Here are summaries of 5 PubMed articles about dry needling of trigger points (arranged in chronological order). They explain the theory behind it, go into chemical details, and demonstrate its pain relieving effects :
J Man Manip Ther. 2011 November (PubMed Full Text);
This article aims to place trigger point dry needling within the context of pain sciences. From a pain science perspective, trigger points are constant sources of peripheral nociceptive input leading to peripheral and central sensitization. Dry needling cannot only reverse some aspects of central sensitization, it reduces local and referred pain, improves range of motion and muscle activation pattern, and alters the chemical environment of trigger points.
Trigger point dry needling should be based on a thorough understanding of the scientific background of trigger points, the differences and similarities between active and latent trigger points, motor adaptation, and central sensitize application
The advantages of dry needling are increasingly documented and include an immediate reduction in local, referred, and widespread pain,restoration of range of motion and muscle activation patterns and a normalization of the immediate chemical environment of active myofascial trigger points.Dry needling can reduce peripheral and central sensitization.
Popular explanations of myofascial pain tend to be relatively simplistic and do not always offer a well-evidenced theoretical foundation to direct clinical treatment strategies.
Historically many researchers and clinicians have considered a vicious cycle hypothesis, known as the pain–spasm–pain cycle, which postulated that muscle pain would cause spasm of the same muscle, and in turn would cause more pain leading to more spasms.
In other words, muscle pain does not appear to cause an increase in fusimotor drive.
The updated pain-adaptation model may reflect more accurately the current thinking. According to this model muscle pain inhibits alpha-motor neurons leading to activation of antagonists and an overall decrease in motor function. Even so, these patterns are not universally applicable either.
it is important to realize that there are significant differences between schools of dry needling
Active and Latent Myofascial Trigger Points
Active trigger points feature spontaneous local and referred pain away from the trigger point, while latent trigger points do not cause spontaneous pain. After stimulation with digital pressure, however, latent trigger points do evoke local and referred pain.
Referred pain from active trigger points may mirror the formation of new effective central nervous connections, meaning that afferent fibers from trigger point nociceptors may make new effective connections with dorsal horn neurons that normally only process information from remote body regions. A nociceptor is a receptor specialized in detecting stimuli that objectively can damage tissue and subjectively are perceived as painful.
Evidence suggests that the first phase of trigger point formation consists of the development of contractured muscle fibers or a taut band, which may or may not be painful.
Characteristic of taut bands and trigger points is that they do not require an electrical activation of the alpha-motor neuron, but get activated by a spontaneous release of acetylcholine from the motor endplate
Motor Aspects of Trigger Points
Trigger points are thought to develop especially following unaccustomed eccentric and concentric loading,68 but also occur after low-load repetitive tasks and sustained postures, with respiratory stress, such as over-breathing,and in association with visceral pain and dysfunction.
Once active trigger points exist, there will be a constant nociceptive input into the dorsal horn, which can perpetuate altered motor control strategies, lead to further muscle overload or even disuse, and result in the development of peripheral and central sensitization.
Muscle Pain and Trigger Points
Muscle pain is associated with many chronic pain conditions. It is difficult to pinpoint and diffuse in nature. Muscle pain is inhibited strongly by descending pain-modulating pathways and under normal circumstances, there is a dynamic balance between the degree of activation of dorsal horn neurons and the descending inhibitory systems. Muscles refer to deep somatic structures,
Trigger points are peripheral sources of persistent nociceptive input, which can excite muscle nociceptors. Nociceptive input from muscle is particularly effective in inducing neuroplastic changes in the spinal dorsal horn and likely in the brainstem.
Sustained contractures of taut bands cause local ischemia and hypoxia in the core of trigger points. Recent Doppler ultrasound studies confirmed significantly different blood flow waveforms and a greater vascular output resistance in active trigger points when compared to latent trigger points and normal muscle tissue.
Hypoxia may trigger an immediate increased release of acetylcholine at the motor endplate
A sensitized muscle nociceptor has a lowered stimulation threshold into the innocuous range and will respond to harmless stimuli like light pressure (allodynia) and muscle movement (mechanical hyperalgesia).
