Myofascial Pain in Athletes Workup

  • Author: Auri Bruno-Petrina, MD, PhD; Chief Editor: Sherwin SW Ho, MD   more...
 
Updated: Nov 17, 2011
 

Laboratory Studies

  • No laboratory test or imaging technique is generally established as useful in the diagnosis of TrPs[4, 5]
    • Three measurable phenomena help to objectively substantiate the presence of characteristic TrP phenomena, and all 3 are valuable as research tools.
    • Two of them, surface EMG and ultrasonography also have much potential for clinical application in the diagnosis and treatment of TrPs.[4, 5]
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Imaging Studies

  • In addition to EMG recording, ultrasonography provides a second way of substantiating and studying the LTR and it also has a strong potential for providing a much needed available imaging technique that could be widely used to objectively substantiate the clinical diagnosis of TrPs.[4, 5, 13]
  • This test would require the examiner to use the skill-demanding snapping palpation technique, or to insert a needle into the TrP, to elicit the twitch response.
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Other Tests

  • Surface electromyography
    • TrPs cause distortion or disruption of normal muscle function.
      • Functionally, the muscle with the TrP evidences a 3-fold problem: It exhibits increased responsiveness, delayed relaxation, and increased fatigability. Together, these effects increase muscle overload and reduce its work tolerance. In addition, the TrP can produce referred spasm and referred inhibition in other muscles.
      • With the recent appearance of online computer analysis of EMG amplitude and mean power spectral frequency, a few pioneer investigators have reported the effects of TrPs on muscle activity. The reports indicate that TrPs can influence the motor function of the muscle in which they occur and that their influence can be transmitted through the central nervous system to other muscles.
      • To date, the number of well-controlled studies to establish the clinical reliability and application of these observations is insufficient, but findings from the few reports of these TrP effects are promising.
    • The strong clinical effects of TrPs on sensation, as evidenced by TrP tenderness and referred pain, are well documented.
      • Strong cutaneous stimuli (eg, electric shocks) are well known to cause reflex motor effects (eg, flexion reflex). If the skin can modulate motor activity and if TrPs can modulate sensory activity, the fact that TrPs can also strongly affect motor activity should not be surprising. In fact, the motor effects of lips may be the most important influence they exert, because the motor dysfunction they produce may result in overload of other muscles and spread the TrP problem from muscle to muscle.
      • Accumulating evidence now indicates that the muscles targeted for referred spasm from TrPs also usually have TrPs themselves. These motor phenomena of TrPs deserve serious competent research investigation.
    • An increased responsiveness of some affected muscles is indicated by abnormally high amplitude of EMG activity when the muscle is voluntarily contracted and loaded.[14] Clinical evidence suggests that some muscles tend to be shortened and abnormally excitable, while others appear to be weak and inhibited.
    • Fatigability noted at EMG and in terms of work tolerance, of the trapezius muscle that had MTrPs is accelerated compared to a contralateral muscle that was pain-free. The EMG amplitude increased and median power frequency decreased significantly in the involved muscle compared to the uninvolved muscle. Both of these changes are characteristic of initial fatigue.
    • Median power frequency generally is accepted as a valid criterion of muscle fatigue. Delayed recovery following fatiguing exercise commonly is seen in patients with muscle-related cumulative trauma disorder (CTD). MTrPs were very common in the involved muscles in this group.
    • Delayed relaxation is commonly seen in muscle-overload work situations. This failure to relax is a common surface EMG finding during repetitive exercises of muscles with MTrPs.
    • In addition, the TrP can induce motor activity (eg, referred spasm) in other muscles.
  • Algometry
    • Sensitivity to pain in patients with TrPs can be measured as the pain threshold to electrical stimulation or applied pressure. The use of pressure algometry is most commonly reported.
    • Pressure algometry involves the induction of a specific pain level in response to a measured force perpendicularly applied to the skin. The following 3 endpoints are reported: (1) onset of local pain (ie, pressure pain threshold), (2) onset of referred pain (ie, referred pain threshold), and (3) intolerable pressure (ie, pain tolerance).
    • Most commonly, the pressure required to reach pain threshold is directly measured on a spring scale that is calibrated in kilograms, newtons, or rounds. Because the pressure is applied through a circular footplate, its diameter is a factor, and the actual measurement is stress (in kilograms per square centimeter) applied to skin.
    • For example, one of the most common algometers has a footplate area of 1 cm2; therefore, its meter, which provides readings in kilograms, is numerically the same as the number of kilograms per square centimeter, and no numeric conversion is needed.
  • Thermography
    • Thermograms can be recorded by using infrared radiometry or films of liquid crystal. Recording infrared radiation (ie, electronic thermography) with computer analysis provides a powerful tool for tile accurate rapid visualization of skin temperature changes over large areas of the body. This technique can demonstrate cutaneous reflex phenomena characteristic of MTrPs. The less expensive contact sheets of liquid crystal have limitations that make reliable interpretation of the findings considerably more difficult.
    • Each of these thermographic techniques is used to measure the skin surface temperature to a depth of only a few millimeters. The temperature changes correspond to changes in the circulation within, but not beneath, the skin. The endogenous cause of these temperature changes is usually sympathetic nervous system activity. Therefore, thermographic changes in skin temperature are comparable in meaning to changes in skin resistance or changes in sweat production. However, electronic infrared thermography is superior to these other two measures (ie, infrared radiometry or with films of liquid crystal) in convenience and in spatial as well as temporal resolution.
    • In summary, Fisher's research studies indicate that the finding a hot spot on the thermogram is not sufficient to identify a TrP beneath it. A similar temperature change can be expected in radiculopathy, articular dysfunction, enthesopathy, or local subcutaneous inflammation. The thermographic hot spot of a TrP is described as a discoid region 5 to 1 (3 cm in diameter, displaced slightly from directly over the TrP).
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Procedures

