Chronic Myofascial Pain Syndrome- Final Case Presentation
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Chronic Myofascial Pain Syndrome- Final Case Presentation

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FINAL CASE PRESENTATION

FINAL CASE PRESENTATION
DDC PT '14

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Chronic Myofascial Pain Syndrome- Final Case Presentation Chronic Myofascial Pain Syndrome- Final Case Presentation Document Transcript

  • Cervical Myofascial Pain Syndrome BACKGROUND 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 fibers. 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. DESCRIPTION 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 palpated). ETIOLOGY 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 shortened position. ➢ 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. EPIDEMIOLOGY 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. ANATOMY 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- permanent contractions. 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. Microanatomy 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 Creatine phosphate Consume Creatine phosphate PHYSIOLOGY 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 calcium channels. 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 sarcoplasmic reticulum. 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 cease. PATHOPHYSIOLOGY 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 CLINICAL PRESENTATION History 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
  • Physical Examination 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 DIFFERENTIAL DIAGNOSIS 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) •Cervical spine During the physical examination, it is important to assess the following: •Stiffness •Tenderness •Pain on motion •Swelling •Deformity •Limitation of motion •Extra-articular manifestations •Rheumatoid nodules 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 paresthesias develop.
  • 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 Similarities ✔ Pain in muscles ✔ Decreased ROM ✔ Postural stresses Differences ✗ Tender points ✗ Poor sleep ✗ No referred patterns of pain ✗ Fatigue ✗ Trigger points on muscles ✗ Referred patterns of pain ✗ Tight band of muscle MEDICAL AND PHARMACOLOGICAL MANAGEMENT Approach Considerations 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 • Anticonvulsants Medication Summary 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 Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) NSAIDs are the drugs of choice for the initial treatment of myofascial pain. Ibuprofen (Motrin, Advil, Neoprofen, Ultraprin) Dizziness, Epigastric pain, Heartburn ,Nausea, Rash, Tinnitus, Edema,Headache, Vomiting Tricyclic Antidepressants 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, Seizure, Weakness Skeletal Muscle Relaxants Muscle relaxants are commonly used to treat muscle pain, but they Cyclobenzaprine (Flexeril, Amrix) Drowsiness, Dry mouth, Headache, Dizziness
  • must be used cautiously because of sedation and because of the addictive potential of some of the medications in this category of drugs (benzodiazepines). Opioid Analgesics 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, ConZip Constipation, Nausea, Dizziness, Vertigo, Headache Anticonvulsants, Other 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, Somnolence
  • 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 trigger points. ➔ 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
  • References: 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 & Wilkins; 1992. 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. 1991:573-583. 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 function. 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 analgesic efficacy. 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 stimulation.