Jeff Watson LMT, CSP
Trigger Point Therapy . Osteopathic Muscle Energy Technique . Myofascial Release
Dear Referring Physician
Thank you for your myofascial pain referrals. Your patient will be treated with the utmost kindness and respect, receiving excellent, cost effective care. I will be the one to personally evaluate and treat your patient’s condition. In a typical visit, which lasts a half hour, I will locate and treat the myofascial trigger points causing their pain as well as educate them on how to remain pain-free. Trigger points are treated by manual manipulation and stretching of the affected muscles.
Your patient will then be given specific self-stretching and strengthening exercises and ergonomic movement suggestions to help keep them free of pain. I actively strive to keep the number of visits to a minimum, preferring self-care education over unnecessary repeated visits.
Please feel free to contact me with any questions or concerns about your patient. For an overview with the “distilled essentials” about myofascial pain and trigger point therapy please read “Diagnosing Myofascial Trigger Point Pain” below.
Sincerely,
Jeff Watson, L.M.T., C.S.P.
Diagnosing Myofascial Trigger Point Pain
Introduction
The leading causes of disability in people in their working years are musculoskeletal conditions.¹ Population surveys also reveal large numbers of people with pain that is labeled as musculoskeletal in origin and that the incidence of distress increases with age.
Musculoskeletal conditions can be classified into two main categories, articular and soft tissue. Articular disorders of diarthrodial joints include articular diseases (arthritic inflammation and injury) and articular dysfunctions (pain and limited joint motion). Soft tissue disorders primarily affect non skeletal structures such as: muscles, fascia, tendons, and ligaments.²
One very common soft tissue disorder which is easily treatable and often overlooked is myofascial trigger point pain. The traditional use of the term myofascial pain was first coined by Drs. Travell and Rinzler in the early 1950’s to specifically describe the effects of trigger points on muscular pain.³
Recently, some authors have morphed the term “myofascial pain” to include not only trigger point generated pain but any regional soft tissue pain syndrome, despite its etiology. To avoid confusion, this article will use the phrase Myofascial Trigger Point Pain (Myofascial TrP pain) as suggested by Drs. Mense and Simons, instead of the traditional definition.²
A Brief Theoretical Background and Nature of Trigger Points
Trigger points (TrPs) can develop in any of the over 400 paired skeletal muscles in the human body, but the muscles in and around the cervical, shoulder, lumbosacral and hip regions are the most common sites. Dysfunctional neuromuscular endplates resulting from “muscular abuse” appear to be the pathophysiologic process that sets off the formation of a myofascial trigger point. Excess acetylcholine release by a dysfunctional motor endplate causes sustained depolarization and the continuous release and inadequate uptake of calcium ions by the local sarcoplasmic reticulum. This in turn causes a sustained contraction of sarcomeres forming a taut band in the effected muscle, and eventually produces a palpable “knot” or trigger point within the band.⁴
This initial endplate depolarization and sarcomere contracture can become self-perpetuating by an ensuing increased metabolic demand and ischemia. This causes a local energy crisis to occur. The local energy crisis in turn causes the failure of the calcium pump and its reuptake of calcium ions back into the sarcoplasmic reticulum. The failure of the reabsorption of Ca²⁺ perpetuates the contraction of the taut band of sarcomeres and the TrP(s) it harbors.⁴ The above cited process is referred to as the integrated hypothesis.
TrPs are either classified as active or latent. Pain, weakness and limited range of motion of a muscle tendon unit are the most common symptoms. Active myofascial TrPs produce both pain and restricted movement. Most often the pain from an active TrP is only felt during movement or muscle loading. However if the active TrP is extremely irritated the patient can experience pain even at rest.
Latent TrPs are far more common than active TrPs, causing stiffness and restricted range of motion but no “active” pain. Both latent and active TrPs when palpated will produce the characteristic pain referral pattern for that muscle. Myofascial TrP pain patients are generally not aware of latent TrPs and the restricted range of motion they cause. They seek help only after latent TrPs become active and produce functional pain. Latent TrPs can become active if the conditions sustaining them become more aggravated and are not addressed.
Left untreated there are three possible outcomes for an active myofascial TrP. With reduced activity and time (2-4 weeks), some TrPs will go on to recover fully without any intervention. A few TrPs that are not addressed will progress into a chronic condition. Others, and probably the majority, will “deceptively” calm down to a latent pain free stage only to reactivate at a later time.
