Myofascial Pain in Athletes Medication

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

Medication Summary

Anti-inflammatory agents, including corticosteroids and analgesics, are generally not useful, and their administration should be avoided. Localized and regional muscle pain syndromes often respond to specific localized therapies. The most common treatment for localized muscle pain is injection. Take great care in locating the TrP, watch for the twitch response on the muscle, and then enter the muscle with the needle.[25]

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Local anesthetics

Class Summary

Amide derivative local anesthetic used to minimize postinjection soreness.

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Lidocaine HCL (Xylocaine)

 

Has rapid onset of action. Stabilizes neuronal membrane by inhibiting the sodium flux required for the initiation and conduction of impulses. In addition, causes inhibition of release of neurotransmitters (eg, substance P), ATP from nociceptive afferent C fibers, modulation in information transfer along primary afferents, and central sympathetic blockade with decrease in pain-induced reflex vasoconstriction.

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Procaine (Novocaine)

 

Regional anesthesia for treatment of painful conditions (eg, neuropathic pain, reflex sympathetic dystrophy, myofascial pain). Least myotonic and has lowest systemic toxicity among commonly used local anesthetics. Procaine is the ester of p-aminobenzoic acid and ethanol with a tertiary diethylamino group attached at the other end of the alcohol. Stabilizes neuronal membrane and prevents the initiation and transmission of impulses. Has a rapid onset of action and relatively short duration depending on anesthetic technique, type of block, concentration, and patient. Greater solution concentration does not increase anesthetic effect.

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Neurotoxin

Class Summary

Botulinum toxin type A (BTA) binds irreversibly to presynaptic cholinergic nerve terminals, which includes the terminals of motor nerve supplying skeletal muscle-fiber endplates. Since the primary dysfunction of motor endplates associated with the TrP phenomenon appears to be excessive release of acetylcholine (ACh), injections into the TrP of a substance (eg, BTA) that only blocks ACh should be specific TrP therapy. This toxin specifically acts only on the neuromuscular junction, effectively denervating that muscle cell.

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OnabotulinumtoxinA (BOTOX®)

 

BTA blocks neuromuscular transmission through a 3-step process, as follows: (1) blockade of neuromuscular transmission; BTA binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. (2) BTA is internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. (3) BTA blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. The toxin does not affect the synthesis or storage of acetylcholine or the

conduction of electrical signals along the nerve fiber.

Typically, a 24-72 h delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 mo.

This purified neurotoxin complex is a vacuum-dried form of purified BTA, which contains 5 ng of neurotoxin complex protein per 100 U.

BTA has to be reconstituted with 2 mL of 0.9% sodium chloride diluent. With this solution each 0.1 mL results in 5 U dose. Patient should receive 5-10 injections per visit.

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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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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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