eMedicine Specialties > Sports Medicine > Introductory Topics in Sports Medicine

Myofascial Pain in Athletes: Treatment & Medication

Author: Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver
Contributor Information and Disclosures

Updated: Feb 8, 2008

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

Effective treatment of an MPS caused by TrPs usually involves more than simply applying a procedure to TrPs. Often, it is necessary to consider and deal with the cause that activated the TrPs, to identify and correct any perpetuating factors (which often are different than what activated the TrPs), and to help the patient restore and maintain normal muscle function. Common misconceptions about the treatment of TrPs include the following:

  • Simply treating the TrP should be sufficient, especially if the stress that activated the TrP is not recurrent and if no perpetuating factors are present.
    • In this case, the TrP is likely to be reactivated by the same stress.
    • Ignoring perpetuating factors invites recurrence. After the TrPs have persisted for some time, failure to retrain the muscle to normal function or failure to reestablish its full-stretch range of motion results in a degree of persistent motor dysfunction.
  • The pain cannot be as severe as the patient says and must be largely psychogenic.
    • The patients are trying to communicate their degree of pain. Believe them. The pain feels severe to them. Patients in a general medical practice rated their pain as severe as or more severe than pain from other causes such as pharyngitis, cystitis, angina, and herpes zoster.
    • An appreciable amount of the pain reported by many patients with fibromyalgia comes from their TrPs. The pain of fibromyalgia rates fully as severe as the pain of rheumatoid arthritis. It is severe enough to cause central nervous system changes characteristic of chronic pain.
    • Because of their chronic lip and fibromyalgia pain, these patients often develop pain behaviors that tend to reinforce dysfunction and further pain. Many patients experience grievous and needless degree and duration of pain, because a series of clinicians unacquainted with MTrPs erroneously (covertly if not overtly) diagnosed a psychogenic condition.
  • MPSs are self-limiting and will cure themselves.
    • An acute uncomplicated TrP activated by an unusual activity or muscle overload can revert spontaneously to a latent TrP within 1 or 2 weeks, if the muscle is not overstressed (used within tolerance, which may be limited) and if no perpetuating factors are present. Otherwise, if the acute syndrome is not properly managed, it evolves needlessly into a chronic MPS.
  • Relief of pain by treatment of skeletal muscles for MTrPs rules out serious visceral disease.
    • Because of the referred pain nature of visceral pain, application of Vapo coolant spray or infiltration of a local anesthetic into the somatic reference zone can temporarily relieve the pain of myocardial infarction, angina, and acute abdominal disease with no effect on the visceral pathology.

Rehabilitation program: The treatment approaches include the use of simple muscle stretch, augmented muscle stretch, post-isometric relaxation, reciprocal inhibition, slow exhalation, eye movement, TrP pressure release, massage, range of motion, heat, ultrasound, high-voltage galvanic stimulation, drug treatment, biofeedback, and new injection techniques.

Physical therapy includes simple muscle stretch, augmented muscle stretch, post-isometric relaxation, reciprocal inhibition, slow exhalation, eye movement, TrP pressure release, massage, range of motion, heat, ultrasound, and high-voltage galvanic stimulation.

Medical Issues/Complications

Table 2. Myofascial Trigger Points Mistakenly Diagnosed as Other Conditions

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Table
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
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

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Table
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
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

  • Complications of injections
    • Pneumothorax by aiming the needle at an intercostal space: The only exception is when the intercostal muscles must be injected. This should be performed with great care.
    • The location of the needle tip can be misjudged readily when using a long slender needle. Furthermore, the needle should be inserted straight, avoiding any side pressure that might bend it, deflecting the tip an unknown distance to one side.
    • It is especially important to avoid using a needle with a burr at the tip because it causes unnecessary bleeding. When the tip of a disposable needle contacts bone, the impact frequently curls the tip to produce a fishhook burr that feels scratchy and drags as the needle is drawn through tissues.
  • Contraindications to TrP injections
    • Patients on anticoagulation therapy
    • If the patient has taken aspirin within 3 days of injection
    • Tobacco smokers, unless they have stopped smoking and have taken at least 500 mg of timed-release vitamin C for 3 days prior to injection
    • Patients who have an inordinate fear of needles
    • Patients should avoid strenuous activity and sports for 10 days.