With the return of pain-free muscle function the patient may erroneously believe that everything is physiologically back to normal. Total recovery from myofascial TrP pain can get delayed or arrested at this “Latent Pain-Free Threshold.” The patient feels “pain-free” and reduces self-care and therapy without realizing that their condition has not yet fully resolved. They are unaware of any remaining taut bands harboring latent TrPs that are still restricting range of motion in the affected muscle(s). However, below the “pain-free surface” their myofascial TrP pain lies dormant, waiting to flare up when future conditions are right. These episodic flare-ups of latent TrPs to active ones and back again can go on for decades. The clinician needs to strongly impress on the patient the importance of continuing self-care beyond the latent pain-free threshold.
There is no way to precisely predict how a TrP will respond without treatment. As mentioned above some TrPs can be self-limiting. If the TrP is of recent onset, and a “first time offender” of a single muscle syndrome, with no perpetuating factors, then there is a reasonable chance that it can return to a normal pain free function without therapy. If however the TrP is of advanced onset, and a “repeat offender,” of a multi muscle syndrome, with perpetuating factors, it’s extremely unlikely to recover without considerable intervention.
Trigger Point Developmental Continuum
Progression:
Normal Taut Band Taut Band Taut Band Taut Band
Muscle Onset→ with → with → with → with
No TrP Latent TrP Active TrP Extremely Active TrP
↗
ǀ← ← ← ‖ ← ← ←Recovery
Latent Pain-Free Threshold
*To date the concept of TrP development has been observed clinically but remains untested experimentally.
__________________________________________________________________________________________________________________________
Features:
Normal Taut Band Taut Band Taut Band Taut Band
Muscle with with with with
No TrP Latent TrP Active TrP Extremely Active TrP
Normal Restricted range Restricted range Restricted range Restricted range
pain-free of motion with of motion with of motion with of motion with
function. no pain referral. pain referral from pain referral from pain referral from
TrP palpation. TrP palpation. TrP palpation.
+ +
Pain with Pain with
movement movement
and muscle and muscle
loading. loading.
+
Pain at rest.
More Common → → → → → → → → Less Common
Without treatment some TrPs will go on to recover fully, Some will progress to a chronic condition, others can deceptively calm down to a latent pain free stage only to reactivate at a later time.
Myofascial TrP affected muscles can cause secondary syndromes which include articular dysfunctions, peripheral nerve entrapments, tendinopathies and occasionally some autonomic nervous system symptomology. The incidence of myofascial TrP pain in humans is clinically ubiquitous. This becomes apparent when all the numerous ways it can present itself are recognized and taken into account. Virtually everyone experiences a stiff neck, tension headaches, muscular low back pain, or soft tissue sports injuries at some point in their life.
In contrast not everyone experiences projected or referred pain associated with an impinged nerve root or visceral pathology. Yet despite its clinical prevalence, historically, most medical schools don’t provide much training on how to diagnose and treat myofascial TrP pain. They focus on looking at nerves, bones, tendons and bursas for the cause of musculoskeletal pain.² Physicians are left on their own to learn how to diagnose and manage their myofascial TrP pain patients.
Sometimes the myofascial TrP pain patient gives an accurate and concise history of acute, sustained, or repeated musculoskeletal overload, which leads to making the correct diagnosis more readily. However, in the majority of cases, there is often a delayed onset of symptoms or the presence of perpetuating factors. Both of these conditions can make a definitive diagnosis more difficult.
Delayed onset of myofascial TrP pain and dysfunction can develop two to four days after the precipitating incident initially occurred. Many times because of this delay the patient may have forgotten the incident and no longer associates their present pain with it. Perpetuating factors which can prolong or exacerbate an episode can also confuse the patient about how or when their pain developed.
To add to the confusion, some trigger points can mimic the classical pain referral zones of distressed organs (e.g., the pain pattern from a trigger point in the left pectorals major muscle can mimic the pain referral of, and present as a “pseudo” myocardial infarction).
TrPs can also form as a secondary symptom of other pathological conditions (e.g., a clinically verified myocardial infarction can generate TrPs in the muscles of its referral zone).
Additionally, the clinician also needs to be able to distinguish myofascial TrP pain from four other musculoskeletal pain generating sources which can present with similar symptoms: radicular afferent, radicular efferent, delayed onset muscular pain, and fibromyalgia (please see the Differential Diagnosis Table below).