  • Procedures to confirm diagnosis of MPS: The first international symposium on myofascial pain and fibromyalgia was held in 1989. It marked one of the first meetings of the principal proponents of the 2 major muscle pain syndromes. In the proceedings of that symposium, Simons listed the clinical criteria for diagnosis of MPS.[4, 5]
  • Clinical criteria for the diagnosis of MPS caused by active TrPs
    • To make the clinical diagnosis of MPS, the findings should include 5 major criteria and at least 1 of 3 minor criteria. The 5 major criteria include the following:[4, 5]
      • Regional pain complaint
      • Pain complaint or altered sensation in the expected distribution of referred pain from a MTrP
      • Taut band palpable in an accessible muscle
      • Exquisite spot tenderness at 1 point along the length of the taut band
      • Some degree of restricted range of motion, when measurable
    • The 3 minor criteria include the following:
      • Reproduction of clinical pain complaint, or altered sensation, by pressure on the tender spot
      • Elicitations of a local twitch response by transverse snapping palpation at the tender spot or by needle insertion into the tender spot in the taut band
      • Pain alleviated by elongating (stretching) the muscle or by injecting the tender spot (TrP)
    • Additional symptoms, such as weather sensitivity, sleep disturbance, and depression, often are present, but they are not diagnostic because they may be attributable to chronic, severe pain perpetuated by multiple mechanical and/or systemic perpetuating factors.
  • The required features include regional pain, referred pain, or disturbed sensation in a predicted location; a taut band; a tender point along the taut band; and restricted range of motion.
  • One of 3 of the following minor criteria also must be present:
    • Pain complaint reproduced by pressure on the tender spot
    • A local twitch response
    • Relief of the pain by stretching or injecting
  • At the same time, Simons listed research criteria for the identification of TrPs. To qualify, the point must be exquisitely tender, located in a taut band of a muscle with restricted range of motion, refer pain when pressed or needled, and exhibit a twitch response when needled.
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Contributor Information and Disclosures
Author

Auri Bruno-Petrina, MD, PhD  Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver

Auri Bruno-Petrina, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Canadian Association of Physical Medicine and Rehabilitation, College of Physicians and Surgeons of British Columbia, and International Society of Physical and Rehabilitation Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Anthony J Saglimbeni, MD  President, South Bay Sports and Preventive Medicine Associates; Private Practice; Team Internist, San Francisco Giants; Team Internist, West Valley College; Team Physician, Bellarmine College Prep; Team Physician, Presentation High School; Team Physician, Santa Clara University; Consultant, University of San Francisco, Academy of Art University, Skyline College, Foothill College, De Anza College