Consultations

The clinical importance of MTrPs to practitioners has been described in the literature for acupuncturists, anesthesiologists, chronic pain managers, dentists, family practitioners, gynecologists, neurologists, nurses, orthopedic surgeons, pediatricians, physical therapists, physiatrists, rheumatologists, and veterinarians.

Other Treatment

Infants have been observed with point tenderness of the rectus abdominis muscle and colic, both of which were relieved by sweeping a stream of Vapo coolant over the muscle, which helps to inactivate MTrPs.

The clinical effectiveness of botulinum A toxin injection for the treatment of MTrPs helps to substantiate dysfunctional endplates as an essential part of the pathophysiology of TrPs (see Image 10). This toxin specifically acts only on the neuromuscular junction, effectively denervating that muscle cell.

  • Sequence of steps when stretching and spraying any muscle for MTrPs (see Image 4)
    • The patient is supported in a comfortable relaxed position.
    • One end of the muscle is anchored.
    • Skin is sprayed with repeated parallel sweeps of the Vapo coolant over the length of the muscle in the direction of pain pattern.
    • After the first sweep of spray, pressure is applied to take up the slack in the muscle and is continued as additional sweeps of spray are applied.
    • Sweeps of the spray are extended to cover the referred pain pattern.
    • Steps 3, 4, and 5 may be repeated 2 or 3 times until the skin becomes cold to the touch or when the range of motion reaches maximum.
  • Technique of spray and stretch
    • For example, treatment for right levator scapulae TrPs; the direction and pattern of the Vapo coolant spray follows the muscle fibers (see Image 5).
    • During the distraction of the spray, the operator presses the patient's head forward and to the opposite side, while using the elbow to press the patient's shoulder down and back. Similar techniques are applied to most other TrPs. The key ingredient is the prolonged stretch of the affected muscle.
    • Unidirectional sweeps cover, first, parallel lines of skin over those muscle fibers that are stretched the tightest, then over the rest of the muscle and its pain pattern. Sequential sweeps of spray should follow the direction of the muscle fibers and progress toward the referred pain zone.
  • TrP injection
    • To prevent bleeding, the fingers of the palpating hand should be spread apart, maintaining tension on the skin to reduce the likelihood of subcutaneous bleeding where the needle has penetrated (see Image 7). Also, during the injection, the fingers exert pressure around the needle tip to provide homeostasis in deeper tissues. When the angle of the needle is changed, the direction of pressure changes.
    • The physician should avoid inserting the needle to the hub where the needle is most likely to break off. Some additional depth of penetration can be obtained safely by indenting the skin and subcutaneous tissues with a finger beside the needle as illustrated in Image 8.
    • The importance of distinguishing between central TrPs, ie, in the central portion of the muscle belly and attachment TrPs when injecting, is illustrated in Image 9.
  • The increased capillary fragility characteristic of a low serum vitamin C level can cause excessive bleeding in muscles injected for TrPs. Capillary hemorrhage augments postinjection soreness and leads to unsightly ecchymoses. A frequent source of increased bleeding due to low vitamin C is tobacco. Mega-dose vitamin C therapy daily for 1 week should correct this deficiency. At least 500 mg of timed-release vitamin C 3 times daily is recommended for a minimum of 3 days prior to injection of TrPs. A daily dose of aspirin increases the susceptibility to bleeding. The patient should take no aspirin for 3 days before TrP injection or needling.

Recovery Phase

Rehabilitation Program

Physical Therapy

See Acute Phase Physical Therapy.

Occupational Therapy

See Acute Phase Physical Therapy.

Maintenance Phase

Rehabilitation Program

Physical Therapy

See above.

Medication

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.

Local anesthetics

Amide derivative local anesthetic used to minimize postinjection soreness.


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.

