Curr Pain Headache Rep (2013) 17:348

DOI 10.1007/s11916-013-0348-5

MYOFASCIAL PAIN (R GERWIN, SECTION EDITOR)

Physiologic Effects of Dry Needling

Barbara Cagnie & Vincent Dewitte & Tom Barbe &
Frank Timmermans & Nicolas Delrue & Mira Meeus

# Springer Science+Business Media New York 2013

Abstract During the past decades, worldwide clinical and triggerpoints: the taut band, local ischemia and hypoxia, pe-
scientific interest in dry needling (DN) therapy has grown ripheral and central sensitization. This article aims to provide
exponentially. Various clinical effects have been credited to the physiotherapist with a greater understanding of the con-
dry needling, but rigorous evidence about its potential phys- temporary data available: what effects could be attributed to
iological mechanisms of actions and effects is still lacking. dry needling and what are their potential underlying mecha-
Research identifying these exact mechanisms of dry needling nisms of action, and also indicate some directions at which
action is sparse and studies performed in an acupuncture future research could be aimed to fill current voids.
setting do not necessarily apply to DN. The studies of poten-
tial effects of DN are reviewed in reference to the different Keywords Myofascial trigger point . Myofascial pain
aspects involved in the pathophysiology of myofascial syndrome . Dry needling . Sensitization . Physiological
Effects . Pain physiology

This article is part of the Topical Collection on Myofascial Pain

B. Cagnie (*) : V. Dewitte : T. Barbe : M. Meeus Introduction
Department of Rehabilitation Sciences and Physiotherapy, Ghent
University, De Pintelaan 185 3B3,
9000 Ghent, Belgium Myofascial pain syndrome (MPS) is a common diagnosis in
e-mail: [email protected] patients with musculoskeletal pain associated with active and
latent myofascial trigger points (MTrPs). A MTrP is defined
V. Dewitte as a hyperirritable spot in a taut band of skeletal muscle fibers.
e-mail: [email protected]
An active MTrP has spontaneous pain or pain in response to
T. Barbe movement, stretch or compression, while a latent MTrP is a
e-mail: [email protected] sensitive spot with pain or discomfort in response to compres-
sion only [1, 2]. The literature suggests several treatment
M. Meeus
e-mail: [email protected] interventions to treat MTrPs: dry needling therapy (DN) being
one of them [3•]. DN uses a fine, solid filiform needle and is
F. Timmermans also known as intramuscular stimulation.
Uplands Physiotherapy Clinic, #121-725 Carmi Avenue, During the past decades, clinical and scientific interest in
Penticton, B.C., Canada V2A 3G8
e-mail: [email protected] DN has grown exponentially and various treatment effects are
being credited to DN, such as: decreased pain and muscle
N. Delrue tension, improved range of motion, muscle strength and coor-
Normandiëstraat 186, dination. However, there is still little scientific backup. A recent
8560 Wevelgem, Belgium
e-mail: [email protected] systematic review of Tough et al. concluded that there is limited
evidence derived from one study that deep needling directly
M. Meeus into myofascial trigger points has an overall treatment effect,
“Pain in Motion” Research Group, Department of Rehabilitation when compared with standardized care [4]. Kim et al. [5•]
Sciences and Physiotherapy, Faculty of Medicine and Health
Science, University of Antwerp, Antwerp, Belgium conclude that, despite the positive results of individual studies,
e-mail: [email protected] the level of evidence supporting the efficacy and effectiveness
348, Page 2 of 8 Curr Pain Headache Rep (2013) 17:348