Myofascial TrP pain, while not a medical emergency, (such as the low back pain associated with an abdominal aortic aneurysm), still can be extremely painful and debilitating for the patient suffering from the condition. Unfortunately when health care providers make the correct diagnosis they often lack the time and resources to treat the patient presenting with myofascial TrP pain.
Clinical Characteristics of Trigger Points
The pain from TrPs can be local but is usually referred to other regional muscles and deep somatic structures, joints, tendons and fascia. Pain can be referred superiorly, inferiorly, peripherally, centrally or locally depending on the specific muscle involved and its characteristic pain referral pattern. Myofascial TrP pain can sometimes present bilaterally but generally manifests unilaterally.
Unlike radicular pain projection, TrP pain referral is not limited to following dermatomes or myotomes (e.g., the pain pattern from the longissimus thoracis division of the erector spinae muscle with a T 10 dermatome & myotome, refers caudally to the inferior aspect of the ipsilateral gluteus maximus muscle which has an S 2 dermatome & S 1 myotome). However most referred pain from TrPs will stay within the same or adjacent dermatome/myotome spinal segments.
Like pain referral from pathological visceral sources, TrP pain is usually “misperceived” as originating in a different location. Muscular pain referral arises when action potentials from nociceptors in a muscle with an active trigger point excite nociceptive connections in the spinal cord. The action potential can “spill over” and excite neurons responsible for processing information outside of the region of the effected muscle. The pain from the TrP is then mislocalized and perceived by the patient as emanating from an area distal from the source.²
To date there are 106 pain referral zones that have been mapped in Travell and Simons’s “Red Myofascial Pain Bibles” to help aide in diagnosing trigger points.⁵ Trying to diagnose and treat myofascial TrP pain without relying on the use of these pain “maps” is like trying to locate and capture hippos in Tibet; you just aren’t going to find too many of them.
The pain produced from TrPs is usually perceived by the patient as hard to localize as well as deep and aching. The pain can restrict motion and can be exacerbated by movement or muscle loading. The pain is reported to be sharp or stabbing only if the TrP pain is severe and muscle spasm/cramping “feedback” from the central nervous system also accompanies the TrP pain.
In addition to pain, TrPs can refer sensory signs like tenderness and occasionally dysesthesia or hypoesthesia to their referral zone. Direct palpation of either an active or latent TrP can produce local pain in the involved muscle and can reproduce its characteristic pain referral pattern. In superficial muscles, a snapping palpation of the taut band containing the TrP can produce a visible local twitch response (LTR), which is a clinical sign of a muscle harboring a myofascial TrP.
As mentioned earlier, tight muscles from TrPs can in turn cause three distinct secondary musculoskeletal dysfunctions to occur: articular dysfunctions (e.g., Spinal Apophyseal Joint Dysfunction), peripheral nerve entrapment syndromes (e.g., Piriformis Syndrome) and tendinopathy syndromes (e.g., Tennis Elbow). All three can add confusing layers to musculoskeletal complaints and can present with or without the classic TrP referred pain patterns depending on whether or not the TrPs in the involved muscle are active or latent.
Articular dysfunction and the pain it presents is usually the indirect result of TrPs in dysfunctional muscles acting adversely on a joint(s). The most common joints to be effected are the apophyseal joints of the spine. The sacroiliac joint is also a very common joint to undergo articular dysfunction and can contribute significantly to low back pain. Since the SI joint is an amphiarthrosis and weight-bearing joint, its dysfunctional etiology may or may not include a myofascial TrP component.
The pain produced from a dysfunctional apophyseal joint is usually felt locally but sometimes, like myofascial TrP pain, can be referred to other locations. The pain from a dysfunctional SI joint is commonly referred distally to the low back, hip, or the posterior thigh.
Peripheral entrapments can occur when a muscle with an active or latent TrP shortens and clamps down on a nerve that lies beneath it. This condition can mimic all the same symptoms of a compromised nerve root. Tendinopathy can arise when a muscle shortened by TrPs puts undue and persistent force on its tendinous attachment and over time causes inflammation and degenerative changes.
Distinguishing Trigger Points from Radicular Pain
In the absence of other neurological signs and symptoms, such as paresthesia, hypoesthesia, reduced reflexes, fasciculations, weakness or atrophy, the pain from a compromised nerve root can sometimes be hard to distinguish from myofascial TrP pain (e.g., the pain pattern from TrPs in the scalene muscles can present almost identical to a C7 radiculopathy).
