Updated: Apr 12, 2009
Descriptions of myofascial pain date back to the mid 1800s when Froriep described muskelschwiele, or muscle calluses. He described these calluses as tender areas in muscle that felt like a cord or band associated with rheumatic complaints. In the early 1900s, Gowers first used the term fibrositis to describe muscular rheumatism associated with local tenderness and regions of palpable hardness. In 1938, Kellgren described areas of referred pain associated with tender points in muscle. In the 1940s, Janet Travell, MD, began writing about myofascial trigger points. Her text, written in conjunction with David Simons, MD, continues to be viewed as the foundational literature on the subject of myofascial pain.1 (See image below and Image 1.)
Pain attributed to muscle and its surrounding fascia has been termed myofascial pain. The diagnosis of this syndrome in clinical, with no confirmatory laboratory tests available. Thus, myofascial pain in any location is characterized on examination by the presence of trigger points located in skeletal muscle. In the cervical spine, the muscles most often implicated in myofascial pain are the trapezius, levator scapulae, rhomboids, supraspinatus, and infraspinatus.2 A trigger point is defined as a hyperirritable area located in a palpable taut band of muscle fibers. According to Hong and Simon's review on the pathophysiology and electrophysiologic mechanisms of trigger points, the following observations help to define them further3 :
Myofascial pain is thought to occur commonly in the general population. As many as 21% of patients seen in general orthopedic clinics have myofascial pain. Of patients seen at specialty pain management centers, 85-93% have a myofascial pain component.
Increased mortality is not associated with cervical myofascial pain.
No studies clarify whether racial differences exist in frequency of cervical myofascial pain.
While fibromyalgia occurs more commonly in women than in men, cervical myofascial pain occurs in both sexes, also with a predominance among women.
Myofascial pain seems to occur more frequently with increasing age until midlife. Incidence declines gradually after middle age.
Typical findings reported by the patient with myofascial pain may include the following:
Common findings noted upon physical examination may include the following:
Cervical myofascial pain is thought to occur following either overuse or trauma to the muscles that support the shoulders and neck. Common scenarios are that the patient recently was involved in a motor vehicle accident or that he or she performed repetitive upper extremity activities. Trapezial myofascial pain commonly occurs when a person with a desk job does not have appropriate armrests or must type on a keyboard that is too high. Other issues that may play a role in the clinical picture include endocrine dysfunction, chronic infections, nutritional deficiencies, poor posture, and psychological stress.
Cervical Disc Disease
Cervical Spondylosis
Cervical Sprain and Strain
Fibromyalgia
Rheumatoid Arthritis
Thoracic Outlet Syndrome
Myopathy
The primary goal of physical therapy is to restore balance between muscles working as a functional unit. The physical therapist may progress toward that goal initially by attempting to diminish pain. This goal can be accomplished using a modality-based approach performed in conjunction with myofascial release techniques and massage. Cervical stretch and stabilization are integral parts of the approach as well. Postural retraining is crucial in cervical myofascial pain. An ergonomic evaluation may be indicated if overuse in the work setting is contributing to the patient's symptoms.
The primary concern for patients with cervical myofascial pain is chronicity. Recurrence of myofascial pain is a common scenario. Prompt treatment prevents other muscles in the functional unit from compensating, thereby producing a more widespread and chronic problem. Migraine headaches and muscle contraction headaches are known to occur frequently in the patient with myofascial pain.4 Temporomandibular joint (TMJ) syndrome also may be myofascial in origin.2
Several treatment options for cervical myofascial pain are discussed in the literature. Trigger point injection probably is one of the most accepted means of treating myofascial pain besides physical therapy and exercise. Injection is performed most commonly with local anesthetic, although dry needling has been shown to be equally effective.5
Palpate the trigger point in the taut band, and place the muscle in a slightly stretched position to prevent it from moving. Hold the trigger point between 2 fingers while injecting with the other hand. (See image below and Image 4.) Then redirect the needle in the area to assure widespread infiltration of the anesthetic. Instruct the patient to be aggressive about compliance with stretching protocols, because they increase the injection's effectiveness. Production of an LTR helps to confirm the diagnosis. Hong and Simon's article describes a fast-in/fast-out method as more successful in eliciting the local twitch response.3 This approach, therefore, generally is the most helpful technique for reducing myofascial pain.