of DN for several conditions remains insufficient, because of cortex, but also to spinal modulation and descending control
concerns about a lack of precision and a high risk of from higher neurological centres.
bias of the studies. Rigorous large-scale, placebo con- An important mechanism in the modulation of pain per-
trolled, clinical trials are needed to evaluate the clinical ception is segmental inhibition, which is the modified “gate
utility of this technique [4, 5•]. theory of pain control”, first published by Melzack and Wall
This article reviews the current state of knowledge of phys- in 1965. This hypothesis describes how activation of Aβ-
iologic effects of DN by an in-depth review of basic and clinical fibres can lead to an inhibition in the spinal cord by blocking
research that has been published. First, a general overview of the synaptic transmission between the Aδ- and C-fibres and
pain pathways and modulation of the pain perception is pro- the cells in the dorsal horn, because of the slower informa-
vided, as this should be the basis and reasonable rationale for all tion transmission of the latter [6].
therapeutic interventions, including DN. Second, after giving a Another possible mechanism of pain modulation is
short overview of the pathophysiology of MTrPs, the different through the endogenous opioid system. It is well known that
underlying mechanisms of DN are described in reference to the the three main groups of opioid peptides: β-endorphin,
different aspects involved in the pathophysiology of MTrPs. enkephalins and dynorphines, and their μ-, δ- and κ-
These findings are then critically discussed. receptors are widely distributed in peripheral primary affer-
We hope to provide the therapist with a better under- ent terminals and areas of the central nervous systems relat-
standing of the contemporary data available and what effects ed to nociception [6]. The analgesic effects of opioids arise
could be attributed to DN, what their potential underlying from their ability to inhibit directly the ascending transmis-
mechanisms of action are and the directions that future sion of nociceptive information from the spinal cord dorsal
research could be aimed at to fill in the current voids. horn. They are also able to activate pain control circuits that
descend from the midbrain [periaqueductal gray (PAG)], via
the rostral ventromedial medulla (RVM) to the spinal cord
Pain Physiology dorsal horn [7].
Besides the endogenous opioids as important neurotrans-
Pain sensations originate mainly in two types of pain recep- mitters in the descending pain control system, serotonin (5-
tors: low-threshold nociceptors that are connected to fast HT) and noradrenaline are the two other, most familiar and
conducting aδ-fibers, and high-threshold nociceptors that con- well investigated, transmitters of this pathway. However,
duct impulses through slower unmyelinated C-fibers. Central descending projections containing dopamine (monoamine)
terminals of these sensory fibers enter the central nervous and many other neurotransmitters can also play a crucial
system (CNS) through the dorsal horn of the spinal cord, role in pain modulation [8].
where they connect with spinal neurons via synaptic transmis-
sion. Neurons of superficial laminae I and deep laminae V Chronic Pain—Central Sensitization
project along the spinothalamic and spinoreticulothalamic
tracts to supraspinal sites such as the thalamus, parabrachial In conditions with chronic pain, the balance in pain modu-
nucleus, and amygdala, where pain signals are further lation can be disturbed due to impaired pain inhibition
processed and sent on to higher cortical centers [6]. and/or enhanced pain facilitation. This may lead to
“centralsensitization”. Central sensitization entails altered
Peripheral Pain Modulation sensory processing in the brain, increased spontaneous ac-
tivity of dorsal horn neurons, dysfunctional endogenous
Peripheral activation of Aδ- and C-fibre nociceptors is mod- analgesia, expansion of receptive field sizes, reduction in
ulated by a number of sensitizing and algogenic agents, such threshold, prolonged after-discharges, and increased activity
as substance P (SP), bradykinin, histamine, calcitonin gene- of brain-orchestrated facilitatory pathways, which augment
related peptide (CGRP), prostaglandins, interleukin-1β nociceptive transmission [8–12]. Central sensitization re-
(IL1β), tumor necrosis factor (TNF), and nerve growth sults in enhanced nociception (hyperalgesia) and pain elic-
factor (NGF). All of these can be released following cellular ited by normally non-noxious stimuli (allodynia) [7, 12].
damage [6]. The local release of some of these chemicals Also, altered states of diffuse noxious inhibitory control
(SP, histamine) causes inflammation and vasodilation, con- (DNIC) have been associated with central sensitization in
tributing to the “protective” function of pain [6, 7]. chronic pain patients [13–15]; often now referred to as
“conditioned pain modulation” (CPM). CPM is a “pain-in-
Central Pain Modulation hibits-pain” paradigm and occurs when two noxious stimuli
are applied heterotopically, i.e., a second nociceptive stim-
The sensation of pain is not only subject to modulation ulus is applied in a more remote location, outside the recep-
during its ascending transmission from the periphery to the tive field of the first. This second nociceptive stimulus (such
Curr Pain Headache Rep (2013) 17:348 Page 3 of 8, 348

