The red shaded area is the referred pain caused by the Trigger Point and the darker red means more people experienced pain in that area. This example diagram is for the Abductor Digiti Minimi for the foot :. These triggerpoint and referred pain diagrams can be purchased from Amazon. The diagrams are available in a very useful flip chart as well as in the original. If you are a healthcare provider and would like advanced training for the treatment of Myofascial Pain Syndrome, visit MyoRehab.
To contact us, please send an email. Black Xs locate the trigger points most likely to be causing the pain patterns illustrated in red. Moreover Medicalstudyzone. If you feel that we have violated your copyrights, then please contact us immediately. Comments Really hoping this helps out my boyfriend. Your email address will not be published. Consequently, a persistent noxious barrage from the periphery can create long-lasting alterations in the central nervous system.
Metabolic and gene induction changes, such as cyclo-oxygenase 2 COX-2 induction in dorsal horn neurons, are maximal at several hours after an initial noxious stimulation, and bolster functional changes after peripheral tissue injury Sensitization of primary afferents is responsible for the transition from normal to aberrant pain perception in the central nervous system that outlasts the noxious peripheral stimulus.
A possible explanation for expanded referral pain patterns is increased synaptic efficiency through activation of previously silent ineffective synapses at the dorsal horn. This concept of opening previously ineffective connections was demonstrated in a rat myositis model.
Experimentally-induced inflammation unmasked receptive fields remote from the original receptive field, indicating that dorsal horn connectivity expanded beyond the original neurons involved in nociceptive transmission In this study, nociceptive input resulted in central hyper-excitability and this finding helps to explain referred pain patterns common to MPS.
Central sensitization may also facilitate additional responses from other receptive fields as a result of convergent somatic and visceral input at the dorsal horn 50 via wide dynamic range WDR neurons. Furthermore, afferent fibers have the ability to sprout new spinal terminals that broaden synaptic contacts at the dorsal horn and may also contribute to expanded pain receptive fields This change in functional connectivity may occur within a few hours, even before metabolic and genetic alterations occur in dorsal horn neurons After activating WDR neurons, afferent input from active MTrPs then ascends the spinothalamic tract to reach higher brain centers.
In addition to activating the thalamus, muscle afferent input preferentially activates the limbic system i. Increased activity in the limbic system leads to greater fear, anxiety, and stress.
Furthermore, Niddam et al. Latent MTrPs are not associated with spontaneous pain; however, they cause local and possibly referred pain upon deep palpation. This begs questions of their underlying pathophysiology and connectivity to the central nervous system. Do latent MTrPs play a role in central sensitization? How is it possible for these lesions to refer pain to distant locations? Two assumptions must be made to explain the mechanism of latent MTrPs. First, these latent MTrPs send nociceptive, sub-threshold signals to the dorsal horn of the spinal cord.
This would effectively sensitize the central nervous system without the perception of pain, as is characteristic of latent MTrPs. Second, ineffective synapses exist within the dorsal horn. In this way, nociceptors from muscle containing the MTrP have connections to dorsal horn neurons, innervating remote muscle regions Sub-threshold potentials and ineffective synapses could serve to explain the sensory phenomenon of latent MTrPs.
Taken together, it could be hypothesized that the characteristics of latent MTrPs occur through a series of events. Although latent MTrPs are not spontaneously painful, they send excitatory, sub-threshold potentials that sensitize the dorsal horn. Sensitization of the dorsal horn opens previously ineffective synapses to distant muscle sites. As a result of sensitization, palpation of the latent MTrP induces pain locally and to distant sites i.
Thereby, following muscle palpation, pain is experienced at the site of the palpated latent MTrP and in distant, seemingly unrelated muscle. Human studies have shown that central sensitization can occur without the experience of acute pain. Intramuscular injection of nerve growth factor NGF results in allodynia and hyperalgesia, both manifestations of sensitization Further, rat studies demonstrated that NGF injections activate an increased proportion of muscle nociceptors.
In concordance with this finding was the presence of excitatory sub-threshold potentials 56 , The thalamus and limbic system are critically involved in the subjective experience of pain.
