen useful to “rub” the skin over
the site of an injury to make it feel better or why interferential current
may relieve pain in patients. While Aδ and C bers open the pain gate,
Aβ stimulation attempts to keep it closed.
In the case of chronic pain, the gate is continually le open. It is
interesting to note that while most GABAergic interneurons of the SG
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 9 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
maintain local connections, some have axons 15 mm-41 mm in length
and project 1-2 levels via Lissauer’s tract, [166] suggesting that
inhibition of the SG at one level can result in disinhibition of dorsal
horn neurons at unrelated levels. at is, in the event of SG inhibition,
Aδ and C ber pain would have greater access to dorsal horn neurons
at the spinal level associated with the pain and at unrelated levels,
propagating both pain and referred pain. However, multiple systematic
reviews have demonstrated increased Aβ ber activation with DN and
EDN [167-169]. DN may, therefore, be able to directly stimulate the
SG, slamming the door shut on pain traveling from the periphery to
CNS and halting symptoms of referred pain.
e Physiology of Aδ ber Stimulation Secondary to
Dry Needling
Boal and Gillette further speculate that the stimulation of
aerents via therapeutic techniques such as spinal manipulation and
DN may result in a limited inux of Ca2+ through NMDA channels of
second order, dorsal horn neurons [69]. e resulting long-term
depression could result in down regulation of AMPA receptors, thereby
reversing the eects of central sensitization [69]. Gilette et al. also
demonstrated decreased receptive eld size and mechanical sensitivity
in the lateral dorsal horn of the spinal cord following “intense
mechanical force” (Aδ stimulation) [170]. While a number of studies
have demonstrated a reduction in wind-up pain in humans pre-post
spinal manipulation [71-73], future studies should explore this
possibility using DN. Like Aβ bers, a number of systematic reviews
have reported Aδ stimulation with DN and EDN [167-169]. Moreover,
investigations of DN have produced a more potent analgesic aect
following Aδ stimulation than Aβ stimulation [168,171].
e Role of the Endocannabinoid System in Dry
Needling-mediated Analgesia
Dry needling is thought to stimulate endogenous opioids (e.g.
dynorphin, enkephalins, and endorphins) from immune cells such as
neutrophils, eosinophils, basophils, lymphocytes, monocytes and
macrophages, which subsequently stimulate μ, δ and κ opioid receptors
expressed on peripheral nerve terminals [146,172,173]. Studies that
have pharmaceutically blocked endogenous opioids and opioid
receptors have been shown to prevent mechanical and thermal
analgesia in animal models secondary to DN [146,174].
Peripherally, DN increases the number of opioids via the
endocannabinoid system. e endocannabinoid system primarily
consists of two types of receptors, cannabinoid CB1 and CB2 receptors.
By employing AM251 and AM630 to block CB1 and CB2 receptors,
respectively, Gondim et al. demonstrated that both receptor types
mediate the anti-nociceptive and anti-inammatory eects of EDN
[175]. However, inamed tissue has been shown to express 10-100
times the number of CB2 receptors compared to CB1 receptor mRNA,
suggesting that EDN may act primarily through CB2 receptors
[176,177]. CB2 receptor mRNA is found primarily on immune cells, to
include mast cells, T lymphocytes, leukocytes, natural killer cells and
macrophages [176,177].
DN also activates the sympathetic nervous system, enhancing the
expression of intracellular adhesion molecule-1 (ICAM-1) in blood
vessels, thereby increasing the recruitment and migration of immune
cells with CB2 receptors to inamed tissue [146,178]. Zhang et al.
further reported an upregulation in the expression of CB2 receptors on
macrophages, T-lymphocytes and keratinocytes already present in
inamed skin tissue [179]. In addition, DN stimulates the release of
endogenous anandmide, a CB2 receptor ligand and an analogue of
tetrahydrocannabinol (THC) [172,173]. A recent study by Su et al.
found that EDN resulted in an increase in mRNA levels of POMC, a β-
endorphin precursor, and protein levels of β-endorphin in
keratinocytes, macrophages and T-lymphocytes [172]. However, sham
EDN and the combination of EDN and AM630, a CB2 antagonist,
signicantly diminished the eects [172]. us, by creating an
environment rich with CB2 receptors and stimulating endogenous
anandmide, EDN may be able to aectively amplify the production
and subsequent release of opioids to block pain.