as heat, high pressure or electric stimulation) will be contraction of affected muscle fibers that are being manually
processed by the dorsal horn wide dynamic range neurons stretched, injected or dry needled. According to Hong et al.
and can lead to inhibition of the first one. [29], DN is most effective when these LTRs are elicited.
Central sensitization can also be enhanced and Clinical results from Ceccherelli et al. [30] demonstrated
maintained by supraspinal processes involving cognitions, that deep stimulation had a better analgesic effect when
attention, emotions and motivation. These forebrain prod- compared with superficial stimulation. It seems obvious to
ucts can make a significant contribution to the clinical pain expect different results from superficial or deeper insertion.
experience in, e.g., MPS and are referred to as cognitive Deeper insertion of the needle affects several structures:
emotional sensitization [16–18]. skin, fascia, and muscle layers, whereas superficial insertion
affects merely the skin and some superficial layers. Itoh et
al. [31] have demonstrated this principle in several other
Pathophysiology of MTrPs studies, too, and conclude that the depth of needle penetra-
tion is important for the relief of muscle pain.
In order to understand the underlying mechanisms of DN, The potential effects of DN will now be reviewed in
some knowledge of the pathophysiology of MTrPs is help- reference to the four different aspects involved in the path-
ful [1, 2]. The most credited local hypothesis for primary ophysiology of MTrPs: the taut band, local ischemia and
MTrP formation is the hypothesis first put forward by hypoxia, peripheral and central sensitization. An overview
Simons et al. [19] and later expanded by Gerwin et al. [20]. of the potential DN physiological effects is shown in Fig. 1.
They suggest that the first phase of trigger point forma-
tion consists of the development of a taut band as a result of
Effects on the Taut Band
abnormal endplate potential caused by excessive acetylcho-
line (ACh) release in the neuromuscular junction at the
A statement that is often found in MPS papers and textbooks
motor endplates [19, 21••]. EMG studies show this as
is “the effectiveness of DN probably lies in the mechanical
‘spontaneous electrical activity’ (SEA), also called ‘endplate
disruption of the integrity of dysfunctional endplate”[19, 32].
noise’. MTrP irritability can be objectively assessed with the
To the best of our knowledge, basic research has not yet
prevalence or amplitude changes of SEA that are recorded in
demonstrated an actual mechanical disruption of the endplate
this region [22].
in recent studies.
It is further hypothesized that, due to this excessive ACh
It has been demonstrated that DN may influence the SEA
release at the motor endplate, sustained sarcomere contrac-
by eliciting a LTR. Both Chen et al. [33] and Hsieh et al.
tures occur, that could lead to local ischemia and hypoxia.
[34] demonstrated in their studies that DN to a MTrP region
Consequently, vasoactive and algogenic substances are re-
could effectively suppress SEA, when LTRs were elicited.
leased that can sensitize peripheral nociceptors (peripheral
They suggest that the insertion of a needle at the endplate
sensitization). Sustained peripheral nociceptive input might
region may lead to increased discharges and thereby imme-
sensitize dorsal horn neurons and supraspinal structures,
diately reduce available ACh stores, leading to a lesser SEA.
leading to hyperalgesia and allodynia, as well as referred
Another working mechanism could be that sufficient me-
pain (central sensitization) [21••, 23–25].
chanical needling activation around the endplate area causes
muscle fibers to discharge and thus elicit a LTR. Baldry [35]
mentioned that a LTR causes alterations in the length and
Physiological Effects of Dry Needling
tension of the muscle fibers and stimulates mechanorecep-
tors like the Aβ-fibers.
There is some emerging DN research, but the exact mech-
anisms of action of direct needling in the deactivation of
trigger points are not yet unraveled. Also, most of our Effects on Blood Flow
current understanding of the systemic physiologic effects
of DN is (in)directly derived from acupuncture literature As previously mentioned, sustained contractures of taut
[26••, 27••, 28]. Indeed, there are some similarities between muscle bands might cause local ischemia and hypoxia in
acupuncture and DN, but, more importantly, many signifi- the core of the MTrPs. Different studies have demon-
cant differences. Not just in the underlying philosophies and strated that needling may increase muscle blood flow and
explanation models, but also in the ‘technical’ details: one oxygenation [36–42]. Several mechanisms have been
of more needles applied, the movement of the needle, the suggested to explain the local muscle response of blood
depth of needle insertion, the amount and force of stimula- flow in needle stimulation. The most plausible one is the
tion and the elicitation of a ‘local twitch response’ (LTR). A release of vasoactive substance, such as CGRP and SP
LTR is an involuntary spinal reflex resulting in a localized which, upon activation of Aδ- and C-fibers via the axon
348, Page 4 of 8 Curr Pain Headache Rep (2013) 17:348