Since sub-threshold potentials provide nociceptive input without subsequent action potentials into higher brain centers, there is no perception of pain. However, these hypotheses did not consider the prevailing theories of pain processing such as the Gate Control Theory of Pain by Melzack and Wall 58 even though Simons and Travell were familiar with them.
The Gate Control Theory was a breakthrough concept in pain research because it suggested that the pain experience was a dynamic one, where afferent nociceptive signaling could be modified and influenced by neurons in the CNS acting as inhibitory or excitatory gates. Specifically, activation of these sensory afferents can inhibit the activation of second-order neurons that receive input from the smaller nociceptor fibers Figure 4.
In addition, supraspinal inputs can also modulate pain perception. Gate Control Theory. Pain stimulation activates small nerve fibers. As a result, the fibers send input to the neurons to block the inhibitory interneuron I , which is now unable to block the output of the projection neuron P that connects with the brain. Since the excitatory gate is open, pain is perceived. Non-painful stimulation activates large nerve fibers primarily. As a result, the projection neuron P and inhibitory interneuron I is activated.
However, because the inhibitory interneuron blocks the signal in the projection neuron P that connects to the brain, the excitatory gate is closed, and no pain is perceived. Without any stimulation, neither large nor small nerve fibers are activated. The inhibitory interneuron I blocks the signal in the projection neuron P that connects to the brain. The excitatory gate is closed and no pain is perceived.
These advances in understanding the pathophysiology of chronic pain had implications for MPS. Travell and Simons were well aware of the mechanistic aspects of the Gate Control Theory of Pain, as well as some of the implications with respect to central sensitization and gene regulation. However, the integration of this theory and their clinical observations did not occur until newer theories of pain perception and modulation were described.
These involved gene regulation, receptor expression, and depolarization thresholds. In particular, more recent findings and data suggest that other processes such as neurogenic inflammation, sensitization of wide dynamic range neurons, and limbic system dysfunction may play a role in the initiation, amplification, and perpetuation of MPS. Another important concept that Simons and Travell did not consider in their theories was the dynamic balance between supraspinal descending facilitation and inhibition, and its influence on pain perception.
The relative amount of descending facilitation versus inhibition modulates the perception of pain from a normal to an aberrant state. The rostral ventral medulla RVM is a critical relay area between the periaqueductal gray and the spinal cord which functions in the descending pain control system. It does so through projections that modulate activity in the dorsal horn. Following initial tissue injury, the ON cells serve a useful and protective purpose designed to prevent further damage.
Under ordinary circumstances, tissue healing would lead to a decrease in ON cell activity and an increase in OFF cell activity. However, in chronic musculoskeletal pain conditions, there appears to be an overall shift to a decrease in inhibition, presumably due to an imbalance of ON cell and OFF cell activity Disrupted descending inhibition in chronic musculoskeletal pain may lead to an increased pain sensitivity of muscle tissue The history of soft tissue pain treatments follows the clinical trends of those physicians and soft tissue specialists e.
Hence, early literature about therapeutics for MPS was mainly descriptive. Publications included recommendations for the use of postural exercise, heat, cold, stretch, fluoromethane spray, electrical stimulation, needling, and acupuncture, to mention a few They stressed the importance of the physical examination including thorough palpation of muscle and surrounding tissue in order to identify MTrPs.
The MTrP requires training and experience to identify, and was the target for their treatment 9. They often relied on pressure pain threshold to supplement their palpation findings in order to distinguish a latent from an active MTrP.
Today, several other methods including intramuscular needling, surface electromyography-guided assessment, infrared thermography, ultrasound, and laser Doppler flowmetry are utilized in an attempt to objectify MTrP findings Nevertheless, palpation by an experienced clinician remains the gold standard in MTrP identification. Travell and Simons were not the first to identify and develop a treatment for MTrPs. They were, however, among the first to recognize the relationship of the trigger point to MPS and clinical soft tissue pain syndromes.
They proposed that deactivating the trigger point was an essential component to successfully treating the pain syndrome 9. One of various techniques that Travell and Simons relied on to treat MTrPs was injection with local anesthetics. The injections were beneficial because they could reach muscles that could not be stretched during manual therapies e.
However, in the ss, the use of local anesthetics raised several concerns including muscle necrosis, fatal anaphylactic shock, and dose-related toxic effects that resulted from multiple treatments using cumulative doses.
