Chronic Myofascial Pain Syndrome- Final Case Presentation
Cervical Myofascial Pain Syndrome
Pain attributed to muscle and its surrounding fascia is termed myofascial pain, with cervical myofascial pain
thought to occur following either overuse or trauma to the muscles that support the shoulders and neck. In the
cervical spine, the muscles most often implicated in myofascial pain are the trapezius, levator scapulae,
rhomboids, supraspinatus, and infraspinatus.
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
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 and,
consequently, producing a more widespread and chronic problem. Migraine headaches and muscle contraction
headaches are known to occur frequently in the patient with myofascial pain.Temporomandibular joint (TMJ)
syndrome also may be myofascial in origin.
Myofascial pain syndrome is defined as a chronic, regional pain syndrome. The hallmark classification of MPS
comprises the myofascial trigger points (MtrPs) in a muscle which have a specific referred pattern of pain. The
trigger point is defined as a hyper-irritable area in a tight band of muscle. The pain from these points is
described as dull, aching, and deep. Additional impairments from the trigger points include decreased ROM
when the muscle is being stretched, decreased strength in the muscle, and increased pain with muscle
stretching. The trigger points may be active (producing a classic pain pattern) or latent (asymptomatic unless
Cervical myofascial pain is thought to occur following either overuse or trauma to the muscles that support the
shoulders and neck. 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. 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.
Possible Causes of Trigger Points
Although the etiology of trigger of trigger points is not completely understood, some potential causes are:
➢ Chronic overload of the muscle that occurs with repetitive activities or that maintain the muscle in a
➢ Acute overload of the muscle, such as slipping and catching oneself, picking up an object that has an
unexpected weight, or following trauma such as in a motor vehicle accident.
➢ Poorly conditioned muscles compared to muscles that are exercised on a regular basis.
➢ Postural stresses such as sitting for prolonged periods of time, especially if the workstation is not
ergonomically correct, and leg length differences.
➢ Poor body mechanics with lifting and other activities.
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.
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.
The anatomy of muscles includes gross anatomy, which comprises all the muscles of an organism, and
microanatomy, which comprises the structures of a single muscle.
Types of tissue
Muscle tissue is a soft tissue, and is one of the four fundamental types of tissue present in animals. There are
three types of muscle tissue recognized in vertebrates:
➢Skeletal muscle or "voluntary muscle" is anchored by tendons (or by aponeuroses at a few places) to bone and
is used to effect skeletal movement such as locomotion and in maintaining posture. Though this postural control
is generally maintained as an unconscious reflex, the muscles responsible react to conscious control like non-
postural muscles. An average adult male is made up of 42% of skeletal muscle and an average adult female is
made up of 36% (as a percentage of body mass).
➢Smooth muscle or "involuntary muscle" is found within the walls of organs and structures such as the
esophagus, stomach,intestines, bronchi, uterus, urethra, bladder, blood vessels, and the errector pili in the skin
(in which it controls erection of body hair). Unlike skeletal muscle, smooth muscle is not under conscious control.
➢Cardiac muscle is also an "involuntary muscle" but is more akin in structure to skeletal muscle, and is found
only in the heart. Cardiac and skeletal muscles are "striated" in that they contain sarcomeres that are packed
into highly regular arrangements of bundles; the myofibrils of smooth muscle cells are not arranged in
sarcomeres and so are not striated. While the sarcomeres in skeletal muscles are arranged in regular, parallel
bundles, cardiac muscle sarcomeres connect at branching, irregular angles (called intercalated discs). Striated
muscle contracts and relaxes in short, intense bursts, whereas smooth muscle sustains longer or even near-
Skeletal (voluntary) muscle is further divided into two broad types: slow twitch and fast twitch:
•Type I, slow twitch, or "red" muscle, is dense with capillaries and is rich in mitochondria and myoglobin, giving
the muscle tissue its characteristic red color. It can carry more oxygen and sustain aerobic activity using fats or
carbohydrates as fuel. Slow twitch fibers contract for long periods of time but with little force.
•Type II, fast twitch muscle, has three major subtypes (IIa, IIx, and IIb) that vary in both contractile speed and
force generated. Fast twitch fibers contract quickly and powerfully but fatigue very rapidly, sustaining only short,
anaerobic bursts of activity before muscle contraction becomes painful. They contribute most to muscle strength
and have greater potential for increase in mass. Type IIb is anaerobic, glycolytic, "white" muscle that is least
dense in mitochondria and myoglobin. In small animals (e.g., rodents) this is the major fast muscle type,
explaining the pale color of their flesh.