Fig. 1 Schematic diagram of the potential physiological effects of DN.

reflex, leads to vasodilatation in small vessels and in- promote angiogenesis, vasodilation, and altered glucose
creased blood flow [43]. metabolism in hypoxic tissues. Repeated localized DN
There is a discrepancy in the literature whether this may thus upregulate the expression of HIF-1, iNOS, and
increase in blood flow is restricted to the needling site or VEGF proteins, and potentially increase capillarity in the
if vasodilatation and increases in blood flow also extend skeletal muscle and improve the circulation in muscles
beyond the site of stimulation (see “remote effects”). Some containing MTrPs. However, long(er) term follow-up stud-
studies have demonstrated remote circulatory effects with ies are needed as the effects on circulation beyond 5 days
needling [37], whereas others did not show an increase in remain unclear.
blood flow at distant sites of the needling [36, 42]. Sandberg
et al. [37] did find a transient significant increase in contra- Neurophysiological Effects: Effects on Peripheral
lateral blood flow in the trapezius muscle after needle stim- Sensitization
ulation. However, this increase was significantly less than in
the stimulated muscle and apparently only there for the first Shah et al. [45, 46] found that the concentrations of SP and
two minutes after the needle stimulation. CGRP were higher in the vicinity of active MTrPs compared
In a recent study by Hsieh et al. [44••] they found an to latent ones or normal muscle tissue. After a LTR was
increase in a number of hypoxic-responsive proteins, includ- elicited, SP and CGRP concentrations were significantly
ing hypoxia-inducible factor-1α (HIF-1α), inducible iso- lowered compared to their pre-LTR values. These results were
form of nitric oxice synthases (iNOS) and vascular endo- consistent with the data of Hsieh et al. [44••]. The data
thelial growth factor (VEGF) production in the biceps obtained from their study showed that a single session treat-
femoris muscle after DN stimulation. These proteins can ment produced a short-term analgesic effect by decreasing the
Curr Pain Headache Rep (2013) 17:348 Page 5 of 8, 348