Travell and Simons stressed the importance of using a low dose and taking precautionary measures by having a tourniquet, intravenous diazepam, equipment for artificial respiration, and cardiac defibrillator available during the injection 9 , Although Travell and Simons utilized this technique, they were concerned about the risks of anaphylactic shock in a susceptible person.
Accordingly, they often preferred to deactivate MTrPs by spray and stretch 9 , which involves spraying the overlying skin with ethyl chloride, introducing a sudden sensory stimulus which distracts the patient from the discomfort associated with stretching the affected muscles 9 Figure 5. One of the benefits of spray and stretch is that it allows for many muscles to be treated in a short period of time.
However, in the event that the MTrP was unresponsive to spray and stretch, injections with anesthetics were still used. Spray and Stretch Application. The lower posterior muscles of the upper back are stretched while the spray is applied in a downward motion, from the patient's neck to the referred pain region.
Drawn from Ferguson, L. Gerwin Clinical mastery in the treatment of myofascial pain. In , Sola and Kuitert introduced saline injections to deactivate MTrPs, which lacked the risks of local anesthetics Interestingly, Frost et al. Naturally, the effectiveness of needling without anesthetics lead to the question of whether saline was even necessary for deactivating MTrPs.
In , Lewit was one of the first physicians to try needling without the use of anesthetic or even saline, a technique that became known as dry needling Given the size of the hypodermic needle and the invasive technique used, this form of dry needling was quite painful, which deterred others from using it instead of injections with procaine. However, Lewit found that the effectiveness of dry needling was related to both the severity of the pain and the precision by which the needle is inserted in relation to the MTrP Currently, clinicians use acupuncture needles to minimize pain and tissue injury, and have found that inserting a needle into the general area of the MTrP as opposed to directly into the MTrP can have the same therapeutic effect 61 Figure 6.
Dry Needling. A series of images are shown in which the MTrP is identified, the needled is inserted in the MTrP using a swift tap, the muscle and surrounding fascia are probed with an up and down motion of the needle in a clockwise direction, and the needle is left in place for minutes for full therapeutic benefit.
In addition to dry needling, clinicians in the mid th century started experimenting with the use of acupuncture, after learning that the Chinese were using acupuncture analgesia to suppress surgically evoked pain In the s, interest in acupuncture surged, and even President Nixon and his personal physician enthusiastically supported its use. Furthermore, MTrPs are palpable, tender nodules, whereas acupuncture points are not palpable, necessarily tender, or nodular Due to the lack of sound scientific studies, interest in acupuncture quickly declined, but continues to be further studied as a topic with important MTrP implications today.
In the s, use of fluoromethane spray, a topical anesthetic, ceased because of its toxic effect on the ozone layer and the fact that its highly flammable properties led to accidental death This occurrence spurred the development of various alternative treatments.
For example, the counterstrain method see online video supplement , a positional release technique developed by Jones in , is shown to be effective at reducing pain and improving function. Ischemic compression, which aims to equalize the length of the sarcomeres, has also been shown to decrease pain sensitivity. Another method is transverse friction massage which, when combined with exercise, has been shown to increase flexibility along with function All three of these techniques stretch the muscles, which is the aim of any manual therapy.
In addition, Travell and Simons stressed the importance of moist heat to relax the underlying muscles and to diminish the tension caused by the MTrPs. They also educated patients on proper postural positioning while sitting, standing, and reading in order to avoid sustained contraction or prolonged shortening of muscles 9. During this time, Travell and Simons also explored the role of drugs with respect to pain relief codeine, aspirin, anti-inflammatory drugs , muscular relaxation Diazepam , sleep anti-histamines , and post-therapy soreness anti-inflammatory action , although their findings were largely empirical.
Travell and Simons noted that many of the side effects for these drugs were often greater than symptoms of MPS. In cases where the drug seemed effective, there was always the possibility of a placebo effect 9. In the s and s, there was significant interest in technologies like transcutaneous electrical nerve stimulation TENS , ultrasound, and laser for the treatment of soft tissue pain. Researchers debate the effectiveness of laser and ultrasound for the deactivation of MTrPs but generally agree that these technologies are effective for pain management.