Interestingly, Zhang et al. reported that inammation and EDN are
able to independently increase the number of CB2 receptors in aected
tissue [173]. Moreover, the combination of inammation and EDN
result in greater CB2 expression than either alone [173]. us, the
purpose of CB2 expression following EDN is a bit unclear. Perhaps the
stimulation provided by EDN initially propagates and exaggerates CB2
receptor increases already initiated by the cycle of inammation [173].
at being the case, the therapeutic eects of EDN may be due more so
to its ability to increase levels of endogenous anandmide than to
recruit and stimulate expression of CB2 receptors.
Complicating the issue further, Whiteside et al. suggested that the
anti-nociceptive eects of EDN might not be dependent on
endogenous opioids [180]. Interestingly, blocking both peripheral and
central opioid receptors with naltrexone in an animal model did not
prevent the anti-nociceptive eect of the CB2 agonist GW405833.
Instead of stimulating the release of opioids, some authors suggest that
the activation of CB2 receptors by endogenous anandmide results in
anti-nociception and anti-inammation by blocking the production
and release of inammatory cytokines such as TNF-α, IL factor and
NGF [180]. Cannabinoids have been shown to inhibit the release of
pro-inammatory cytokines such as TNF-α, IL-4, IL-6, IL-8, and IL-10
from immune cells [146,181]. Su et al. further used EDN to decrease
mRNA and protein levels associated with IL-1B, IL-6, and TNF in
inamed skin tissue via activation of CB2R [181]. us, while the exact
mechanism responsible for the anti-nociceptive and anti-inammatory
eects of EDN are still not fully realized, the stimulation of CB2
receptors by endogenous anandmide likely results in a combination of
opioid release and inammatory cytokine inhibition to block pain and
inammation, respectively.
e up regulation of CB2 receptors on keratinocytes is particularly
interesting, given their non-immune function and location in the
epidermis. Remarkably, keratinocytes also have the ability express
opioid receptors and release opioids [172,173,182]. A recent study by
Moett et al. (2012) used pulsed radio frequency energy to increase
precursor mRNA for enkaphalin and dynorphin in both human
dermal broblasts and keratinocytes, suggesting that both non-neural
cell types have the ability to create and release opioids [183]. While the
exact role that non-neural cells such as keratinocytes and broblasts
play in EDN is still unknown, these cells may account for some of the
positive benets of supercial needling.
e Role of the Sympathetic Nervous System in Dry
Needling Mediated Analgesia
EDN also activates the sympathetic nervous system (SNS), which
seems to work additively with the endocannabinoid system to reduce
pain and inammation. In addition to upregulating ICAM-1 [146,178]
the SNS also releases norepinephrine. When norepinephrine activates
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 10 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
B2-adrenergic receptors on immune cells, it stimulates the release of B-
endorphins and blocks inammatory cytokine production [146,184].
e SNS also activates the HPA axis, stimulating cortisol release
[150,152]. As previous mentioned, corticosterone inhibits cytokines,
prostaglandin and cox-2, thereby blocking inammation in rats [151].
Since Cox-2 metabolizes endogenous anandmide, cortisol also
aectively conserves endogenous anandmide, prolonging the pain and
inammation reducing eects of the endocannabinoid system [146].
e role of Spinal Opioids/Non-opioids in Dry
Needling Mediated Analgesia
Spinally, DN needling has been shown to activate the descending
pain modulatory system, which is mediated by a synergic relationship
between opioids and non-opioids, including serotonin and
norepinephrine [185]. Guo et al. found that EDN results in the
reciprocal stimulation of β-endorphin containing neurons in the
arcuate nucleus (ARC) and periaqueductal grey (PAG) via glutamate
transporter-3 [186]. While stimulation of the ARC enhances the
analgesic eects of DN, lesioning of the nucleus almost abolishes it
[168,187]. Similarly, injection of ARC and PAG with the opioid
receptor antagonist naloxone signicantly inhibits the analgesic eects
of DN [168,187-189]. Activation of ARC and PAG results in the release
of dynophorin and enkaphalin down into the spinal cord. At the same
time, nociceptive aerents activate the spinothalamic/spinoreticular
tract, which stimulates the locus coeruleus and raphe nucleus to
release norepinephrine and serotonin, respectively [189,190].
