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12 Articles in Volume 13, Issue #1
A Modest Proposal (Thanks to Jonathan Swift—1667-1745)
Chronic Pain: Study of Complementary and Alternative Treatments
Decompression Surgery to Reduce Diabetic Peripheral Neuropathy
Extracorporeal Shock Wave Therapy—Application for Trigger Points
Improving a Practice Model for Prescribing Opioids
Interpretations and Actions Following Cytochrome P450 Testing
Is It Safe to Restart an NSAID Following an Endoscopically Confirmed NSAID-Induced GI Bleed?
January/February 2013 Pain Research Updates
Massage Therapy in an Ambulatory Pain Clinic
Practical Tips in the Treatment of Osteoarthritis of the Hip
Quantum Theory Underpins Electromagnetic Therapies for Pain Management
When a Pain Patient Insists on Alternative Treatments Alone

Extracorporeal Shock Wave Therapy—Application for Trigger Points

Part three of a three-part series examining the role of extracorporeal shock wave therapy in pain management.

Most clinicians who practice pain management are familiar with the contributions of Drs. David Simons and Janet Travell, who are credited with pioneering the importance of trigger points (TPs) in many of the pathologies we see in the clinic.1 The emergence of TPs as both a primary and secondary form of muscle pathology has been a gradual one, culminating in today’s more complete understanding.

In preparation for this report I reviewed or, more accurately, scoured the literature for a complete historical perspective on TPs. Surprisingly, the early descriptions of TPs do not look much different than today’s versions. From a descriptive sense, TPs have been characterized rather well right from the start. What has changed over time is our understanding of the importance that TPs play in myriad conditions affecting the muscles, joints, and skeleton.

Over the last 50 years, we also have evolved more interventions to treat TPs. The problem has been that none of the interventions have enough convincing data to support widespread use. What is also surprising is that not until the 21st century were TPs actually imaged, which, logically, should then lead to a better and more lucid understanding of how to treat this entity.1 Figure 1 illustrates the concept of the TP whereby “X” indicates the location (foci) of a TP followed by the pain radiation pattern (red) that a patient describes as symptomatic.

Trigger Point IllustrationFigure 1

In fact, the ultrasonic image of a TP might surprise many readers. The search for truth is a process of acquiring, validating, and discarding (when necessary) information and in the process, challenging our assumptions so we end up giving shape to a conceptual schema that is meaningful in our clinical endeavors.

For a myofascial condition that has been identified for many years, for which we have so many apparently valid treatments, and about which we also have such a complete understanding, why is it we are still debating TPs? The topic should have been relegated to old news a long time ago. Unlike infectious diseases, TPs don’t respond to vaccines, inoculation, medications, or surgery. Yet TPs are ubiquitous in North American society and occur at a much higher frequency than any old or newly emerging infectious disease. They have indeed become the focal point in many discussions surrounding musculoskeletal pathology so any treatment that demonstrates an efficacy for resolving TPs in muscle is a welcome addition to the pain practitioner’s arsenal.

Overview of TPs

In preparing this report, I gathered a fairly large amount of data—at least more than the usual amount of reports/citations. The availability of information on this subject is really quite abundant with scientific validation studies continuing to increase and far surpassing those unequivocal reports based solely on observation and opinion. The reason for the extra volume of data is that this is a report that should focus on the efficacy of a new technology (shock wave therapy); however, since it is described within the treatment context of myofascial pain, whose hallmark features are of that highly controversial entity known as the TP, we should first validate the target condition.

The existence of TPs has now been confirmed by a large and growing body of funded (including by the National Institutes of Health) research. We can now see TPs using ultrasonography; we can now measure their electrical activity and stiffness using electromyography (EMG) and acoustic elastography, respectively; we can palpate them, provoke, measure their size, and assess their tenderness (algometry); assay their biochemical environment (in vitro studies); and treat them with various interventions and watch them change shape and disappear.