Skeletal muscles are sheathed by a tough layer of connective tissue called the epimysium. The epimysium
anchors muscle tissue to tendons at each end, where the epimysium becomes thicker and collagenous. It also
protects muscles from friction against other muscles and bones. Within the epimysium are multiple bundles
called fascicles, each of which contains 10 to 100 or more muscle fibers collectively sheathed by a perimysium.
Besides surrounding each fascicle, the perimysium is a pathway for nerves and the flow of blood within the
muscle. The threadlike muscle fibers are the individual muscle cells (myocytes), and each cell is encased within
its own endomysium of collagenfibers. Thus, the overall muscle consists of fibers (cells) that are bundled into
fascicles, which are themselves grouped together to form muscles. At each level of bundling, a collagenous
membrane surrounds the bundle, and these membranes support muscle function both by resisting passive
stretching of the tissue and by distributing forces applied to the muscle. Scattered throughout the muscles are
muscle spindles that provide sensory feedback information to thecentral nervous system.
This same bundles-within-bundles structure is replicated within the muscle cells. Within the cells of the muscle
aremyofibrils, which themselves are bundles of protein filaments. The term "myofibril" should not be confused
with "myofiber", which is a simply another name for a muscle cell. Myofibrils are complex strands of several
kinds of protein filaments organized together into repeating units called sarcomeres. The striated appearance of
both skeletal and cardiac muscle results from the regular pattern of sarcomeres within their cells. Although both
of these types of muscle contain sarcomeres, the fibers in cardiac muscle are typically branched to form a
network. Cardiac muscle fibers are interconnected byintercalated discs, giving that tissue the appearance of a
syncytium. The filaments in a sarcomere are composed of actin and myosin.
Type I fibers (red) Type II a fibers (red) Type II b fibers (white)
Contraction time Slow Moderately Fast Very fast
Size of motor neuron Small Medium Very large
Resistance to fatigue High Fairly high Low
Activity Used for Aerobic Long-term anaerobic Short-term anaerobic
Maximum duration of use Hours <30 minutes <1 minute
Power produced Low Medium Very high
Note Consume lactic acid Produce lactic acid and
The three types of muscle (skeletal, cardiac and smooth) have significant differences. However, all three use the
movement of actin against myosin to create contraction. In skeletal muscle, contraction is stimulated by electrical
impulses transmitted by the nerves, the motoneurons (motor nerves) in particular. Cardiac and smooth muscle
contractions are stimulated by internal pacemaker cells which regularly contract, and propagate contractions to
other muscle cells they are in contact with. All skeletal muscle and many smooth muscle contractions are
facilitated by the neurotransmitter acetylcholine.
Contractions, by muscle type
There are three general types of muscle tissues:
•Skeletal muscle responsible for movement
•Cardiac muscle responsible for pumping blood
•Smooth muscle responsible for sustained contractions in the vascular system, gastrointestinal tract, and other
areas in the body.
Skeletal and cardiac muscles are called striated muscle because of their striped appearance under a
microscope, which is due to the highly organized alternating pattern of A band and I band.
Skeletal muscle contractions
1.An action potential originating in the CNS reaches an alpha motor neuron, which then transmits an action
potential down its own axon.
2.The action potential propagates by activating voltage-gated sodium channels along the axon toward the
neuromuscular junction. When it reaches the junction, it causes a calcium ion influx through voltage-gated
3.The Ca2+ influx causes vesicles containing the neurotransmitter acetylcholine to fuse with the plasma
membrane, releasing acetylcholine out into the extracellular space between the motor neuron terminal and the
neuromuscular junction of the skeletal muscle fiber.
4.The acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on
the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel,
causing sodium to rush in and potassium to trickle out. Because the channel is more permeable to sodium, the
charge difference between internal and external surfaces of the muscle fiber membrane becomes less negative,
triggering an action potential.
5.The action potential spreads through the muscle fiber's network of T-tubules,depolarizing the inner portion of
the muscle fiber.
6.The depolarization activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T
tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent
7.Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them,
causing the sarcoplasmic reticulum to release calcium.