Surprisingly, while the ARC-PAG-NRM-dorsal horn pathway
stimulates the raphe nuclei, it inhibits the locus coeruleus [168].
However, this may reect the fact that norepinephrine has opposite
aects in the brain and the spinal cord [168]. While norepinephrine
potentiates EDN analgesia in the spine, it inhibits it in the brain
[168,191]. In fact, EDN has been shown to decrease brain
norepinephrine [192] while increasing spinal norepinephrine [193].
us, the activation of the descending pain modulatory system results
in increased opioids, serotonin and norepinephrine in the spine and
decreased norepinephrine in the brain [168].
Spinal Serotonin and Norepinephrine
Both serotonin and norepinephrine travel down the dorsal lateral
funiculus to inhibit pain in the dorsal horn of spinal cord.
Norepinephrine and serotonin can directly or indirectly aect the
communication between rst order and second order neurons in the
dorsal horn of the spinal cord. Recent work by Zhang et al. used
immunohistochemical staining to demonstrate that α2-adrenergic
receptors are positioned on CGRP-containing primary aerents, while
5-hydroxytryptamine (HT) rectors are located on second order
neurons containing NR-1, a subunit of NMDA receptors [194]. As
previously mentioned, the transmission of pain information requires
the release of glutamate from rst order sensory aerents and the
subsequent receipt of glutamate from second order dorsal horn
neurons. A number of authors have suggested that the activation of α2-
adrenergic receptors by norepinephrine work to presynaptically
decrease glutamate release from primary sensory aerents [195]. At
the same time, activation of 5-HT receptors prevents the
phosphorylation of NR-1 subunits, decreasing the ability of NMDA
receptors to post-synaptically receive glutamate [196]. Notably, studies
that have pharmaceutically blocked α2-adrenergic and 5HT receptors
in the spine reported an inhibition of the analgesic eects of EDN
[146,197].
Spinal Opioids
Indirectly, norepinephrine and serotonin also inuence the
transmission of pain in the dorsal horn of the spinal cord via
interneurons. Enkephalinergic interneurons have both α2-adrenergic
receptors and 5HT receptors [194,198]. In the presence of
norepinephrine and/or serotonin, the interneurons release enkephalin,
which is recognized by μ and δ opioid receptors pre and post
synaptically to inhibit pain transmission. Notably, EDN results in the
stimulation of pre and post-synaptic μ, δ and κ receptors during acute
pain conditions but only μ and δ receptors during chronic pain
conditions [199,200]. is may be due to the adaptive nature of δ
receptors, leading to reduced sensitivity [146]. However, the fact that
opioids mediate the anti-nociceptive eects of DN suggests that DN
may be used to reduce the need for opioid medications (Figure 6)
[201].
Figure 6: A. Transmission of pain from rst-order sensory aerents
to second order dorsal horn neurons in the spine. B. DN- mediated
analgesia in the spine secondary to opioids (pre-synaptically and
post-synaptically), norepinephrine (pre-synaptically), and serotonin
(post-synaptically).
Nociceptin/Orphanin FQ
While opioids, serotonin and norepinephrine all play a part in
reducing pain and inammation secondary to EDN, the role of
nociceptin/orphanin FQ (N/OFQ) is perhaps the most intriguing.
N/OFQ is an opioid related peptide and endogenous agonist of opioid
receptor-like receptor (ORL-1). e actions of N/OFQ depend on its
location in the body [202]. While supraspinal and peripheral N/OFQ
leads to increased nociception, its spinal actions have a powerful anti-
nociceptive eect that mimics opioids [202]. In as little as 3-hours
following the induction of inammation with carrageenan in a rat
model, Carpenter et al. noted increased spinal ORL-1 receptor density,
which correlated with decreased pain behavior [202]. Similarly, EDN
at GB30 and GB34 also increased spinal N/OFQ and ORL-1 receptors
density, and N/OFQ antagonist blocked the analgesic eects of EDN
[203].