Early Myofascial Work

The first edition of Travell and Simons appeared circa 1983, and was the first organized attempt to provide a detailed accounting of what TPs were and how TPs behaved, which illuminated, to some degree, how best to locate them.2 This was one of the few examples where much of the discovery work was performed, and data collected, many years before the actual publication. The authors, Janet Travell, MD, (White House physician to Presidents Kennedy and Johnson) and David Simons, MD, (National Aeronautics and Space Administration flight surgeon) described TPs in two forms: latent and active, with characteristics linked to each form. The preferred form of treatment, as recommended by these pioneers, was injection therapy and/or spray and stretch techniques using a vapo-coolant such as fluoromethane. Along the way, other forms of treatment—such as ischemic compression—became popular but eventually fell out of favor with both Travell and Simons. They preferred, instead—at least later on—to advocate for less intense digital pressure in their manual approach.2

There was much work by both Travell and Simons prior to the publication of the first manual, but they were not the only group to be studying myofascial pain. In 1957, the prolific pain physician John Bonica, MD, published a report in the Journal of the American Medical Association and made references to the existence of hypersensitive regions (referring to pain syndromes) called the “trigger area” and recognized that this area formed as part of muscle and connective tissue.3 Dr. Bonica goes on to make reference to an anatomical mapping of these trigger areas, quite possibly a similar conceptualization of pain referral zones mapped out by Travell and Simons. In his description, he also makes references to a vicious cycle that becomes self-sustaining (pain-spasm-pain) and has both a motor and sensory component.

Although the focal point of his paper is about two forms of local anesthesia as the primary intervention for treatment of trigger area pain, he does acknowledge physical therapy, specifically corrective and restorative exercises, along with psychotherapy, as being beneficial in these types of conditions. Presumably, Bonica realized early on that there was a connection between psychic stress and somatic dysfunction, thereby including psychotherapy as a treatment recommendation.

In 1978, Burnell Brown, Jr., MD, PhD, wrote a paper outlining the differential diagnostic algorithm best used to distinguish between primary myofascial syndrome and the then thought to be more sinister disc/facet dysfunctions and vertebral body fractures.4 Even Ronald Melzack, PhD, (of Melzack and Wall’s “gate theory”) chimed in on possible physiological mechanisms underlying the genesis of TPs and remarked that his gate control theory of pain—which essentially provides a rationale for using hyperstimulation analgesia techniques such as dry needling, intense heat/cold or electrotherapy, and ischemic compression—was the mechanism responsible for these analgesic effects.5 Intense sensory input might “close the gate” by means of a central biasing mechanism possibly located in the brainstem’s reticular formation. The memory of pain was probably linked to a reverberating neural circuit that had to be disrupted (painful stimulus), thus providing pain relief in many patients. This conservative method of achieving analgesia was certainly preferable to surgical methods of sensory input interruption.

Clinical Features

The clinical features of a TP, as described by Travell and Simons, were that TPs existed within a taut muscle band near the muscle belly, had a palpable nodule/knot, were painful on palpation, often referred pain to distal regions, and had a palpatory twitch response. Firm palpation could give rise to sensory, motor, and autonomic dysfunction.6 Much has been written in the last 20 years to try and distinguish or differentiate the characteristics between a TP, as seen in myofascial syndromes, and the tender points of a condition such as fibromyalgia. Essentially, some key differences would be that the tender points do not have palpable nodules; are often close to musculotendinous attachments, not muscle bellies; have pain/tenderness in their vicinity (unlike TPs); and poor or undiscovered unique histologic biomarker assay (Table 1).7

Table 1. Comparison of Trigger Points vs Tender PointsTable 1In the 1990s, we witnessed the application of EMG technology to try and further validate what manual therapists were feeling with their hands as they performed various soft tissue treatments.8 The idea of psychoneuroimmunology was not well known or understood at the time. Myofascial pain syndromes and TPs were still not widely known and were considered by many as a “functional syndrome”—a mysterious, unexplained, and highly variable condition probably having its origins in the psychosocial realm. If we have no biomarkers for it, and we can’t see it (and, therefore, can’t measure it), then it probably doesn’t exist.

Pressure algometry (measuring tissue tenderness) became an option to further characterize TPs in the 1980s,9 but even those measures were ultimately determined by patient response and, therefore, could be managed and would be considered an unconvincing “soft” outcome measure. Thermography (measuring heat in tissues) as an outcome measure had been given a bad reputation in the courts, ultimately was relegated to bad science, and eventually became nonreimbursable as a result.

