Cervical Myofascial Pain

Cervical myofascial pain is thought to occur following either overuse of or trauma to the muscles that support the shoulders and neck. It can also occur as a reaction to an underlying spinal pathology such as facet joint arthropathy or an annular tear in one of the cervical discs. Common scenarios among patients are recent involvement in a motor vehicle accident or performance of repetitive upper extremity activities.

In the cervical spine, the muscles most often implicated in myofascial pain are the trapezius, levator scapulae, rhomboids, supraspinatus, and infraspinatus.[1] 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 of cervical myofascial pain include endocrine dysfunction, chronic infections, nutritional deficiencies, poor posture, and psychological stress.

Occurrence in the United States

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 to their condition.

International occurrence

A South American study, by Munoz-Ceron et al, reported that of emergency department patients with nontraumatic headaches, cervical myofascial pain was the most frequent nonprimary cause.[9]

Sex- and age-related demographics

Cervical myofascial pain occurs in both sexes, but with a predominance among women. Myofascial pain seems to occur more frequently with increasing age until midlife. The incidence declines gradually after middle age.

When the patient with cervical myofascial pain undergoes appropriate treatment (eg, physical therapy, massage therapy, stretch and spray, trigger point injections, identification and elimination of an underlying, triggering pathology), the prognosis is generally good. However, recurrence can be a common scenario. Outcomes seem to be better when treatment is initiated early in order to prevent compensation patterns that exacerbate pain. Increased mortality is not associated with cervical myofascial pain.

A Turkish study found evidence that patient disability in chronic myofascial pain is most strongly linked to the duration of pain. The report's assessment was based on data collected from 103 female patients with the chronic disorder and from 30 healthy female participants, using the Neck Pain and Disability Scale, the Beck Depression Inventory, and a visual analog scale, as well as pain pressure threshold measurements from common cervical myofascial pain trigger points.[1]

Patients with cervical myofascial pain need to be educated regarding the factors or underlying problems that may contribute to their pain and loss of mobility. The physical therapist can educate the patient on proper exercise habits and instruct them in a home exercise program for stretching and reconditioning. The patient also may benefit from specific exercises and strategies to improve posture awareness and body mechanics with activities of daily living. If poor workplace ergonomics contribute to the patient's condition, offer instruction in proper ways to modify and revamp the workstation. Cervical myofascial pain is a treatable condition if the patient is educated on the condition and takes an active role in the recovery process.

For patient education information, see Temporomandibular Joint (TMJ) Syndrome, Fibromyalgia, and Chronic Pain.

The diagnosis of myofascial pain is clinical, with no confirmatory laboratory tests available. The patient with cervical myofascial pain may present with a history of acute trauma associated with persistent muscular pain. However, myofascial pain can also manifest insidiously, without a clear antecedent accident or injury. It may be associated with repetitive tasks, poor posture, stress, or cold weather. Typical findings reported by patients also include the following:

• Cervical spine range of motion (ROM) is often limited and painful

• The patient may describe a lumpiness or painful bump in the trapezius or cervical paraspinal muscles

• Massage is often helpful, as is superficial heat

• The patient's sleep may be interrupted because of pain

• The cervical rotation required for driving is difficult to achieve

• The patient may describe pain radiating into the upper extremities, accompanied by numbness and tingling, making discrimination from radiculopathy or peripheral nerve impingement difficult

• Dizziness or nausea may be a part of the symptomatology

• The patient experiences typical patterns of radiating pain referred from trigger points

Common findings noted upon physical examination include the following:

• Patients with cervical myofascial pain often present with poor posture; they exhibit rounded shoulders and protracted scapulae

• Trigger points frequently are noted in the trapezius, supraspinatus, infraspinatus, rhomboids, and levator scapulae muscles

• The palpable, taut band is noted in the skeletal muscle or surrounding fascia; a local twitch response often can be reproduced with palpation of the area

• ROM of the cervical spine is limited, with pain reproduced in positions that stretch the affected muscle

• While the patient may complain of weakness, normal strength in the upper extremities is noted on physical examination

• Sensation typically is normal when tested formally; no long tract signs are observed on examination

Myofascial pain in any location is characterized on examination by the presence of trigger points located in skeletal muscle. 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 further[10] :