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 11 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
According to Carpenter et al. the purpose of the added ORL-1
receptors may be to amplify the eects of N/OFQ in the spinal cord
[202]. Interestingly, a number of studies have demonstrated that spinal
N/OFQ inhibits C-ber pain signals while preserving pain
[204,205]. e fact that N/OFQ and ORL-1 receptor are manufactured
in DRG neurons and expressed in the DRG and spinal cord further
suggest that the actions of N/OFQ may specically target presynaptic
sensory aerents rather than postsynaptic neurons [206]. As such,
N/OFQ is perfectly positioned to inhibit C-ber pain, thereby
preventing and/or blocking central mediated sensitization [202,204].
Previous research has demonstrated that N/OFQ is able to pre-
synaptically block the release of glutamate [207] and substance-P [208]
preventing the up regulation of glutamatergic receptors on dorsal horn
neurons and the disinhibition of receptive elds. Carpenter et al.
further suggests that N/OFQ may provide negative feedback to
postsynaptic neurons, facilitating a down regulation of glutamatergic
receptors [202].
e Physiology and Relevance of Dry Needling Distal
Points
e intimately connected but distinct physiology responsible for the
perception of itch and pain may provide the justication for needling
points outside the site of discomfort. Huang et al. found that the
analgesic eect of DN was inhibited if histamine receptors (H1) were
blocked by clemastine [209]. While histamine also mediates the
perception of itch, there is evidence to suggest that the perception of
itch travels from the periphery to the CNS via a pathway that is
independent of pain [209,210]. According to Schmelz et al., a unique
subgroup of mechano-insensitive C-bers is responsible for initiating
itch in humans [211,212]. Likewise, Liu et al. reported unique
MrgprA3 and GRPR / MOR1D-positive second order neurons in the
DRG and the dorsal horn, respectively that are responsible for
processing itch [210]. ese neurons independently project through
the ventromedial thalamic nucleus to the anterior cingulate cortex, le
inferior parietal lobe, dorsal insular cortex, and supplementary motor
area [213]. e latter typically results in the desire to scratch [213]. e
purpose of the scratch is to introduce pain stimuli at the site of the itch,
as GRPR and MOR1D-negative, dorsal horn neurons are able to
inhibit GRPR and MOR1D-positive itch neurons in the presence of
pain via Bhlhb5 positive interneurons [210]. Notably, topical capsaicin
has been shown to prevent histamine-induced itch experimentally, and
it is widely used by dermatologists clinically to treat various disorders
associated with itch [214].
While perception of pain clearly has the ability to inhibit the
perception of itch peripherally, this is not necessarily the case
supraspinally. Sensory aerents associated with itch stimulate the
histaminergic system in the tuberomammillary nucleus of the
hypothalamus [215]. ese neurons send axonal projections
throughout the CNS. More specically, histamine receptors (H1 and
H2) have been found in the limbic system, to include the
hippocampus, the periaqueductal grey and raphe nuclei [216]. General
intracerebralventricular injections and specic microinjections of
histamine into the periaqueductal grey and raphe nuclei all had anti-
nociceptive eects in animal models [215]. Tamaddonfard et al. further
demonstrated a synergistic eect of morphine and histamine in the
hippocampus [215].
Taken together, the degranulation of MCs and subsequent release of
histamine at an acupoint close to the site of pain (i.e. the MTrP) may
be less advantageous, as the pain would likely dominate TRPv1
channels and mitigate the analgesic eects of the histamine in the
brain [209]. However, needling an acupoint oset or distal from a
trigger point (>10 cm) could stimulate the release of histamine from
mast cells in the absence of pain, thereby facilitating histamine-
mediated pain reduction supraspinally [209]. is is one of the
primary justications for including distal points as part of evidence-
based DN treatment. It also provides direct evidence that trigger points
should not be the only target of DN treatment (Figure 7).
Figure 7: When itch (DN-mediated histamine release) and pain are
presented at the same location, second order dorsal horn neurons
are able to inhibit the perception of itch in the spinal cord (blue
pathway). However, if itch (DN-mediated histamine release) is
presented distal to the site of pain, the sensation is able to inhibit
pain in the brain (red pathway) [91].
Conclusion
Dry needling has gained increased popularity in Western-based
medicine over the past 20-30 years. Physicians, osteopaths,
chiropractors and physical therapists presently use needling modalities
to treat muscles, ligaments, tendons, subcutaneous fascia, scar tissue
and peripheral nerves for the management of a number of
neuromusculoskeletal conditions. As specialists in the treatment of
neuromusculoskeltal conditions, DN has become particularly popular
in the U.S. within the physical therapy profession over the past decade.