Anthony J Saglimbeni, MD, is a member of the following medical societies: California Medical Association and Santa Clara County Medical Association

Disclosure: South Bay Sports and Preventive Medicine Associates, Inc Ownership interest Other

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Russell D White, MD  Professor of Medicine, Professor of Orthopedic Surgery, Director of Sports Medicine Fellowship Program, Medical Director, Sports Medicine Center, Head Team Physician, University of Missouri-Kansas City Intercollegiate Athletic Program, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center-Lakewood

Russell D White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Family Physicians, American Association of Clinical Endocrinologists, American College of Sports Medicine, American Diabetes Association, and American Medical Society for Sports Medicine

Disclosure: Nothing to disclose.

Jon B Whitehurst, MD  Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital

Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America

Disclosure: Nothing to disclose.

Chief Editor

Sherwin SW Ho, MD  Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy Association of North America, and Herodicus Society

Disclosure: Breg, Inc. Consulting fee Consulting; Biomet, Inc. Consulting fee Consulting; GMV, Inc. Arthroscopy Simulator Evaluation and teaching; Smith and Nephew Grant/research funds Fellowship funding; DJ Ortho Grant/research funds Course funding; Athletico Physical Therapy Grant/research funds Course, research funding

References

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  17. Sarrafzadeh J, Ahmadi A, Yassin M. The Effects of Pressure Release, Phonophoresis of Hydrocortisone, and Ultrasound on Upper Trapezius Latent Myofascial Trigger Point. Arch Phys Med Rehabil. Oct 7 2011;[Medline].

  18. Rha DW, Shin JC, Kim YK, Jung JH, Kim YU, Lee SC. Detecting local twitch responses of myofascial trigger points in the lower-back muscles using ultrasonography. Arch Phys Med Rehabil. Oct 2011;92(10):1576-1580.e1. [Medline].