Central Sensitization and Trigger Points
sensitization is not specific for myofascial trigger points. Trigger points are, however, involved in nearly every pain syndrome131 and it is likely that central sensitization involves trigger points,
The immediate environment of active trigger points is characterized by significantly increased levels of substance P (SP), CGRP, BK, 5-HT, norepinephrine, tumor necrosing factor-alpha, and interleukin-1beta compared to latent trigger points and normal muscle tissue. These chemicals sensitize and activate not only muscle nociceptors, but can also activate glia cells
Dry Needling and Trigger Points
There is overwhelming scientific evidence that trigger points are not just peripheral phenomena limited to muscles. Treatments directed at inactivating trigger points do have an impact on central processes by removing a common and peripheral source of persistent nociceptive input
It is nearly impossible to develop double blind, placebo-controlled studies of dry needling or acupuncture, given the invasive nature of the stimulus
Dry Needling and Acupuncture
In the context of acupuncture treatments, dry needling would be considered a technique of acupuncture. Dry needling is, however, not in the exclusive scope of any discipline.
Dry needling or trigger point inactivation rarely is a stand-alone kind of intervention and is just one aspect of a comprehensive manual physical therapy approach.
In this review, we have postulated that dry needling is a potent therapeutic measure to remove a constant source of peripheral nociceptive input originating from myofascial trigger points. As such, dry needling does not replace other manual physical therapy technique, but may be useful in facilitating a rapid reduction of pain and a return to function. A thorough understanding of the role of trigger points in peripheral and central sensitization is important in manual physical therapy practice. Trigger points can be inactivated with manual techniques and joint manipulations,but dry needling may be a more efficient and quicker method.
Published online 2011 March 25 (PubMed Full Text)
Active myofascial trigger points are one of the major peripheral pain generators for regional and generalized musculoskeletal pain conditions.
Current evidence shows that spontaneous electrical activity at myofascial trigger point originates from the extrafusal motor endplate. The spontaneous electrical activity represents focal muscle fiber contraction and/or muscle cramp potentials depending on trigger point sensitivity.
Nociceptor and non-nociceptor sensitization at myofascial trigger points may be part of the process of muscle ischemia associated with sustained focal muscle contraction and/or muscle cramps.
Active myofascial trigger points may play an important role in the transition from localized pain to generalized pain conditions via the enhanced central sensitization, decreased descending inhibition and dysfunctional motor control strategy.
Myofascial trigger points (MTPs) are hyperirritable spots in skeletal muscle associated with palpable nodules in the taut bands of muscle fibers.
An active MTP is one that refers pain either locally to a large area and/or to another remote location, the local and referred pain can be spontaneous or reproduced by mechanical stimulation which elicits a patient-recognized pain. A latent MTP does not reproduce the clinical pain complaint but may exhibit all of the features of an active MTP to a minor degree. Myofascial pain syndrome due to MTPs can be acute or chronic, regional or generalized; it can also be a primary disorder leading to local or regional pain syndromes or a secondary disorder as a consequence of other conditions
New evidence has emerged suggesting an important role of spontaneous electrical activity (SEA) at MTPs in the induction of muscle pain and central sensitization. This article reviews the literatures in the last decade about the SEA at MTPs; in particular, how SEA contributes to the induction of local and referred pain and how active MTPs are involved in the transition from the localized pain to generalized pain conditions.
Published online 2012 July 27 (PubMed Full Text)
TrPs [Trigger Points] are defined as exquisitely tender spots in discrete taut bands of hardened muscle that produce local and referred pain, among other symptoms. A TrP is composed of numerous so-called contraction knots. An individual contraction knot appears as a segment of a muscle fiber with extremely contracted sarcomeres and an increased diameter.
Although muscle damage is not required for the development of TrP, there may be a disruption of the cell membrane, damage to the sarcoplasmic reticulum with a subsequent release of high amounts of calcium-ions, and disruption of cytoskeletal proteins, such as desmin, titin, and dystrophin. Ragged red (RR) fibers and increased numbers of cytochrome-c-oxidase (COX) negative fibers are common in patients with myalgia, which are suggestive of an impaired oxidative metabolism .