Interestingly, despite signicant evidence to the contrary, many within
the profession have conned their use of DN to only targeting trigger
points in muscle. Importantly, this narrow philosophy is likely due to
the general exclusion of the acupuncture literature from the PT
Profession [217] which ironically is conducted in the main by
physiotherapists, [218] medical physicians [219-222] and PhDs,
[223,224] not traditional Chinese acupuncturists. Certainly the
terminology, theoretical constructs, and underlying science
surrounding the insertion of needles without injectate is dierent
among traditional Chinese acupuncture and Western-based DN
communities; however, the actual technical delivery and the analgesic
mechanisms underpinning such have many similarities between
professions [2,225]. e complexity of this topic cannot be
underestimated, and more, high-quality research must be conducted to
fully appreciate the potential of needling therapies for the management
of neuromusculoskeletal conditions.
Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
Page 12 of 18
Int J Phys Med Rehabil
ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
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Citation: Butts R, Dunning J, Perreault T, Mourad F, Grubb M (2016) Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated
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Analgesia: A Clinical Resource Guide for Health Care Professionals. Int J Phys Med Rehabil 4: 327. doi:10.4172/2329-9096.1000327
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ISSN:2329-9096 JPMR, an open access journal Volume 4 • Issue 2 • 1000327
... In this study, the USG mechanical needling with injection of sterile water may break the myofascial trigger points, reduce sensitization of the muscles and soft tissue at the facet joints, and block the medial branches of the dorsal rami that innervate the facet joints. e mechanical needling and sterile water can reduce peripheral and central sensitization and might create the mechanical effect of removing calcification and fibrosis around the facet joints [9,[24][25][26] and alter the neurochemistry [9,[24][25][26][27][28][29][30][31][32][33][34] of the deeper tissue structures that may provide an enhanced analgesic response [30][31][32][33][34]. From a neurophysiological standpoint, mechanical needling may reduce both peripheral and central sensitization by removing the source of peripheral nociception, such as the trigger point (TrP) region, calcification, and fibrosis of the facet joint, as seen in this study, changing spinal dorsal horn activity, and activating central inhibitory pain pathways. e insertion of a needle into the body is known to elicit a variety of natural neurophysiological mechanisms, such as stimulation of the A and C fibers or activation of cortical brain areas [9,10,[24][25][26][27][28][29][30][31][32][33][34][35][36]. ...
... In this study, the USG mechanical needling with injection of sterile water may break the myofascial trigger points, reduce sensitization of the muscles and soft tissue at the facet joints, and block the medial branches of the dorsal rami that innervate the facet joints. e mechanical needling and sterile water can reduce peripheral and central sensitization and might create the mechanical effect of removing calcification and fibrosis around the facet joints [9,[24][25][26] and alter the neurochemistry [9,[24][25][26][27][28][29][30][31][32][33][34] of the deeper tissue structures that may provide an enhanced analgesic response [30][31][32][33][34]. From a neurophysiological standpoint, mechanical needling may reduce both peripheral and central sensitization by removing the source of peripheral nociception, such as the trigger point (TrP) region, calcification, and fibrosis of the facet joint, as seen in this study, changing spinal dorsal horn activity, and activating central inhibitory pain pathways. e insertion of a needle into the body is known to elicit a variety of natural neurophysiological mechanisms, such as stimulation of the A and C fibers or activation of cortical brain areas [9,10,[24][25][26][27][28][29][30][31][32][33][34][35][36]. ...
... e mechanical needling and sterile water can reduce peripheral and central sensitization and might create the mechanical effect of removing calcification and fibrosis around the facet joints [9,[24][25][26] and alter the neurochemistry [9,[24][25][26][27][28][29][30][31][32][33][34] of the deeper tissue structures that may provide an enhanced analgesic response [30][31][32][33][34]. From a neurophysiological standpoint, mechanical needling may reduce both peripheral and central sensitization by removing the source of peripheral nociception, such as the trigger point (TrP) region, calcification, and fibrosis of the facet joint, as seen in this study, changing spinal dorsal horn activity, and activating central inhibitory pain pathways. e insertion of a needle into the body is known to elicit a variety of natural neurophysiological mechanisms, such as stimulation of the A and C fibers or activation of cortical brain areas [9,10,[24][25][26][27][28][29][30][31][32][33][34][35][36]. e mechanical needling with sterile water action as the water jet mechanism can clear the calcification and fibrosis from the facet joint, nerves, and muscle. ...