Botulinum toxin injection therapy has gotten mixed reviews in the literature. Injection directly into the trigger point produces inconsistent results. The best use of botulinum toxin may be for correcting abnormal biomechanics that incite a myofascial response.6,7
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
The goal of medication for patients with cervical myofascial syndrome is to reduce pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs DOC for initial treatment of myofascial pain. Keep narcotic analgesics at a minimum if at all possible. If the clinical picture is one of more chronic pain accompanied by sleep dysfunction, consider use of a tricyclic antidepressant (TCA).
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. Used to provide relief of cervical myofascial pain.
400-600 mg PO tid with food; 800 mg if pain is severe and patient has no history of gastric ulceration
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
TCAs are commonly used for chronic pain. They help to treat insomnia and reduce painful dysesthesia. They treat nociceptive and neuropathic pain syndromes.
Inhibits reuptake of serotonin and/or norepinephrine at presynaptic neuronal membrane, which increases concentration in CNS. May increase or prolong neuronal activity since reuptake of these biogenic amines is important physiologically in terminating transmitting activity.
30-100 mg PO qhs
Children: 0.1 mg/kg PO qhs; increase, as tolerated, over 2-3 wk to 0.5-2 mg/d qhs
Adolescents: 25-50 mg/d PO initially; increase gradually to 100 mg/d in divided doses
Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Documented hypersensitivity; use of MAOIs within 14 d of initiating therapy; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in cardiac conduction disturbances and history of hyperthyroidism, renal or hepatic impairment; avoid using in the elderly
Muscle relaxants are commonly used to treat muscle pain, but they must be used cautiously because of sedation and because of the addictive potential of some of the medications in this category of drugs (benzodiazepines).
Acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons. Structurally related to TCAs.
Skeletal muscle relaxants have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle strains and, used intermittently, for diffuse and certain regional chronic pain syndromes. Long-term improvement over placebo has not been established.
Often produces a "hangover" effect, which can be minimized by taking the nighttime dose 2-3 h before going to sleep.
10 mg PO tid with a range of 20-40 mg/d in divided doses; not to exceed 60 mg/d
Not established
Coadministration with MAOIs and TCAs may increase toxicity; cyclobenzaprine may have additive effect when used concurrently with anticholinergics; effects of alcohol, CNS depressants, and barbiturates may be enhanced with cyclobenzaprine
Documented hypersensitivity; MAOIs within last 14 d
B - Usually safe but benefits must outweigh the risks.
Caution in angle closure glaucoma, and urinary hesitance
Centrally acting muscle relaxant metabolized in liver and excreted in urine and feces.
4-8 mg PO q8h prn; not to exceed 36 mg/d
Not established
May interact with alcohol (increase somnolence, stupor) and oral contraceptives (which decrease its clearance), and can cause increased hypotensive effects when administered concurrently with diuretics
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
Caution in renal impairment
Tramadol is a weak opioid and an inhibitor of serotonin and norepinephrine reuptake in the dorsal horn. Studies have shown efficacy when treating fibromyalgia, although no formal studies have been performed for myofascial pain. Tramadol is known to help with chronic low back pain and osteoarthritis pain, both of which are commonly associated with myofascial pain.
Analgesic probably acting over monoaminergic and opioid mechanisms. Monoaminergic effect shared with TCAs. Tolerance and dependence appear to be uncommon.
100-400 mg PO qd shown to be effective in diabetic neuropathic pain
Not established
Decreases carbamazepine effects significantly; cimetidine increases toxicity, risk of serotonin syndrome with coadministration of antidepressants
Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 d; use of SSRIs, TCAs, opioids, acute alcohol intoxication
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism; pregnancy, breast-feeding; seizure; development of tolerance or dependency with extended use
Anticonvulsants used as neuropathic analgesics may be helpful, because myofascial pain may at its core be a spinal-mediated disorder affected by neuropathic dysfunction. Gabapentin has been shown to be effective in treating myofascial and neuropathic pain.
Membrane stabilizer, a structural analogue of inhibitory neurotransmitter GABA, which paradoxically is thought to not exert effect on GABA receptors. Appears to exert action via the alpha(2)delta1 and alpha(2)delta2 auxiliary subunits of voltage-gaited calcium channels.
Used to manage pain and provide sedation in neuropathic pain.
Titration to effect occurs over several days (300 mg on day 1, 300 mg bid on day 2, and 300 mg tid on day 3).