Since the capillary blood pressure ranges from approximately 35 mm Hg at the beginning (arterial side) to 15 mm Hg at the end of the capillary beds (venous side), the capillary blood flow is temporarily obstructed during muscle contractions. The blood flow recovers immediately with relaxation, which is consistent with its normal physiological mechanism. In dynamic rhythmic contractions, intramuscular blood flow is enhanced by this contraction-relaxation rhythm, also known as the muscular pump. During sustained muscle contractions, however, muscle metabolism is highly dependent upon oxygen and glucose, which are in short supply.
Even contractions performed at only 10 % and 25 % of capacity or maximum voluntary contraction (MVC) may produce intramuscular pressures high enough to significantly impair the intramuscular blood circulation. The association of the percentage of MVC and intramuscular pressure (IMP) is highly dependent upon the architecture of the muscle.
Under aerobic circumstances, oxygen reacts with pyruvic acid producing a high amount of ATP (16 molecules per pyruvic acid molecule), carbon dioxide and water. Under anaerobic circumstances, however, most of the pyruvic acid produced during glycolysis is converted into lactic acid, thereby increasing the intramuscular acidity (pH). Most of the lactic acid diffuses out of the muscle into the bloodstream; post-exercise lactic acid is washed out within 30 minutes after exercise. Unfortunately, when the capillary circulation is restricted, as in sustained low-level contractions, this process comes to a standstill
in the direct environment of active TrPs, the pH may be well below 5, which is more than sufficient to excite muscle nociceptors
It is conceivable that in sustained low-level contractions and in dynamic repetitive contractions, ischemia, hypoxia and insufficient ATP synthesis in type I motor unit fibers are responsible for increasing acidity, Ca2+ accumulation, and subsequently sarcomere contracture. Furthermore, starting with the sarcomere (super-) contraction, the intramuscular perfusion slows down and ischemia and hypoxia will occur. This may lead to the release of several sensitizing substances causing peripheral sensitization
When ongoing ATP demands are within the capacity of the aerobic pathway, muscular activity can continue for hours in well-conditioned individuals. However, when the demands of exercise begin to exceed the ability of the muscle cells to carry out the necessary reactions quickly enough, anaerobe glycolysis will contribute more and more of the total generated ATP. Finally, the muscle will run out of ATP and sustained sarcomere contractions may occur, starting the development of TrPs.
In spite of a lack of well-designed studies, the best available evidence supports that TrPs develop after muscle overuse. Several potential mechanisms may play a role, such as eccentric overload, submaximal sustained, and (sub)-maximal concentric contractions. A key factor is the local ischemia, which leads to a lowered pH and a subsequent release of several inflammatory mediators in muscle tissue.
Published online 2013 March 27
The aim of this study was to determine whether the dry needling of myofascial trigger points (MTrPs) is superior to placebo in the prevention of pain after total knee arthroplasty.
All available reviews about the effectiveness of dry needling [11–13] reached the conclusion that dry needling appears to be an effective treatment, although studies are needed to elucidate whether its effects are superior to placebo
A single, brief, and safe dry needling treatment applied under anaesthesia in lower limb MTrPs reduced the pain in the first month after total knee replacement surgery, when pain is highest. Dry needling of MTrPs in the lower limb allowed patients to reach the same degree of pain reduction in 1-month as the subjects with a natural history or placebo intervention achieved in 6-months. It significantly decreased the need for postsurgical analgesia.
Curr Rheumatol Rep. 2014 Jan;
Trigger points (TrP) are hyperirritable spots in a taut band of a skeletal muscle, which usually have referred pain. There is controversy over whether TrP are a peripheral or central nervous system phenomenon. Referred pain, the most characteristic sign of TrP, is a central phenomenon initiated and activated by peripheral sensitization, whereby the peripheral nociceptive input from the muscle can sensitize dorsal horn neurons that were previously silent. TrP are a peripheral source of nociception, and act as ongoing nociceptive stimuli contributing to pain propagation and widespread pain. Several studies support the hypothesis that TrP can induce central sensitization, and appropriate TrP treatment reduces central sensitization. In contrast, preliminary evidence suggests that central sensitization can also promote TrP activity, although further studies are needed. Proper TrP management may prevent and reverse the development of pain propagation in chronic pain conditions, because inactivation of TrP attenuates central sensitization.