Radicular pain from an afferent nerve root impingement is experienced as sharp, pricking, superficial and is easily localized to specific dermatomes. This differs significantly from the deep, aching, and hard to localize pain of myofascial TrPs. The pain projection from an afferent nerve can be aggravated or relieved by changing spinal positions, whereas referred pain from TrPs is not.
Radicular pain from efferent nerve root impingement can mimic the same deep aching quality of myofascial TrPs. Additionally, the efferent generated pain, like TrP pain, is not confined to following dermatome distributions. However, the painful muscle(s) will always share a common myotome with its compromised nerve root. TrP induced pain may share but is not limited to specific myotomes or dermatomes. Movement or loading of the radicular pain affected muscle does not exacerbate its pain level as readily as movement or loading of a muscle with TrPs.
Like afferent impingement and unlike myofascial TrP pain, efferent pain can be aggravated or relieved by spinal positioning. Efferent nerve root impingement can also “trigger” myofascial TrPs to form in the muscles of their myotome distribution. Sometimes myofascial TrP pain is the first sign or symptom to appear before any of the other classic signs present themselves. Understanding these differences can help in distinguishing afferent and efferent radicular pain from myofascial trigger point pain.
Distinguishing Trigger Points from Delayed Onset Muscular Pain
Simple delayed onset muscular pain arises as the result of overuse when a muscle(s) has been “eccentrically” abused. The condition emerges as a reaction to excessive, or unaccustomed to, eccentric (lengthening) muscle contractions. Sarcomeres are more tolerant of overuse from concentric and isometric muscle contractions than eccentric.
Work load forces from unpredictable eccentric contractions can far exceed the forces developed during maximum voluntary concentric or isometric contractions. Delayed onset muscular pain can occur from any vigorous activity requiring repeated eccentric contractions used to decelerate joint movement. However the condition is often times related to a sport or recreational activity.⁶ In weight- lifting the term “negatives” is used to describe eccentric muscle contraction and is a very common instigator of the condition.
The pain associated with delayed onset muscular pain can be hard to distinguish from myofascial TrP pain. Both conditions can be caused by muscular overload and produce dull and achy muscular pain that is exacerbated by movement. In the case of post exercise muscular pain there is often an inflamed feeling along with an associated erythema or swelling involving the whole muscle.
The involved muscle will also lack the classic taut band and palpable tender “knot.” The pain is always limited to the involved muscle(s) itself with no pain referral to other regional muscles or deep somatic structures, joints, tendons and fascia as it is with myofascial TrP pain.⁶ The muscles of the appendicular skeleton are the most likely to be affected. The condition often presents bilaterally, unlike myofascial TrP pain which usually presents unilaterally.
Delayed onset muscular pain is always self-limiting, generally resolving in 5 to 7 days. Myofascial TrP pain as mentioned earlier can sometimes be self-limiting, but usually it is not. Instead, active TrPs either become chronic or will “deceptively” calm down to a non-painful latent state.
Distinguishing Trigger Points from Fibromyalgia
Fibromyalgia patients report that their pain feels constant, diffuse, deep, aching and throbbing and covers a generalized distribution. The widespread muscular pain is the main distinguishing symptom of fibromyalgia as opposed to the local or regional pain of myofascial TrPs. The pain of fibromyalgia can present on both sides of the body, or above and below the waist at the same time.
Myofascial TrP pain never presents in such a widespread generalized distribution. Other distinguishing differences with fibromyalgia include soreness upon palpation of the classic 11 out of 18 tender points, widespread tenderness, soft and doughy feeling to the muscles, and hypermobility. Myofascial TrP pain patients present with focal tenderness, palpable tension in the muscle, and restricted range of motion, as opposed to hypermobility.
The examining clinician always keeps in mind that with radicular pain, delayed onset pain, and fibromyalgia pain syndromes, the patient may also have myofascial trigger point pain.
Note: This paper does not take into account other possible pain generating sources (e.g., acute anaerobic exercise muscle pain, muscle pain from rupture or sprain, referred pain from distressed viscera, neuropathic pain, or disease processes). The focus was on those pain generators that are most likely to be confused with myofascial TrP pain.