• Trigger points are known to elicit local pain and/or referred pain in a specific, recognizable distribution

• Palpation in a rapid fashion (ie, snapping palpation) may elicit a local twitch response, a brisk contraction of the muscle fibers in or around the taut band; the local twitch response also can be elicited by rapid insertion of a needle into the trigger point (see the images below)

• Restricted ROM and increased sensitivity to stretch of muscle fibers in a taut band are noted frequently

• The muscle with a trigger point may be weak because of pain; usually, no atrophic change is observed

• Patients with trigger points may have associated localized autonomic phenomena (eg, vasoconstriction, pilomotor response, ptosis, hypersecretion)

• An active myofascial trigger point is a site marked by generation of spontaneous pain or pain in response to movement; in contrast, latent trigger points may not produce pain until they are compressed

  Cross-sectional drawing shows flat palpation of a taut band and its trigger point. Left: A. The skin is pushed to one side to begin palpation. B. The fingertip slides across muscle fibers to feel the cord-line texture of the taut band rolling beneath it. C. The skin is pushed to the other side at completion of the movement. This same movement performed vigorously is called snapping palpation. Right: A. Muscle fibers are surrounded by the thumb and fingers in a pincer grip. B. The hardness of the taut band is felt clearly as it is rolled between the digits. C. The palpable edge of the taut band is sharply defined as it escapes from between the fingertips, often with a local twitch response.

  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, which usually is seen most clearly as skin movement between the trigger point and the attachment of the muscle fibers.

As previously stated, the diagnosis of myofascial pain is clinical, with no confirmatory laboratory tests available. In addition, imaging studies often reveal nonspecific change only and typically are not helpful in making the diagnosis of cervical myofascial pain.

However, cervical myofascial pain can be present at the same time as other, more serious medical conditions. If the patient's symptoms are resistant to traditional treatment for cervical myofascial pain, further workup is indicated. If a history of trauma exists, order cervical flexion/extension films to rule out the possibility of instability.

Magnetic resonance imaging (MRI) may be helpful in ruling out any significant abnormality within the structure of the cervical vertebrae or spinal canal. The cervical discs also may be evaluated. If the pain is in the shoulders or chest wall, be aware that visceral pain may refer to these areas and even produce some myofascial findings on examination. Be open-minded to the possibility that another problem also may be present.

It may also be reasonable, depending on the clinical presentation, to check for indicators of inflammation, assess thyroid function, and perform a basic metabolic panel to rule out a concomitant medical illness.

Travell and Simons described a study looking at lactate dehydrogenase (LDH) isoenzymes in which a shift was noted in the distribution of the isoenzymes, with higher levels of LDH1 and LDH2, while the total LDH remained within normal limits.[4]

Several research articles have attempted to identify changes on electromyograms/nerve conduction velocity studies that may be unique to patients with myofascial pain. The research has been somewhat contradictory, with some studies finding no real electromyographic activity and others finding nonspecific electrical activity.

Studies by Simons and by Hobbard and Berkoff described low-amplitude action potentials recorded at the region of the myofascial trigger point. Spontaneous electrical activity apparently can be detected using high-sensitivity recordings at the site of the trigger point. The spontaneous electrical activity may be a type of endplate potential.

A study by Ballyns et al describes the use of sonoelastography in classifying myofascial trigger points by active, latent, and normal sites. Although not yet clinically useful, employing sonoelastography to assess the trigger point areas and pulsatility index may help to determine myofascial pain syndrome's natural history.[11]

Treatments for cervical myofascial pain include physical therapy, trigger point injection, stretch-and-spray therapy, and ischemic compression. Injection of botulinum toxin (BoNT) has also been used, although this procedure has received mixed reviews in the literature.

Various pain-relieving medications can also be employed in treatment, including the following:

• Nonsteroidal anti-inflammatory drugs (NSAIDs)

• Tricyclic antidepressants

• Muscle relaxants[12]

• Nonnarcotic analgesics

• Anticonvulsants

A study by Park et al indicated that extracorporeal shock-wave therapy (ESWT) can effectively treat myofascial pain syndrome of the upper trapezius, producing improvement in verbal numeric pain scale and Neck Disability Index scores, as well as in pressure threshold and neck range of motion (ROM). The investigators also reported that posttreatment improvements in the Neck Disability Index and in neck flexion were significantly greater in patients who received high-energy ESWT than in those who underwent low-energy therapy.[13]

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.