8.The calcium binds to the troponin C present on the actin-containing thin filaments of the myofibrils. The
troponin then allosterically modulates the tropomyosin. Under normal circumstances, the tropomyosin sterically
obstructs binding sites for myosin on the thin filament; once calcium binds to the troponin C and causes an
allosteric change in the troponin protein, troponin T allows tropomyosin to move, unblocking the binding sites.
9.Myosin (which has ADP and inorganic phosphate bound to its nucleotide binding pocket and is in a ready
state) binds to the newly uncovered binding sites on the thin filament (binding to the thin filament is very tightly
coupled to the release of inorganic phosphate). Myosin is now bound to actin in the strong binding state. The
release of ADP and inorganic phosphate are tightly coupled to the power stroke (actin acts as a cofactor in the
release of inorganic phosphate, expediting the release). This will pull the Z-bands towards each other, thus
shortening the sarcomere and the I-band.
10.ATP binds to myosin, allowing it to release actin and be in the weak binding state (a lack of ATP makes this
step impossible, resulting in the rigor state characteristic of rigor mortis). The myosin then hydrolyzes the ATP
and uses the energy to move into the "cocked back" conformation. In general, evidence (predicted and in vivo)
indicates that each skeletal muscle myosin head moves 10–12 nm each power stroke, however there is also
evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.
11.Steps 9 and 10 repeat as long as ATP is available and calcium is freely bound within the thin filaments.
12.While the above steps are occurring, calcium is actively pumped back into the sarcoplasmic reticulum. When
calcium is no longer present on the thin filament, the tropomyosin changes conformation back to its previous
state so as to block the binding sites again. The myosin ceases binding to the thin filament, and the contractions
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:
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
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
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
➢Trigger points frequently are noted in the trapezius, supraspinatus, infraspinatus, rhomboids, and levator
➢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
➢Sensation typically is normal when tested formally; no long tract signs are observed on examination
Cervical Disc Disease is defined as localized displacement of nucleus, cartilage, fragmented apophyseal
bone, or fragmented anular tissue beyond the intervertebral disc space. Most of the herniation is made up of the
annulus fibrosus. Cervical radiculopathy can result from nerve root injury in the presence of disc herniation or
stenosis, most commonly foraminal stenosis, leading to sensory, motor, or reflex abnormalities in the affected
nerve root distribution. Depending on whether primarily motor or sensory involvement is present, radicular pain is
deep, dull, and achy or sharp, burning, and electric. Such radicular pain follows a dermatomal or myotomal
pattern into the upper limb. Cervical radicular pain most commonly radiates to the interscapular region, although
pain can be referred to the occiput, shoulder, or arm as well. Neck pain does not necessarily accompany
radiculopathy and frequently is absent. Patients may present with distal limb numbness and proximal weakness
in addition to pain. Atrophy may be present.
Cervical Spondylosis is a chronic degenerative condition of the cervical spine that affects the vertebral
bodies and intervertebral disks of the neck (in the form of, for example, disk herniation and spur formation), as
well as the contents of the spinal canal (nerve roots and/or spinal cord). Chronic suboccipital headache may be
present. Mechanisms include direct nerve compression; degenerative disk, joint, or ligamentous lesions; and
segmental instability. Pain can be perceived locally, or it may radiate to the occiput, shoulder, scapula, or arm.
The pain, which is worse when the patient is in certain positions, can interfere with sleep.
Cervical Sprain and Strain Cervical strain is one of the most common musculoskeletal problems
encountered by generalists and neuromusculoskeletal specialists in the clinic. One cause of cervical strain is
termed cervical acceleration-deceleration injury; this is frequently called whiplash injury. Whiplash, one of the
most common sequela of nonfatal car injuries, is one of the most poorly understood disorders of the spine, and
the severity of the trauma is often not correlated with the seriousness of the clinical problems. A history of neck
injury is a significant risk factor for chronic neck pain.
Rheumatoid Arthritis is a chronic systemic inflammatory disease of unknown cause. An external trigger
(eg, cigarette smoking, infection, or trauma) that triggers an autoimmune reaction, leading to synovial
hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized
to occur in genetically susceptible individuals.