The theoretical constructs supporting the existence of TPs became more difficult to advance until the late 1990s and 2000s with the advent of musculoskeletal ultrasonography, and more recently acoustic sonoelastography.10,11 Diagnostic musculoskeletal ultrasound has the potential to become a sentinel diagnostic tool stemming from its ability to confirm the presence or absence of many conditions inherent in muscles, tendons, ligaments, and peripheral nerves, as well as act as a tool to measure change, stage a lesion, and confirm the value of an intervention by documenting the treatment effect (Figures 2 and 3).12 Figure 4 depicts an artistic rendering of what a masseter muscle TP might look like and its orientation within the belly of the muscle.

Figure 2Figure 2

Figure 3Figure 3Figure 4Figure 4

Anatomy of a TP

We believe that the genesis of a TP is related to muscle overuse, injury, disease, chronic postural strain, and perhaps even age-related musculoskeletal decline (deconditioning) and sarcopenia. The TP has been characterized in several different ways including functional (impairment), pathological (symptoms), histological (assays), electrophysiological (EMG), and most recently, radiological using diagnostic ultrasound imaging (DUI). The appearance of a TP on ultrasound is consistent with an encapsulated structure similar to a synovial cyst (hypoechoic) in echotexture. There appears to be a wall boundary (encapsulation) that can be compressed if the entity is superficial enough, and on compression will deform. Our studies show that the entity can either return, or it can dissipate post-treatment.

Treatment Options

Treatment recommendations for TPs are more anecdotal than scientific. However, using ultrasonography as an outcome tool, at least we can now compare the effectiveness of various forms of treatment and be able to measure structural changes in a TP post intervention. The dark or hypoechoic appearance of the TP entity is consistent with an inflammatory nodule, which is also consistent with the histological descriptions provided by in vitro researchers studying TP milieu assays. Shah et al have studied micro-analytical assays of normal muscle tissue versus both active and latent TP-infested tissues and have provided some interesting insights into the differences between these tissue types.13 This level of research helps validate the clinical observations for myofascial syndromes and provides insight into how best to treat the condition. Between new imaging capabilities and some excellent basic histological research, more definitive evidence for the existence of TPs has arrived.

Shock Wave in TP Therapy

Figure 5Figure 5

Diagnostic ultrasound appears to be a useful tool to identify, monitor, and evaluate TPs as part of myofascial syndromes/disorders. Figure 5 illustrates an ultrasound scan depicting a TP just medial to the scapular insertion of the levator scapulae. Other landmarks are labeled to provide anatomical orientation to those of you who are new to ultrasonography. Figure 6 illustrates this same area after a 15-minute treatment using acoustic compression or shock wave therapy. There are some clear differences between the pre- and post-scans, with the post-scan appearing significantly more echo-normal. The patient did experience an audible “popping” noise during the treatment, after which tenderness abated and the TP was no longer visible on DUI. We are not certain whether the pop was related to the irritable point we were treating (ie, actually related to the acoustic energy build up) or was an incidental occurrence related to random scapular motion that occurred during the treatment.

Figure 6Figure 6

The histology data emerging clearly support the active TP as having an inflammatory component, which is also consistent and supported by the ultrasonic appearance of an active TP.14 Areas of the same muscle both with and without TPs show entirely different levels of inflammatory and pain-related analytes on lab analysis.14 The problem with TPs that are left untreated is that they can eventually lead to bigger problems. TPs that continue to elicit noxious stimulation will initiate both motor and sensory changes in the peripheral and central nervous systems (sensitization). TPs have demonstrated spontaneous EMG activity, the property most likely responsible for what the clinician interprets as a hyperirritability nodule or knot during palpation.15 There are a number of possible underlying physiological explanations noted over the years including end-plate firing dysfunction,16 muscle perfusion deficits,17 muscle hypoxia,18 mitochondrial dysfunction,19 alteration in acetylcholinesterase levels,20 and dysfunctional feed-forward neurogenic inflammation.21 The sensitizing biochemicals found within the TP milieu can eventually lead to unwanted spinal plasticity events such as sensitization and chronic pain.