Day 1: 100 mg PO tid or 300 mg hs
Day 2: 400 mg PO tid for 3 d and titrate prn; not to exceed 1200 mg PO tid
<12 years: Not established
>12 years: Administer as in adults
Antacids may significantly reduce bioavailability (administer at least 2 h following antacids); may increase norethindrone levels significantly
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in severe renal disease
Deterrence/Prevention
Complications
Prognosis
Patient Education
Travell JG, Simons DG. Myofascial Pain and Dysfunction. vol 2. Baltimore, Md: Lippincott Williams & Wilkins; 1992.
Duyur Cakit B, Genc H, Altuntas V, et al. Disability and related factors in patients with chronic cervical myofascial pain. Clin Rheumatol. Feb 18 2009;[Medline].
Hong CZ, Simons DG. Pathophysiologic and electrophysiologic mechanisms of myofascial trigger points. Arch Phys Med Rehabil. Jul 1998;79(7):863-72. [Medline].
Harden RN, Cottrill J, Gagnon CM, et al. Botulinum toxin A in the treatment of chronic tension-type headache With cervical myofascial trigger points: a randomized, double-blind, placebo-controlled pilot study. Headache. Oct 10 2008;[Medline].
Lee SH, Chen CC, Lee CS, et al. Effects of needle electrical intramuscular stimulation on shoulder and cervical myofascial pain syndrome and microcirculation. J Chin Med Assoc. Apr 2008;71(4):200-6. [Medline].
Jabbari B. Botulinum neurotoxins in the treatment of refractory pain. Nat Clin Pract Neurol. Dec 2008;4(12):676-85. [Medline].
Jeynes LC, Gauci CA. Evidence for the use of botulinum toxin in the chronic pain setting--a review of the literature. Pain Pract. Jul-Aug 2008;8(4):269-76. [Medline].
Borg-Stein J, Simons DG. Focused review: myofascial pain. Arch Phys Med Rehabil. Mar 2002;83(3 Suppl 1):S40-7, S48-9. [Medline].
De Andres J, Cerda-Olmedo G, Valia JC, et al. Use of botulinum toxin in the treatment of chronic myofascial pain. Clin J Pain. Jul-Aug 2003;19(4):269-75. [Medline].
Gnatz SM. Referred pain syndromes of the head and neck. In: Physical Medicine and Rehabilitation: State of the Art Reviews. Vol 5. 1991:585-596.
Hou CR, Tsai LC, Cheng KF, et al. Immediate effects of various physical therapeutic modalities on cervical myofascial pain and trigger-point sensitivity. Arch Phys Med Rehabil. Oct 2002;83(10):1406-14. [Medline].
Jacob AT. Myofascial pain. In: Physical Medicine and Rehabilitation: State of the Art Reviews. Vol 5. 1991:573-583.
Rosen NB. Myofascial pain: the great mimicker and potentiator of other diseases in the performing artist. Md Med J. Mar 1993;42(3):261-6. [Medline].
Wheeler AH. Myofascial pain disorders: theory to therapy. Drugs. 2004;64(1):45-62. [Medline].
cervical myofascial pain, neck pain, fascia, myofascial, cervical spine, trigger point, myalgia, myofascial pain, neck and shoulder pain, trigger point therapy, trigger points, trigger point injections, TMJ, TMJ pain, temporomandibular joint, trigger point injection, myofasciitis, interstitial myofibrositis, fibrositis, nonarticular rheumatism affecting the cervical spine, tension myalgia
Beth B Froese, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Orthopaedic Associates of DuPage Ltd
Beth B Froese, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, and Illinois State Medical Society
Disclosure: Nothing to disclose.
Martin K Childers, DO, PhD, Associate Professor, Department of Neurology, Wake Forest University Health Services
Martin K Childers, DO, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Osteopathic Association, Christian Medical & Dental Society, and Federation of American Societies for Experimental Biology
Disclosure: Allergan pharma Consulting fee Consulting
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Related eMedicine topics:
Back Pain, Mechanical
Cervical Spine Sprain/Strain Injuries
Cervical Sprain and Strain
Cervical Strain
Mechanical Low Back Pain
Myofascial Pain
Myofascial Pain in Athletes
Therapeutic Injections for Pain Management
Guidelines:
ACR Appropriateness Criteria Chronic Neck Pain
Assessment and Management of Chronic Pain
Clinical studies:
The Natural History of Upper Trapezius Myofascial Trigger Points: Comparison of Local and Remote Tissue Milieu in Normal Muscle, Latent and Active Myofascial Trigger Points Over Time
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