The physical examination should address the following:
•Upper extremities (metacarpophalangeal joints, wrists, elbows, shoulders)
•Lower extremities (ankles, feet, knees, hips)
During the physical examination, it is important to assess the following:
•Pain on motion
•Limitation of motion
Thoracic Outlet Syndrome is not the name of a single entity, but rather a collective title for a variety of
conditions attributed to compression of these neurovascular structures as they traverse the thoracic outlet. The
thoracic outlet is bordered by the scalene muscles, first rib, and clavicle. Neurovascular structures pass from the
neck and thorax into the axilla through this space. The examination should begin with an assessment of the
patient’s posture. A slumped posture of the shoulders and upper back and a “poked-forward” position of the head
and neck are comfortable but potentially damaging for the scapular and neck muscles and are thought to
contribute to the susceptibility for thoracic outlet syndrome. The symmetry of both arms should be evaluated.
Cervical active range-of-motion assessment and the Spurling test (ie, patient’s head is placed in extension and
lateral flexion, with axial compression applied by the examiner to the patient’s head in an effort to recreate
radicular pain) should be performed. Active and passive range of motion of both shoulders should be examined.
A careful neurovascular examination of both upper extremities is needed, taking care to remember that the
muscles and nerves supplied by the lower brachial plexus are most commonly affected.
The Adson maneuver is performed by positioning the tested shoulder in slight abduction and extension. Then,
the patient extends his or her neck and turns the head toward this affected shoulder. The patient inhales while
the examiner simultaneously palpates the ipsilateral radial pulse. If the pulse diminishes or the patient has
paresthesias, the test result is considered positive as long as this maneuver does not cause symptoms on the
asymptomatic contralateral side.
The Wright test is performed by progressively hyperabducting and externally rotating the patient’s affected arm
while assessing the ipsilateral radial pulse. Again, the test result is considered positive if the pulse diminishes or
The Roos stress test is performed with the patient positioning both of his or her shoulders in abduction and
external rotation of 90° with elbow flexion at 90°. The patient then opens and closes his or her hands for several
minutes. Reproduction of symptoms or a sensation of heaviness or fatigue is considered a positive test result.
Fibromyalgia is now recognized as one of many central pain-related syndromes that are common in the
general population. Research advances have lead to the conclusion that disturbances within the central nervous
system (CNS) known as central sensitization represent the most likely source.
Similarities and differences between Fibromyalgia and Myofascial Pain Syndrome
FIBROMYALGIA MYOFASCIAL PAIN SYNDROME
✔ Pain in muscles
✔ Decreased ROM
✔ Postural stresses
✗ Tender points
✗ Poor sleep
✗ No referred patterns of pain
✗ Trigger points on muscles
✗ Referred patterns of pain
✗ Tight band of muscle
MEDICAL AND PHARMACOLOGICAL MANAGEMENT
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.
Treatments for cervical myofascial pain include physical therapy, trigger point injection, stretch-and-spray
therapy, and ischemic compression. Injection of botulinum toxin 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
• Nonnarcotic analgesics
The goal of medication for patients with cervical myofascial syndrome is to reduce 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 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.
Examples Adverse effects
NSAIDs are the drugs of choice for
the initial treatment of myofascial
Ibuprofen (Motrin, Advil, Neoprofen,
Dizziness, Epigastric pain,
Heartburn ,Nausea, Rash, Tinnitus,
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 (Elavil, Levate)
Ataxia, ECG changes, Fatigue,
Headache, Hypertension, Lethargy,,
Orthostatic hypotension, Palpitation,
Skeletal Muscle Relaxants
Muscle relaxants are commonly
used to treat muscle pain, but they
Cyclobenzaprine (Flexeril, Amrix)
Drowsiness, Dry mouth, Headache,
must be used cautiously because of
sedation and because of the
addictive potential of some of the
medications in this category of
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.
ltram, Ultram ER, Rybix ODT,
Constipation, Nausea, Dizziness,
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, Gralise
Ataxia, Dizziness, Fatigue,
PHYSICAL THERAPY MANAGEMENT
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.
Treatment consists of three main components: eliminating the trigger point, correcting the contributing factors,
and strengthening the muscle. If the cause of the trigger point is a chronic overload of the muscle, the
contributing factor should be eliminated prior to addressing the trigger point. When ROM is restored and the
trigger point has been addressed, muscle strengthening is initiated. Several techniques are used to eliminate
➔ Contract-relax-passive stretch done repeatedly until the muscle lengthens.
➔ Contract-relax-active stretch also done in repetition
➔ Trigger point release
➔ Spray and stretch
➔ Dry needling or injection
1.Kisner C, Colby L. Therapeutic Exercise. 5th
Ed. F.A . Davis Company. 2007: 316-318
2.Travell JG, Simons DG. Myofascial Pain and Dysfunction. vol 2. Baltimore, Md: Lippincott Williams &
3.Hong CZ, Simons DG. Pathophysiologic and electrophysiologic mechanisms of myofascial trigger
points.Arch Phys Med Rehabil. Jul 1998;79(7):863-72.