As alluded to earlier, several methods for the treatment of TPs have become popular with practitioners including using cold laser; CryoProbe or ischemic compression; dry needling using acupuncture needles; and extracorporeal shock wave therapy, or myotripsy (Figures 7-10). At our facility, we are fortunate in that we have the opportunity to use all four methods interchangeably, with varying degrees of success for any one method. We have not performed a comparative effectiveness study to evaluate superiority between treatments to date. So, this report is really not about comparing effectiveness between methods; it is, however, about illuminating the advantages of using shock wave therapy for the treatment of TPs.

Figure 7Figure 7

Figure 8Figure 8

Figure 9Figure 9

Figure 10Figure 10



The two primary advantages in using this technology are that the acoustic energy used to treat a TP can also be used to identify both latent and active TPs. For all we know, it might even be identifying the pre-TP status of taut band formation or preclinical TP areas. This statement is purely speculative at this time and based on the results of the pretreatment scan we have performed on approximately 150 patients to date. The  WellWave unit we use has a scan function that allows the practitioner to virtually locate a tender, painful, irritable, or pre-irritable area. It does this by directing energy, of lower power densities than treatment dosages, to the painful region. The patient with an irritable knot will feel the acoustic energy as soreness—sometimes quite intense. What we also find during our “sono-isolation” (tissue evaluation function) is that pre-tender points become tender and are identified and treated as part of that session. We are currently evaluating these patients with latent TPs to see if in fact these points go on to become active or at least, more tender with time. We expect treatment-related pain to dissipate within 48 hours versus the evolution of a latent to active TP to be more permanent.

Besides the sono-isolation function unique to the machine we use for shock wave treatment, there is another interesting finding that needs more formal confirmation in clinical testing, but for now, serves as a point of interest and discussion—that is, those patients treated for TPs using shock wave acoustic energy appear to have a longer remission period. The time between successive treatments is considerably longer when patients have been treated with acoustic compression. This might be explained purely as a treatment effect, or possibly by other confounding factors such as co-interventions (medications/therapies, etc), inherent differences between subjects (severity, gender, age, comorbidities), or exposures to perpetuating and maintaining factors such as activities/exercises (eccentric exercise) and postures (fatigue/static tension states) since the link between TPs and certain muscle states (ischemia/hypoxia) have been postulated.22 There is some evidence to suggest that shock wave acoustic compression energy systems achieve their results from reducing the concentration of nociceptor-stimulating substances inherent in TPs, which would in turn abort the cycle leading to possible plastic changes in the spinal cord by averting the sensitization phenomenon.23 There are a multitude of possible biochemical pathways and substance cascades that could be operating through this excellent example of mechanotransduction, or how an outside mechanical force (acoustic energy) applied at the tissue/cellular level can initiate a complex series of cellular signaling events that lead to changes in the cellular environment manifesting, in this case, as analgesia.


Practitioners have developed numerous ways to eradicate human muscle tissue of TPs, those extra tender, irritable, and pain-inducing areas that lie buried within muscle bellies. There are still more questions than answers when we engage in a discussion about TPs. There are no clear answers regarding which treatment is best for a TP. Clinicians have expounded on the original Travell and Simons recommendations for TP treatment, those being injection, compression, and spraying and stretching the tissue. In the future, more effort into translational and comparative effectiveness research should narrow down the list of treatment options—or maybe not. Are all TPs inherently similar or are there subsets or subtypes of TPs within the more common TP population? A case in point: synovial/ganglion cysts, plantar warts, and growths/masses/tumors in general all demonstrate there can be individual differences within these entities that make their treatment amenable to a different form of therapy.

Treatment optimization is dependent on having several frontline strategies, much like the role of chemotherapy in certain malignant tumors. The value of acoustic compression treatment for TP therapy is that it appears to have a very beneficial treatment effect duration, thus minimizing the time interval between subsequent treatments. The included feature of sono-isolation can be an additional benefit, especially to the novice TP practitioner. Now that many of the salient features of a TP can be measured to some degree and with more clarity, research efforts in the future should help elucidate which treatments are the most cost effective, including those treatments administered at home by patients themselves. Recent evidence has suggested that patients can effectively treat TPs themselves,24 which has raised some concern in terms of how this type of data will be interpreted by payers. The use of inexpensive DUI with or without tissue assays should provide a good comparative analysis of whether TPs can effectively be managed at home by the patient, and which interventions will yield the greatest return.

Last updated on: March 27, 2013
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