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Objective. This present study aimed to explore the clinical effects of ultrasound-guided (USG) mechanical needling with sterile water injection for lumbar facet joint syndrome. Methods. This was a retrospective cohort study that assessed the clinical outcome of ageing patients who received USG mechanical needling with sterile water injection. In addition, the clinical outcome of age- and gender-matched patients randomly selected from patients who received mechanical needling with sterile water was compared to the patients injected with steroids in a 2 : 1 ratio. The data were extracted from the medical records of ageing patients with facet joint syndrome who received USG injection at the lumbosacral spine by the first author. Low back pain or axial pain, and leg pain or radicular pain were assessed by the visual analogue scale (VAS), and gait ability with walking distance was obtained at 6 different time points. Results. A total of 4,276 medical records were examined. Four thousand two hundred twenty-eight ageing patients received needling with sterile water injection and found that the efficacy lasted up to 6 months. Ninety-six patients were compared with 48 patients who received steroid injection. Those who received steroids had less back and leg pain at 1 week after injection; however, pain returned at 3 months and 6 months after injection. Conclusions. USG mechanical needling with sterile water could help relieve axial and radicular pain for at least 6 months. Reduced sensitization and removal of calcification and fibrosis were all possible mechanisms.Keywords: Mechanical needling, Sterile water, Ultrasound guided (USG) injection, Facet joint syndrome, Pain
... This hypothesis is integrated into a pain neuroscience paradigm and has been suggested for other needling techniques such as dry needling, acupuncture, or electroacupuncture [20][21][22]. The neurophysiological effect of these therapies might be produced by the activation of descending pathways, stimulation of the neuroendocrine system, conditioned pain modulation, or segmental inhibition [20][21][22][23][24]. These potential mechanisms should be included in the concept of endogenous pain modulation (EPM), which is the ability of the central nervous system to modulate nociceptive input from peripheral tissues as it ascends to the spinal cord/brainstem and the brain [25]. ...
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Abstract: The purpose of this double-blinded randomized controlled trial was to investigate whether percutaneous electrolysis (PE) is able to activate endogenous pain modulation and whether its effects are dependent on the dosage of the galvanic current. A total of 54 asymptomatic subjects aged 18–40 years were randomized into three groups, receiving a single ultrasound-guided PE intervention that consisted of a needle insertion on the lateral epicondyle tendon: sham (without electrical current), low-intensity (0.3 mA, 90 s), and high-intensity (three pulses of 3 mA, 3 s). Widespread pressure pain thresholds (PPT), conditioned pain modulation (CPM), and temporal summation (TS) were assessed in the elbow, shoulder, and leg before and immediately after the intervention. Both high and low intensity PE protocols produced an increase in PPT in the shoulder compared to sham (p = 0.031 and p = 0.027). The sham group presented a significant decrease in the CPM (p = 0.006), and this finding was prevented in PE groups (p = 0.043 and p = 0.025). In addition, high-intensity PE decreased TS respect to sham in the elbow (p = 0.047) and both PE groups reduced TS in the leg (p = 0.036 and p = 0.020) without significant differences compared to sham (p = 0.512). Consequently, a single PE intervention modulated pain processing in local and widespread areas, implying an endogenous pain modulation. The pain processing effect was independent of the dosage administrated.
... Dry needling (DN) refers to the insertion of monofilament needles without injectate into muscles, ligaments, tendons, connective tissue, scar tissue, and peri-neural tissue for the management of neuromusculoskeletal conditions [27,28]. While the terminology and theoretical constructs of acupuncture and DN are different [29], both have been shown to elicit biochemical, biomechanical, endocrinological, and neurovascular changes associated with reductions in pain and disability [30]. ...