SP at peripheral sites, however, no lasting effect was observed It has been proposed that “satellite or secondary” MTrPs
5 days after DN. In contrast, five consecutive sessions (one per may develop in the referred pain zone from “key or prima-
day) of DN, increased the SP levels immediately after the nee- ry” MTrPs. Hsieh et al. [51] conducted a clinical study and
dling and was maintained 5 days after the DN. This was accom- provided evidence that DN-evoked inactivation of a primary
panied by higher levels of TNF-α, iNOS, HIF-1, COX-2 and (key) MTrP inhibited the activity in ipsilateral secondary
VEGF. Studies have demonstrated that increased COX-2 and (satellite) MTrPs situated in its referral pain zone. Ferandez-
TNF levels are associated with muscle damage [47]. It is likely Carnero et al. [52] showed that an increased nociceptive
that the five sessions of DN accumulated to an excessive level of activity at latent MTrPs in the infraspinatus muscle in-
intramuscular manipulation and caused damage in the fibers with creased motor activity and sensitivity of a MTrP in distant
noxious inputs (C-fibers) and increased release of SP. muscles connected to the same segmental level.
Secondly, peripheral opioid analgesia has received con-
siderable attention as an endogenous pathway of inhibiting Release of Endogenous Opioids
pain, mainly in the acupuncture literature, although clear
mechanisms remain elusive. Hsieh et al. [44••] have also Knowledge of the central effects of DN upon opioid release
shown that increased β-endorphin levels can suppress neu- is limited. Using functional magnetic resonance imaging,
rons from releasing SP and thus inhibit pain transmission Niddam et al. [53] showed that pain following the insertion
[44••]. Using an animal model, they demonstrated that one of a needle into a trigger point, combined with electrical
session of DN in the biceps femoris enhanced the beta- stimulation, is mediated through the PAG in the brainstem.
endorphin levels in the biceps muscle and serum immedi- The PAG is a central part of the opioid circuitry that controls
ately after needling, but no lasting effect was observed nociceptive transmission at the level of spinal cord and
5 days after the needling. In contrast, the five consecutive cortex [8]. The change in PAG-activity was correlated with
sessions of DN reversed this effect. the change in PPT. It is hypothesized that DN, via stimula-
tion of the nociceptive fibers, may activate the
enkephalinergic inhibitory dorsal horn interneurons. It is
Neurophysiological Effects: Effects on Central Sensitization
unclear whether the needle manipulation or the electrical
stimulation is responsible for these results or both. This
According to Chou et al. [26••], the most likely mechanism
combination, being “electro-acupuncture”, is also men-
of pain relief through needle stimulation is hyperstimulation
tioned in clinical studies on acupuncture-induced analgesia
analgesia, which was originally proposed by Melzack [48].
and laboratory results report endogenous opiate peptides to
DN may stimulate, both large myelinated fibers (i.e., Aβ-
be involved.
and Aδ-fibers), as well as C-fibers, indirectly via the release
of inflammatory mediators. As a result of mechanical stim-
Effect on the Release of Neurotransmitters: Serotonin
ulation, Aβ- and Aδ-fibers are both activated and send
and Noradrenaline
afferent signals to the dorsolateral tracts of the spinal cord
and could activate the supraspinal and higher centres in-
Stimulation of Aδ-nerve fibers may also activate the sero-
volved in pain processing. Different mechanisms can occur,
tonergic and noradrenergic descending inhibitory system.
either in isolation or concurrently.
Although there are no known specific experimental or clin-
ical studies supporting the proposed serotonergic and nor-
Segmental Inhibition/Gate Control adrenergic mechanisms of DN, it is hypothesized that DN
may have an effect on both systems, often based again on
Chu [49] stated that, when an needle is rapidly thrust into a acupuncture literature [27••].
MTrP, the LTRs evoked lead to a large diameter-sensory Shah et al. [45, 46] found that the concentration of 5-HT
afferent proprioceptive input into the spinal cord. This could and noradrenaline, was higher in the vicinity of active
have a “gate-controlling” effect of blocking the intra-dorsal MTrPs compared to latent MTrP or normal muscle tissue.
horn passage of noxious information generated in the 5-HT receptors are primarily pronociceptive in the periph-
MTrP’s nociceptors. ery, acting directly on afferent nerves and indirectly by
Srbely et al. [50] identified an immediate increase in the release of other mediators (e.g., SP and glutamate).
pain pressure threshold (PPT) at the infraspinatus MTrP,
compared with the gluteus medius point, at 3 and 5 minutes Conditioned Pain Modulation
after DN the infraspinatus muscle. They hypothesized that
site-specific DN may be mediated by segmental inhibitory Patients with chronic musculoskeletal pain have impaired
effects, evoked by selective stimulation of large myelinated CPM. Depressed CPM will lead to a reduction of endoge-
fibers in the MTrP. nous pain inhibition and can contribute to a chronic pain
348, Page 6 of 8 Curr Pain Headache Rep (2013) 17:348