In a study by Sherman et al, the authors concluded that massage may provide short-term relief for chronic neck pain. In this randomized, controlled trial, the investigators evaluated whether therapeutic massage is more beneficial than a self-care book for patients with chronic neck pain. Patients (n=64) were randomized to receive up to 10 massages over 10 weeks or a self-care book. Measurement of the Neck Disability Index at 10 weeks demonstrated more participants randomized to massage experienced clinically significant improvement (39%) than did the participants in the self-care book group (14%). However, a larger trial is warranted to confirm these results.[14]

In a study by Ma et al, patients who underwent biofeedback training to the bilateral upper trapezius showed greater reduction in work-related pain and better neck muscle activation than did patients who underwent exercise therapy or passive treatment modalities.[15]

A study by Bronfort et al concluded that both spinal manipulation treatment and a home exercise program were both superior to medication alone in the treatment of acute and subacute neck pain. No significant differences were seen in the outcome when comparing 12 weeks of manipulation to a home exercise program taught by a therapist in 2 separate sessions.[16]

A randomized, double-blind, placebo-controlled study by Ay et al indicated that kinesiology taping improves pain, the pressure pain threshold, and cervical ROM in patients with cervical myofascial pain syndrome but does not improve disability in the short-term. The study included 31 patients who underwent kinesiology taping and 30 patients who underwent sham taping.[17]

A study by Moustafa et al indicated that in patients with chronic cervical myofascial pain syndrome and defined abnormalities in cervical sagittal posture, the use of a Denneroll cervical orthotic device in combination with integrated neuromuscular inhibition technique (INIT) leads, possibly through improvement of sagittal cervical posture alignment, to better results with regard to pressure pain thresholds and cervical range of motion than does INIT alone.[18]

A prospective, randomized clinical study by Aydin et al indicated that exercise therapy can effectively treat dizziness associated with cervical myofascial pain syndrome, with a combination of exercise and dry needling producing better results than exercise alone. The severity of dizziness, weekly number of dizziness attacks, fall index, and Dizziness Handicap Inventory were among the measurements used in deriving the results.[19]

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.[6]

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, and then redirect the needle in the area to assure widespread infiltration of the anesthetic. (See the image below.)

Cross-sectional schematic drawing shows flat palpation to localize and hold the trigger point for injection. A and B show the use of alternate pressure between 2 fingers to confirm the location of the palpable module of the trigger point. C shows the trigger point being positioned halfway between the fingertips to keep it from sliding to one side during the injection.

Instruct the patient to be aggressive about compliance with stretching protocols, because they increase the injection's effectiveness. Production of a local twitch response 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.[10] This approach, therefore, generally is the most helpful technique for reducing myofascial pain.

A retrospective study by Affaitati et al indicated that in patients in whom target areas of myofascial cervical trigger points coincide with migraine pain sites, topical treatment of the trigger points with 3% nimesulide gel is as effective against migraine headache as injection of the trigger points with local anesthetic.[20]

Stretch and spray

Stretch and spray is another method of treating cervical myofascial pain (see the images below). This technique is performed using a vapocoolant spray applied to the affected muscle after it has been placed in passive stretch. Apply the vapocoolant spray to the region around the trigger point and the area of referred pain using parallel strokes in the same direction. Some authors recommend first spraying, then stretching, and only then repeating the spraying.

Sequence of steps to use when stretching and spraying any muscle for myofascial trigger points.

Schematic drawing showing how the jet stream of vapocoolant is applied.

Ischemic compression

Ischemic compression involves application of sustained pressure on the trigger point. Have the patient place the muscle in a fully stretched position. Press firmly on the trigger point with a thumb. Gradually increase the pressure as the pain lessens.