Differential Diagnosis Table
Pain Generator
Myofascial Radicular Radicular Delayed Onset Fibromyalgia
Trigger Point Afferent Efferent Muscular Pain
__________________________________________________________________________________________________________________________
Features:
Localized Yes No No Yes No
Pain
_____________________________________________________________________________________________________________________
Regional Yes Yes Yes Yes No
Pain
_____________________________________________________________________________________________________________________
Generalized No No No No Yes
Pain
____________________________________________________________________________________________________________________
Pain No Yes Yes Yes Yes
At Rest Unless highly irritated But Minimal
____________________________________________________________________________________________________________________
Pain with Yes No Yes Yes Yes
Movement But Minimal But Minimal ___________________________________________________________________________________________________________________
Muscle Yes No Yes Yes No
Loading But Minimal
____________________________________________________________________________________________________________________
Affected ± by No Yes Yes No No
Spinal Position
_____________________________________________________________________________________________________________________
Burning No Yes No No No
Tingling Pain
_____________________________________________________________________________________________________________________
Dull Ache Yes No Yes Yes Yes
Deep Pain
____________________________________________________________________________________________________________________
Superficial No Yes No No No
Pain
_____________________________________________________________________________________________________________________
Tender to No No No Yes Yes
Palpation Whole Muscle Muscles Feel "Doughy" Regional
_____________________________________________________________________________________________________________________
Tender to Yes No No No Yes
Palpation Trigger Points Tender Points
Focal and Taut Band
___________________________________________________________________________________________________________________________
Treatment
To date the successful pharmaceutical management of myofascial TrP pain remains elusive. Analgesics, nonsteroidal anti-inflammatories and skeletal muscle relaxants have marginal effect on the pathophysiology of TrP pain. They do not directly address or relieve the sustained sarcomere contracture cycle responsible for TrP formation. At best they offer only a limited degree of pain control. However NSAID’S can help with the temporary muscle soreness that can sometimes develop after manual manipulation or injection of myofascial tissues. Muscle relaxants can prove beneficial in relieving muscle spasm/cramping which sometimes may accompany sever myofascial TrP pain.
The treatment of myofascial TrP pain and dysfunction and its associated syndromes of articular dysfunction, peripheral nerve entrapment and tendinopathy can be accomplished through several methods. Specific manual manipulation techniques, augmented stretching, and injection of local anesthetics are some of the more common options. Augmented stretching involves adding the application of intermittent cold, reciprocal inhibition or post-isometric relaxation techniques to enhance the efficacy of the stretch.
In the case of early onset pain, most single-muscle myofascial TrP pain syndromes can be eliminated with just simple stretching. TrP therapy has no discernable effect on afferent radicular pain; however it can help relieve some of the severe spasm/ cramping pain from efferent nerve root impingement. Classic massage techniques of petrissage and effleurage can be used to successfully treat delayed onset muscular pain and to give symptomatic relief for fibromyalgia.
Reference List:
1. Russell IJ: A New Journal. J Musculoskeletal Pain 1 (1): 1-7, 1993
2. Mense S., Simons DG: Muscle Pain Understanding Its Nature, Diagnosis, and Treatment, Lippincott Williams & Wilkins, 2001.
3. Travell JG, Rinzler SH: The myofascial genesis of pain. Postgrad Med 11:425 – 434, 1952
4. Travell JG., Simons DG: Myofascial pain and Dysfunction: The Trigger Point Manual, Volume 1. Upper Half of the Body. Ed. 2 Williams & Wilkins, Baltimore, 1999.
5. Travell & Simons: Myofascial Pain and Dysfunction: The Trigger Point Manual, Volumes 1 & 2, Williams & Wilkins, Baltimore, 1983 & 1992
6. Mense S., Gerwin RD: Muscle Pain: Understanding the Mechanisms, Springer 2010
Not directly quoted but used for concepts and fact checking:
Mense S., Gerwin RD: Muscle Pain: Diagnosis and Treatment, Springer 2010
Campbell WW: Dejong’s the Neurologic Examination, 7th ed., Lippincott Williams & Wilkinds, 2013
Greenman PE: Principles of Manual Medicine, 2nd ed., Williams & Wilkins 1996
Lewit KL: Manipulative Therapy in Rehabilitation of the Locomotor System, 2nd ed., Butterworth-Heinemann Ltd 1991
Borenstein DG, Wiesel SW: Low Back Pain, W. B. Saunders Company 1989
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