4.[Best Evidence] Sherman KJ, Cherkin DC, Hawkes RJ, Miglioretti DL, Deyo RA. Randomized trial of
therapeutic massage for chronic neck pain. Clin J Pain. Mar-Apr 2009;25(3):233-8.
5.Ma C, Szeto GP, Yan T, Wu S, Lin C, Li L. Comparing biofeedback with active exercise and passive
treatment for the management of work-related neck and shoulder pain: a randomized controlled trial.
Arch Phys Med Rehabil. Jun 2011;92(6):849-58.
6.Bronfort G, Evans R, Anderson AV, Svendsen KH, Bracha Y, Grimm RH. Spinal manipulation,
medication, or home exercise with advice for acute and subacute neck pain: a randomized trial. Ann
Intern Med. Jan 3 2012;156(1 Pt 1):1-10.
7.Jacob AT. Myofascial pain. In: Physical Medicine and Rehabilitation: State of the Art Reviews.Vol 5.
8.Wheeler AH. Myofascial pain disorders: theory to therapy. Drugs. 2004;64(1):45-62.
EVIDENCE- BASED PRACTICE
Title: Differential Diagnosis and Treatment in a Patient With Posterior Upper Thoracic Pain
Author: Stacie J Fruth
Abstract: Determining the source of a patient’s pain in the upper thoracic region can be difficult. Costovertebral
(CV) and costotransverse (CT) joint hypomobility and active trigger points (TrPs) are possible sources of upper
thoracic pain. This case report describes the clinical decision-making process for a patient with posterior upper
thoracic pain. Case Description. The patient had a 4-month history of pain; limited cervical, trunk, and shoulder
active range of motion; limited and painful mobility of the right CV/CT joints of ribs 3 through 6; and periscapular
TrPs. Interventions included CV/CT joint mobilizations, TrP release, and flexibility and postural exercises. Phys
Ther. 2006;86:254 –268.]
Results: This patient was able to return to his normal daily and recreational activities after 7 physical therapy
sessions over the course of 4 weeks. He actively participated in his care, reported adherence to his HEP, and did
not miss or cancel any sessions. His pain rating at rest decreased from an average of 7.5/10 to 0–1/10, and his
pain rating with UE activities decreased from 9/10 to 1–2/10. Upon re-examination, the patient demonstrated
symmetrical, nonguarded sitting and standing postures. Cervical, trunk and UE AROM were normal and pain-
free. There was no pain and full strength during MMT. The patient said he had no pain with accessory motion
testing of the right CV and CT joints or the upper thoracic spine. All of the patient’s initial physical therapy goals
were fully met. He reported a considerable decrease in daily pain, full ability to play with and care for his
children, unrestricted participation in softball, and minimal to no difficulty sleeping. This patient also was seen
informally several times following his discharge. Each time he reported normal function and no residual pain. The
last time this individual was seen was 5 years following his discharge, and he again reported full, pain-free
Recommendations: This case suggests that CV/CT mobilizations and active TrP release may have been
beneficial in reducing pain and restoring function in this patient. The author suggested that based on her
estimation of joint hypomobility, the presence of pain with mobility assessment, and the limited available
literature, I hypothesized that the patient might benefit from joint mobilizations. One similar description is in the
literature regarding a patient with CV and CT joint dysfunction at ribs 2, 3 and 5. However, local analgesic
injections were a part of the interventions and, therefore, a direct comparison with this case could not be made.
Several aspects of this case report highlight the need for further research. Compared with the literature available
in the lumbar and cervical areas, information regarding pain and dysfunction in the thoracic area is limited. There
is also a lack of research concerning the reliability of assessments of joint mobility, the reliability of detecting of
TrPs, the efficacy of providing joint mobilizations, and the efficacy of TrP release. Because these are all common
physical therapist examination or intervention techniques, additional research is important to provide patients
with evidence-based examinations and interventions.