Botulinum toxin

BoNT injection therapy has received mixed reviews in the literature. Injection directly into the trigger point produces inconsistent results. The best use of BoNT may be for correcting abnormal biomechanics that incite a myofascial response.[7, 8]

A study by Nicol et al of patients with cervical myofascial pain found improvements in pain when BoNT-A was injected directly into painful muscle groups. The study began with 114 patients with cervical and shoulder girdle myofascial pain who were injected with BoNT-A and assessed for their response to it. The investigators then conducted a 12-week, randomized, double-blind, placebo-controlled trial with 54 responders, who received either a second injection of BoNT-A, administered directly into a painful muscle group, or a placebo. Improvements in pain, as measured with visual numerical pain scores and Brief Pain Inventory general activity and sleep interference scores, were seen in the BoNT-A group, in comparison with the placebo group. Patients in the BoNT-A group also experienced a decrease in the weekly number of headaches.[21]

The goal of medication for patients with cervical myofascial syndrome is to reduce pain. Avoid the use of opioid analgesics. If the clinical picture is one of more chronic pain accompanied by sleep dysfunction, consider the use of a tricyclic antidepressant (TCA). Anticonvulsants used as neuropathic analgesics may be helpful, because myofascial pain may at its core be a spinal-mediated disorder affected by neuropathic dysfunction. Muscle relaxants, although commonly administered to treat muscle pain, must be used cautiously because of their sedative effects and, in some cases, addictive potential.[12]

Class Summary

NSAIDs are the drugs of choice for the initial treatment of myofascial pain.

Ibuprofen (Motrin, Advil, Neoprofen, Ultraprin)

Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. It is used to provide relief of cervical myofascial pain.

Indomethacin (Indocin)

Indomethacin is thought to be the most effective NSAID for the treatment of ankylosing spondylitis, although no scientific evidence supports this claim. It is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Naproxen (Naprosyn, Naprelan, Aleve, Anaprox)

Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Diclofenac (Voltaren, Cataflam XR, Zipsor, Cambia)

Diclofenac inhibits prostaglandin synthesis by decreasing COX activity, which, in turn, decreases formation of prostaglandin precursors.

Ketoprofen

Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.

Class Summary

Tricyclic antidepressants are commonly used for chronic pain. They help to treat insomnia and reduce painful dysesthesia. These agents treat nociceptive and neuropathic pain syndromes.

Amitriptyline

Amitriptyline inhibits the reuptake of serotonin and/or norepinephrine at the presynaptic neuronal membrane, which increases their concentration in the central nervous system (CNS). Amitriptyline may increase or prolong neuronal activity, since the reuptake of these biogenic amines is important physiologically in terminating transmitting activity.

Class Summary

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).

Cyclobenzaprine (Flexeril, Fexmid, Amrix)

Cyclobenzaprine acts centrally and reduces motor activity of tonic somatic origins, influencing alpha and gamma motor neurons. It is structurally related to the tricyclic antidepressants.

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.

Cyclobenzaprine often produces a "hangover" effect, which can be minimized by taking the nighttime dose 2-3 hours before going to sleep.

Baclofen (Lioresal, Gablofen)

Baclofen is metabolized in the liver and excreted primarily in urine. This agent is not a controlled substance under the Drug Enforcement Administration (DEA).

Carisoprodol (Soma)

Carisoprodol is a short-acting medication that may have depressant effects at the spinal cord level.

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.

Tizanidine (Zanaflex)

Tizanidine is a centrally acting muscle relaxant that is metabolized in the liver and excreted in the urine and feces. It is used in patients with predominantly upper motor neuron involvement. It is not a DEA-controlled substance.

Class Summary

Tramadol is a weak opioid and an inhibitor of serotonin and norepinephrine reuptake in the dorsal horn. Studies have shown efficacy when it has been used to treat fibromyalgia, although no formal studies have been performed for myofascial pain. Tramadol is known to help with chronic low back pain and osteoarthritic pain, both of which are commonly associated with myofascial pain.

Tramadol (Ultram, Ryzolt)

Tramadol is an analgesic that probably acts over monoaminergic and opioid mechanisms. Its monoaminergic effect is shared with tricyclic antidepressants. Tolerance and dependence appear to be uncommon.

Class Summary

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.

Gabapentin (Neurontin)

Gabapentin is a membrane stabilizer. It is a structural analogue of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), but, paradoxically, it is thought not to exert an effect on GABA receptors. Gabapentin appears to exert action via the alpha(2)delta1 and alpha(2)delta2 auxiliary subunits of voltage-gaited calcium channels. It is used to manage pain and provide sedation in neuropathic pain.

Titration to effect occurs over several days (300 mg on day 1, 300 mg twice on day 2, and 300 mg 3 times on day 3).