Adult

1% solution without vasoconstrictor: 0.2 mL SC per TrP 2 times/wk until symptoms disappear (usually within 3 wk)

Pediatric

Not established

May potentiate the neuromuscular blocking effect of succinylcholine, tubocurarine; reduced clearance with concomitant use of beta-blocking agents, cimetidine; benzodiazepines, barbiturates, and volatile anesthetics increase seizure threshold; duration of regional anesthesia prolonged by vasoconstrictor agents; alkalinization increases rate of onset and potency of local or regional anesthesia

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Caution in patients with hypovolemia, severe congestive heart failure, shock, and all forms of heart block; adverse reactions include hypotension, bradycardia, arrhythmias, respiratory depression, tinnitus, seizures, loss of hearing, euphoria, anxiety, diplopia, palsies, urticaria, pruritus, angioneurotic edema


Procaine HCL 0.5% solution (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.

Adult

0.2 mL SC per TrP 2 times/wk until symptoms disappear (usually within 3 wk); not to exceed 1 g per injection

Pediatric

Not established

Prolongs the effect of succinylcholine; metabolite (PABA) inhibits action of sulfonamides and aminosalicylic acid; benzodiazepines, barbiturates, and volatile anesthetics increase seizure threshold; duration of regional anesthesia prolonged by vasoconstrictor agents (eg, epinephrine) and alpha 2-agonists (eg, clonidine); alkalinization increases rate of onset and potency of local or regional anesthesia

Documented hypersensitivity to procaine or ester-type local anesthetics and in individuals with allergy to suntan lotion, which contains PABA derivatives

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Do not use vasoconstrictor drugs for this kind of regional anesthesia because of risk of muscle damage, including necrosis; caution in patients with severe disturbances of cardiac rhythm or heart block; reduce doses in obstetric, elderly, hypovolemic, and high-risk patients; bacteriostatic agent commonly added to procaine is sodium bisulphite, which can be irritating and contribute to postinjection soreness (can reduce this effect by diluting 2% procaine solution to 0.5% with isotonic sodium chloride solution)

Neurotoxin

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. See Images 10-15 for the mechanism of action of BTA.


Botulinum Toxin Type A (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.

Adult

5-10 U of BTA per TrP (0.1-0.2 mL), not to exceed 90 U; recurrent injections, if necessary to inactivate the TrP, should be given after 8 wk

Pediatric

Not established

With >92 U of BTA over 6 wk, effectiveness may be reduced due to antibody production; effects of BTA therapy may be increased with the use of aminoglycoside antibiotics or other drugs that interfere with neuromuscular transmission

Patients with myasthenia gravis or other muscular endplate disorders; adverse effects associated with BTA usually transient and mild to moderate and may include drooping of the eyelid, eye irritation, dry eye, tearing or light sensitivity (in patients treated for blepharospasm), and superficial punctate keratitis at injection site

Pregnancy

C - Safety for use during pregnancy has not been established

Precautions

High doses, frequent injections, and exposure to neurotoxin complex proteins are all thought to play important roles in the formation of neutralizing antibodies, which may lead to nonresponse or resistance; using neurotoxins with a low protein load, the lowest effective dose, and the longest interval between injections may help to minimize the potential for antibody formation; axon sprouting and muscle fiber reinnervation terminate the clinical toxic effect of BTA, which results in the reestablishment of neuromuscular transmission
Chemical denervation of the neuromuscular junction by BTA results in an expansion of the endplate region and growth stimulation of collateral axonal sprouts; a nerve sprout eventually establishes a new neuromuscular junction, and muscle activity gradually returns; however, new research suggests that this new nerve sprout retracts and the original junction returns to functionality; in either case, repeat injections may be required to maintain the desired clinical effect
Intramuscular injections of BTA typically result in a dose-dependent reduction of hyperactive muscle contraction that lasts for approximately 3 mo and is ultimately reversible

More on Myofascial Pain in Athletes

Overview: Myofascial Pain in Athletes
Differential Diagnoses & Workup: Myofascial Pain in Athletes
Treatment & Medication: Myofascial Pain in Athletes
Follow-up: Myofascial Pain in Athletes
Multimedia: Myofascial Pain in Athletes
References

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Further Reading

Keywords

myofascial pain syndromes, trigger points, MPS, myofascial trigger points, TrPs, MTrPs

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.

Medical Editor

Anthony J Saglimbeni, MD, Staff Physician, Family Practice Residency, 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
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, 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
Sherwin SW Ho, 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.

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