state [13]. Several reviews have hypothesized that needling with respect to the methodological characteristics. It seems
may affect CPM [27••]. However, recent findings in both logical that mechanisms and effects of DN actions differ
healthy and whiplash-patients have demonstrated that CPM depending on: the location(s) of the needle placement(s), the
on temporal summation of pressure pain did not respond to depth of the insertion(s), the needle forces and motions
acupuncture needling [54, 55]. used, and whether or not a LTR is elicited [59].
Most recommended clinical and research parameters are
Remote Effects based on experts’ opinions. Recently, Davis et al. [60••]
have developed an innovative device to quantify needling
Different studies have investigated the remote effects of DN, motion and force parameters in a treatment-like setting.
both ‘distal to proximal’ effects and contralateral effects. Needling data can then subsequently be analyzed, providing
Tsai et al. [56] and Fu et al. [22] both found that DN of a a more objective method for characterizing needling in basic
distal MTrP could provide a remote effect to reduce the and clinical needling research. Studies are needed to identify
irritability of a proximal MTrP. The literature is conflicting optimal intervention parameters for DN.
with respect to contralateral effects. Hsieh et al. [34] did find Further insights into the MPS’ pathophysiology mecha-
contralateral effects in an animal study, whereas Fu et al. nisms are welcomed, in order to find out more how pain
[22] did not find these. modulation systems are being affected by it. Most of the
The neural pathway for the remote effects appears to be existing studies on needling analgesia have focused on
mediated via a spinal reflex, which depends on an intact physiological pain in “normal” animals and human volun-
afferent pathway from the remote stimulating site to the teers. However, current evidence points to far more complex
spinal cord and normal spinal cord function at the level pain mechanisms, especially in chronic pain patients. To
corresponding to the innervations of the proximally affected better explore the mechanisms of analgesia, adequate
muscle [34]. It is further hypothesized that the remote ef- models of chronic pain should be developed and applied
fects may relate to a consequence of CPM, but firm evi- in research. This may prevent scientists from an overexcited
dence is lacking [26••]. search for DN effects and explanation models, which might
not be applicable given the complex modified circumstances
Placebo Effects in ‘real’ patients.
When chronic pain and central sensitization are present,
It is well known that expectation can significantly modulate there is an increased responsiveness to a variety of peripheral
pain perception, a mechanism frequently referred to as pla- stimuli. A general recommendation in these patients is to not
cebo analgesia [57]. Neuroimaging data demonstrate that increase pain during treatment, as any therapeutic intervention
placebo analgesia recruits subcortical and opioid sensitive could serve as a new peripheral source of nociceptive barrage
brain regions, also involved in pain perception (including sustaining the process of central sensitization [12, 61].
PAG, rostral anterior cingulate cortex, thalamus, insula, DN activates several types of receptors, including
amygdala, and in some studies the prefrontal cortex). nociceptors, and daily practice shows it is not always well
Many of these areas overlap with those modulated by nee- tolerated in patients with central sensitization and therefore
dling. Functional magnetic resonance studies have con- may not be a suitable choice. In a recent educational re-
firmed that expectancy can influence acupuncture analgesia source paper, published by the American Physical Therapy
[58]. Obviously, placebo effects have to be considered when Association (February 2013), it is highlighted that severe
designing and conducting DN studies. hyperalgesia or allodynia may interfere with the application
of DN. However, it should not be considered as an absolute
contraindication. Several authors suggest in their reviews
Discussion that treatment of concurrent MTrPs in, e.g., fibromyalgia
should be systematically performed before any specific fi-
DN has become a popular treatment technique with an bromyalgia therapy is undertaken [32]. Their idea is that any
increasing amount of studies demonstrating its clinical ef- peripheral source of nociception should be removed before
fects. Rigorous evidence about its physiological mecha- desensitization of the central nervous system can become
nisms of actions and effects is needed now in order to start the focus of the therapy.
supporting it as evidence based practice. The difficult meth-
odological characteristics related to experimental studies
and the complex network in pathological conditions may Conclusions
certainly account for this lack of research so far.
Direct comparison between existing needling studies is We can conclude, after reviewing the current basic science
difficult as the intervention parameters vary considerably findings, that the physiological mechanisms and effects of
Curr Pain Headache Rep (2013) 17:348 Page 7 of 8, 348

DN are highly complex and recruit central and peripheral 5. • Kim TH, Lee CR, Choi TY, et al. Intramuscular stimulation
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Further insight in MPS and its pathophysiological mech- large-scale clinical trials on dry needling.
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Mr. Vincent Dewitte reported no potential conflicts of interest pain states. Curr Opin Anaesthesiol. 2010;23(5):611–5.
relevant to this article. 14. Meeus M, Nijs J, Van de Wauwer N, et al. Diffuse noxious
Mr. Tom Barbe reported no potential conflicts of interest relevant to inhibitory control is delayed in chronic fatigue syndrome: an
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