Biofeedback, introduced by Keefe in , and other relaxation techniques like hypnotherapy, are also available to help patients manage their pain by training them to regain control of their pain condition. It is important to note that clinicians have been treating MPS based on what they believe is its underlying pathophysiology and what are considered safe and effective treatments.
For example, Travell and Simons primarily utilized the spray and stretch technique because they attributed MPS to muscle overload, whereas Sola and Kuitert 65 and Lewit 67 utilized saline injections and dry needling, respectively, because they believed their methods mechanically disrupted the dysfunctional endplates located near the MTrP. Both of these theories are still considered plausible and discussed today.
While the etiology of MPS and the pathophysiology of MTrPs are not yet fully understood, some investigators are suggesting that treatments should focus not only on the MTrP, but also the surrounding environment e.
The biochemical contributors to pain are very important. The role of muscle, fascia, and their cellular components are also important factors to both MPS and the formation of the MTrP. This thinking has led clinicians to try to reduce the size of the MTrP, correct underlying contributors to the pain, and restore the normal working relationship between the muscles of the affected functional units According to Dommerholt, all treatments fall into one of these two categories or both: a pain-control phase and a deep conditioning phase.
During the pain-control phase, trigger points are deactivated, improving circulation, decreasing pathological nociceptive activity, and eliminating the abnormal biomechanical force patterns.
During the deep conditioning phase, the intra- and inter- tissue mobility of the functional unit is improved, which may include specific muscle stretches, neurodynamic mobilizations, joint mobilizations, orthotics, and strengthening muscle Current approaches for management of MPS include pharmacological and nonpharmacological interventions.
Among the pharmacological approaches are anti-inflammatory, analgesic, and narcotic medications, topical creams, and trigger point injections, which are now safer and more effective. Non-pharmacological interventions include manual therapies, which continue to include post-isometric relaxation, counterstrain method 72 , trigger point compression, muscle energy techniques, and myotherapy 73 , along with other treatments like laser therapy 74 , dry needling, and massage 35 , According to Simons, stretching and strengthening of the affected muscles is important for any treatment While many of the manual treatment methods stay the same or are only slightly modified all include some form of mechanical pressure , it is the underlying theory as to why they are effective that continues to evolve with further study.
Modalities and manual treatments are often clinically effective for deactivating active MTrPs and desensitizing sensitized spinal segments, and are commonly employed as a first line of treatment before attempting more invasive therapies.
While a number of recent reviews and meta-analyses have focused on needling, the effectiveness of manual therapy should not be overlooked and may possibly be just as effective as needling Among the invasive therapies, the scientific articles report mixed results.
Generally, dry needling, anesthetic injection, steroids, and botulinum toxin-A [BTA] of the trigger point have all been shown to provide pain relief 70 , 77 - Regardless of the method used, there is considerable agreement that elicitation of a LTR produces more immediate and long-lasting pain relief than no elicitation of LTR 81 - 86 , although some still believe that eliciting an LTR is not necessary for improvement.
Nevertheless, within minutes of a single induced LTR, Shah et al. While treatment options for soft tissue pain have not changed dramatically, researchers today have certainly discovered better ways of categorizing and analyzing the clinical data they collect and determining if a treatment is effective.
Gerber et al. Clinicians are shifting the focus from not only pain relief and increasing function, but to improving the patient's quality of life as well. When Kennedy won the presidential election in , he appointed her as his personal physician. Kennedy, with his successor Lyndon B. She continued through Johnson's re-election, but decided to leave the White House in While serving as the President's personal physician, Travell also took on the role of Associate Clinical Professor of Medicine at the George Washington University in Even after leaving the White House, she continued teaching at the University as a faculty for the School of Medicine.
Travell remained active in the medical field until the end: writing articles, giving lectures, and attending conferences. Her personal interest led her to investigate, explain and expound on the phenomenon of myofascial pain syndrome, secondary to trigger points, first written about in the s by Dr Dudley J. Travell's research resulted in over scientific articles, as well as the acclaimed co-authored book with David G.
Simons: Myofascial Pain and Dysfunction. The Trigger Point Manual. She also wrote her autobiography, Office Hours: Day and Night , which sheds light on her career and life.
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