Article
Full-text available
Objective: To compare the effects of dry needling and upper cervical spinal manipulation with interocclusal splint therapy, diclofenac, and temporomandibular joint (TMJ) mobilization in patients with temporomandibular disorder (TMD). Methods: One hundred-twenty patients with TMD were randomized to receive six treatment sessions of dry needling plus upper cervical spinal manipulation (n = 62) or interocclusal splint therapy, diclofenac, and joint mobilization to the TMJ (n = 58). Results: Patients receiving dry needling and upper cervical spinal manipulation experienced significantly greater reductions in jaw pain intensity over the last 7 days (VAS: F = 23.696; p < 0.001) and active pain-free mouth opening (F = 29.902; p < 0.001) than those receiving interocclusal splint therapy, diclofenac, and TMJ mobilization at the 3-month follow-up. Conclusion: Dry needling and upper cervical spinal manipulation was more effective than interocclusal splint therapy, diclofenac, and TMJ mobilization in patients with TMD.
... Butts reports that, from a neurophysiological standpoint, DDN reduces both peripheral and central sensitivity by neutralizing nociceptors in the area, modeling de activity of the dorsal spine through the inhibition of the activity of central pain pathways [48,49]. In their studies, Shah et al proved that with DDN, there is an immediate concentration in the area of neurotransmitters, such as calcitonin, as well as of various cytokines and interleukins, both outside and in cellular fluids [50,51]. ...
Article
Full-text available
Background and Objectives: The objective of our clinical trial was to determine the effectiveness of the deep dry needling technique (DDN) (neuromuscular deprogramming) as a first step in the treatment of temporomandibular disorders. Methods and Materials: The double-blind randomized clinical trial comprised 36 patients meeting the inclusion criteria who had signed the corresponding informed consent form. The participants were randomly distributed into two groups, the Experimental group (Group E) and the Control group (Group C). Group E received bilateral DDN on the masseter muscle, while Group C received a simulation of the technique (PN). All the participants were evaluated three times: pre-needling, 10 min post-needling, and through a follow-up evaluation after 15 days. These evaluations included, among other tests: pain evaluation using the Visual Analog Scale (VAS) and bilateral muscle palpation with a pressure algometer; evaluation of the opening pattern and range of the mouth, articular sounds and dental occlusion using T-scans; and electromyography, which was used to evaluate the muscle tone of the masseter muscles, in order to control changes in mandibular position. Results: Digital control of occlusion using Tec-Scan (digital occlusion analysis) showed a significant reduction both in the time of posterior disclusion and in the time needed to reach maximum force in an MI position after needling the muscle, which demonstrated that there were variations in the static position and the trajectory of the jaw. The symmetry of the arch while opening and closing the mouth was recovered in a centric relation, with an increase in the opening range of the mouth after the procedure. Conclusions: facial pain is significantly reduced and is accompanied by a notable reduction in muscle activity after needling its trigger points.
... A number of synergistic mechanisms are proposed to mediate analgesia via biochemical and mechanical processes in neural, connective, and muscle tissue. 80 Dry needling is an invasive technique, and although the overall risks are considered very low, any therapist desiring to offer this intervention should undertake adequate training. In addition, dry needling is not universally included in all state therapy practice acts, and contact with local professional associations and state licensure boards would be prudent before undertaking training in dry needling. ...
Article
Full-text available
Dry needling is a therapeutic method that involves inserting a filiform needle into a target area. Osteoarthritis is a degenerative joint disease that affects the articular cartilage, causes discomfort, and changes the biomechanics. ling is a component of conservative or comprehensive physiotherapeutic management. Increased blood flow, metabolic changes, spontaneous electrical activity, pain gating, and other mechanisms of action of dry needling may generate therapeutic advantages in osteoarthritis. The history of dry needling is extensively discussed. Needling can be defined as superficial or deep needling depending on the depth of the needle insertion, and it can also be classified as trigger point dry needling, fascial needling, scar tissue needling, and so on. The mechanism of Dry Needling is explained by a variety of ideas. The local effects of dry needling were also explored in this review, as well as the mechanism of analgesic effects. The needles can be utilized to provide therapeutic current to the tissues in a variety of ways. It can be done with PENS (Percutaneous Electrical Nerve Stimulation) or ETOIMS (Electro Transcutaneous Electrical Nerve Stimulation) (Electrical Twitch Obtaining Intramuscular Stimulation).