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Myofascial pain in athletes. Schematic of a trigger point complex of a muscle in longitudinal section.A: The central trigger point (CTrP) in the endplate zone contains numerous electrically active loci and numerous contraction knots. A taut band of muscle fibers extends from the trigger point to the attachment at each end of the involved fibers. The sustained tension that the taut band exerts on the attachment tissues can induce a localized enthesopathy that is identified as an attachment trigger point (ATrP).B: Enlarged view of part of the CTrP shows the distribution of 5 contraction knots. The vertical lines in each muscle fiber identify the relative spacing of its striations. The space between 2 striations corresponds to the length of one sarcomere. The sarcomeres within one of these enlarged segments (ie, contraction knot) of a muscle fiber are markedly shorter and wider than the sarcomeres in the neighboring normal muscle fibers, which are free of contraction knots.
Myofascial pain in athletes. Cross-sectional drawing shows flat palpation of a taut band and its trigger point.Left: Skin pushed to one side to begin palpation (A). The fingertip slides across muscle fibers to feel the cord-line texture of the taut band rolling beneath it (B). The skin is pushed to other side at completion of movement. This same movement performed vigorously is snapping palpation (C).Right: Muscle fibers surrounded by the thumb and fingers in a pincer grip (A). The hardness of the taut band is felt clearly as it is rolled between the digits (B). The palpable edge of the taut band is sharply defined as it escapes from between the fingertips, often with a local twitch response (C).
Myofascial pain in athletes. Longitudinal schematic drawing of taut bands, myofascial trigger points, and a local twitch response. A: Palpation of a taut band (straight lines) among normally slack, relaxed muscle fibers (wavy lines). B: Rolling the band quickly under the fingertip (snapping palpation) at the trigger point often produces a local twitch response that usually is seen most clearly as skin movement between the trigger point and the attachment of the muscle fibers.
Myofascial pain in athletes. Sequence of steps to use when stretching and spraying any muscle for myofascial trigger points.
Myofascial pain in athletes. Schematic drawing showing how the jet stream of Vapo coolant is applied.
Myofascial pain in athletes. Cross-sectional schematic drawing shows flat palpation to localize and hold the trigger point for injection. A and B show use of alternate pressure between 2 fingers to confirm the location of the palpable module of the trigger point. C shows positioning the trigger point half way between the fingertips to keep it from sliding to one side during the injection.
Myofascial pain in athletes. Schematic top view of 2 approaches to the flat injection of a trigger point area in a palpable taut band. Injection away from the fingers (A) and injection toward the fingers (B).
Myofascial pain in athletes. C. Z. Hong's technique. Finger pressure beside the needle is used to indent the skin, subcutaneous, and fat tissues so that the needle can reach the trigger point in a muscle that would be inaccessible otherwise.
Myofascial pain in athletes. Diagrammatic representation of pre-injection sites (open circles) and injection sites (solid circles) of local anesthetic to the trigger point. The enclosed stippled area represents the taut band. This diagram distinguishes the central trigger point within the large broken circle from the attachment trigger points located at the myotendinous junction and at the attachment of the tendon to the bone. Each of these 3 trigger point regions can be identified by their individual spot tenderness and anatomical locations. No rationale is apparent for injecting the part of the taut band that lies between the central trigger point and the attachment trigger point (solid circles numbers 7-10).
Myofascial pain in athletes. Mechanism of botulinum toxin type A.
Myofascial pain in athletes. Binding of neuromuscular transmission with botulinum toxin type A, which binds the motor nerve terminal.
Myofascial pain in athletes. After botulinum toxin type A is internalized, the light chain of the toxin molecule is released into the cytoplasm of the nerve terminal.
Myofascial pain in athletes. Botulinum toxin type A blocks acetylcholine by cleaving a cytoplasmic protein on the cell membrane.
Myofascial pain in athletes. After the botulinum toxin type A exerts its clinical toxic effect, a nerve sprout eventually establishes a new neuromuscular junction, and muscle activity gradually returns. However, new research findings suggest that this new nerve sprout retracts and the original junction returns to functionality.
Myofascial pain in athletes. After the clinical toxic effect of botulinum toxin type A occurs, axon sprouting and muscle fiber reinnervation terminate the clinical effect of the toxin, which results in the reestablishment of neuromuscular transmission.
Table 1. Prevalence of Myofascial Pain
RegionPracticeNumber StudiedPrevalence of Myofascial Pain, %
GeneralMedical17230
GeneralPain medical center9693
GeneralComprehensive pain center28385
CraniofacialHead and neck pain clinic16455
LumboglutealOrthopedic clinic9721
Table 2. Myofascial Trigger Points Mistakenly Diagnosed as Other Conditions
Initial DiagnosisTrPs
Angina pectoris, atypicalPectoralis major
AppendicitisLower rectus abdominis
Atypical facial neuralgiaMasseter, temporalis, sternal division of the sternocleidomastoid, upper trapezius
Atypical migraineSternocleidomastoid, temporalis, posterior cervical
Back pain, middleUpper rectus abdominis, thoracic paraspinals
Back pain, lowLower rectus abdominis, thoracolumbar paraspinals
Bicipital tendinitisLong head of the biceps brachii
Chronic abdominal wall painAbdominal muscles
DysmenorrheaLower rectus abdominis
Earache, enigmaticDeep masseter
EpicondylitisWrist extensors, supinator, triceps brachii
Frozen shoulderSubscapularis
Myofascial pain dysfunctionMasticatory muscles
Occipital headachePosterior cervicals
Post-therapeutic neuralgiaSerratus anterior, intercostals
Radiculopathy, C6Pectoralis minor, scalenes
Scapulocostal syndromeScalenes, middle trapezius, levator scapulae
Subacromial bursitisMiddle deltoid
Temporomandibular joint disorderMasseter, lateral pterygoid
Tennis elbowFinger extensors, supinator
Tension headacheSternocleidomastoid, masticatory, posterior cervicals, suboccipital, upper trapezius
Thoracic outlet syndromeScalenes, subscapularis, pectoralis minor and major, latissimus dorsi, teres major
Table 3. Differences in Clinical Features that Distinguish Myofascial Pain due to TrPs from Fibromyalgia
FeatureMyofascial Pain (TrPs)Fibromyalgia
Female-to-male ratio1:14-9:1
PainLocal or regionalWidespread, general
TendernessFocalWidespread
MuscleFeels tense (taut bands)Feels soft and doughy
MotionRestricted range of motionHypermobility
ExaminationExamine for TrPsExamine for tender points
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