Title: Effectiveness of a Home Program of Ischemic Pressure Followed by Sustained Stretch for
Treatment of Myofascial Trigger Points
Author: William P Hanten, Sharon L Olson, Nicole L Butts and Aimee L Nowicki
Abstract: Myofascial trigger points (TPs) are found among patients who have neck and upper back pain. The
purpose of this study was to determine the effectiveness of a home program of ischemic pressure followed by
sustained stretching for the treatment of myofascial TPs. Subjects. Forty adults (17 male, 23 female), aged 23 to
58 years (X530.6, SD59.3), with one or more TPs in the neck or upper back participated in this study. Methods.
Subjects were randomly divided into 2 groups receiving a 5-day home program of either ischemic pressure
followed by general sustained stretching of the neck and upper back musculature or a control treatment of active
range of motion. Measurements were obtained before the subjects received the home program instruction and
on the third day after they discontinued treatment. Trigger point sensitivity was measured with a pressure
algometer as pressure pain threshold (PPT). Average pain intensity for a 24-hour period was scored on a visual
analog scale (VAS). Subjects also reported the percentage of time in pain over a 24-hour period. A multivariate
analysis of covariance, with the pretests as the covariates, was performed and followed by 3 analyses of
covariance, 1 for each variable.
Findings: The purpose of our study was to investigate the effectiveness of a home program of ischemic
pressure followed by sustained stretching in reducing TP sensitivity, average pain intensity, and percentage of
time in pain in individuals with neck and upper back pain. Our results indicate that clinicians can manage neck
and upper back pain associated with TPs through a home program of ischemic pressure and sustained
stretching with periodic monitoring by a physical therapist. We do not know, however, whether the pain relief
influences patients’ functional abilities or disability status. These results were obtained with minimal patient-
clinician contact, providing evidence of effective treatment in the age of managed care, which places emphasis
on shorter treatment times and decreased number of clinic visits.
Recommendations: The results of our study demonstrate the effectiveness of ischemic pressure followed by
sustained stretching, performed as a home program, in reducing TP sensitivity as measured with a PA and pain
intensity scored with a VAS. Direct comparison of these results with the results found in other TP treatment
experiments is only possible in a general way due to different treatment techniques, subject populations,
measurements taken, duration of treatment, and time between treatment cessation and posttest measurement.
They did not examine effectiveness relative to any other outcome such as functional limitation or disability.
Studies of TP pain typically focus on patients with chronic pain, most of whom are being medically treated for
Tps. The subject sample in our study did not include anyone undergoing treatment for TPs or myofascial pain.
The differences in subject groups should be noted when comparing results. We believe that our results might
have been different if we had studied a clinical population of individuals with chronic pain. A limitation of our
study is that it may be possible that either the ischemic pressure or the sustained stretching produced the results
independently. This study could be repeated with one group performing only ischemic pressure, one group
performing only sustained stretching, and one group performing both techniques together.
Title: Effectiveness of Interferential Current Therapy in the Management of Musculoskeletal Pain: A
Systematic Review and Meta-Analysis
Authors: Jorge P. Fuentes, Susan Armijo Olivo, David J. Magee, Douglas P. Gross
Abstract: Interferential current (IFC) is a common electrotherapeutic modality used to treat pain. Although IFC is
widely used, the available information regarding its clinical efficacy is debatable. The aim of this systematic
review and meta-analysis was to analyze the available information regarding the efficacy of IFC in the
management of musculoskeletal pain
Results: Interferential current therapy included in a multimodal treatment plan seems to produce a pain relieving
effect in acute and chronic musculoskeletal painful conditions compared with no treatment or placebo.
Interferential current therapy combined with other interventions was shown to be more effective than placebo
application at the 3-month follow-up in subjects with chronic low back pain. However, it is evident that under this
scenario, the unique effect of IFC is confounded by the impact of other therapeutic interventions. Moreover, it is
still unknown whether the analgesic effect of IFC is superior to that of these concomitant interventions. When
IFC is applied alone, its effect does not differ from placebo or other interventions (ie, manual therapy, traction, or
massage). However, the small number of trials evaluating the isolated effect of IFC, heterogeneity across
studies, and methodological limitations identified in these studies prevent conclusive statements regarding its
Recommendations: Because only 4 studies that evaluated the isolated effect of IFC were identified, and these
studies had mixed results, further research examining this issue is needed, ideally in homogeneous clinical
samples. Further research also is needed to study the effect of IFC on acute painful conditions. Also of interest
would be the study of the effect of IFC in chronic conditions using a theoretical framework for the selection of
parameters associated with suprasegmental analgesic mechanisms (ie, noxious stimulus) instead of sensory