. Myofascial pain syndrome. OrthopaedicsOne Articles. In: OrthopaedicsOne - The Orthopaedic Knowledge Network. Created Oct 20, 2011 14:35. Last modified Jun 28, 2012 13:26 ver.5. Retrieved 2015-11-29, from http://www.orthopaedicsone.com/x/8ABCB.
Myofascial pain syndrome (MPS) is a common cause of pain and dysfunction in the musculoskeletal system that accounts for 20% to 95% of patients with musculoskeletal pain complaints.1-5 Despite the prevalence of MPS, awareness among clinicians is still inadequate, which results in this condition often being misdiagnosed or underdiagnosed and thus not treated effectively.6-8
The purpose of this literature review is to define and differentiate MPS from other muscle pain syndromes and to describe effective evaluation and treatment methods to effectively diagnose and manage this condition.
Anatomy and Physiology of Skeletal Muscle
Approximately 40% of the human body is comprised of skeletal muscle.9 Skeletal muscles are comprised of numerous muscle fibers, which in turn are comprised of successively smaller subunits described below from the gross to the molecular level.
The sarcomere is the basic functional unit within muscle cells. The sarcolemma is the cell membrane of the muscle fiber whose outer coat consists of numerous thin collagen fibrils that fuse with tendon fibers that, in turn, collect into bundles which form muscle tendons that insert into the bones.
Each muscle fiber contains several hundred to several thousand myofibrils, which are comprised of thousands of long proteins called myosin and actin filaments; they are responsible for muscle contraction. Titin filaments are also found at this level, and they act to keep myosin and actin filaments in place. The myofribrils are suspended in the muscle fiber by an intracellular matrix called the sarcoplasm, which also houses the kidney-shaped mitochondria — responsible for generating cellular energy for muscular contractions.
The sliding filament mechanism of contraction describes the mechanism behind muscle contraction, which results in shortening of the sarcomere with contraction followed by a return to normal muscle length through a slower chemical reaction.
The body recruits as many of these fibrils in any muscle as needed for the task at hand. If the task is significant, the number of fibrils needed may not be available to do the job. This is noted by an inability of an individual to lift certain objects that are too heavy or the inability to lift a lighter object after several repetitions. If the muscle is allowed to rest, then most of the myofibrils will recover to perform further contractile shortening
We are all aware of this action in our own bodies and most, if not all, of us have experienced the muscle pains that develop after an excessive and unusual or vigorous activity. Most of us have learned to walk it out, loosen up, and return to function as quickly as possible, as our life pursuits demand this.
Muscles are the engine of they body, and like all engines, they require care. This means proper nourishment through good dietary and exercise habits; it is imperative for optimal and efficient muscle function. Regular exercise to maintain muscle strength, length, and conditioning is paramount, along with maintenance of weight, especially abdominal girth, and maintenance of proper posture.
If an individual is involved in day-to-day work loads that are often heavy and repetitive, it is the individual's responsibility to maintain a healthy lifestyle and regular exercise to ensure that the body can meet these daily physical demands. Professional athletes would not consider engaging their sports without a muscle conditioning program that would allow them to perform at their very best. Thus, it is our contention that the same level of discipline should be employed by individuals who expects to perform at their very best when engaging in their activities of daily living: work, recreational activities, home care tasks, and so on. Failure to do so is to invite muscle pain and stiffness that may progress to chronic pain, not because of pathology in the muscle but due to de-conditioning and failure to maintain healthy muscle hygiene habits on a daily basis.
Types of Muscle Pain
Acute Muscle Pain
Acute muscular pain may arise from muscle overload, a single episode of macrotrauma, or recurrent episodes of microtrauma. Macrotraumas typically arise from contusions and lacerations to the muscle, whereas delayed onset muscle soreness and muscle strain may result from repetitive exposure to microtrauma and muscle overloading.10 Contusions are typically produced by direct blunt force impact or trauma to the muscle. Laceration of a muscle is not common and usually results following severe trauma. In cases where a muscle is lacerated, surgical consultation and management may be warranted. Delayed-onset muscular soreness is common with physical activity and usually begins several hours following heavy exercise or over activity, and gradually worsens reaching maximal levels of discomfort in 24 to 72 hours.
Chronic Muscular Pain
Chronic muscle pain typically arises from repetitive activities that cause cumulative strain of specific muscle groups over time. When evaluating chronic muscular pain, one must consider metabolic, systemic, and inflammatory causes along with physical causes, especially if muscle weakness is identified. Diagnostic evaluation should be pursued in such cases. Physical examination typically reveals increased tone and reduced muscle length with associated dysfunction.
Myofascial Pain Syndrome
Myofascial pain syndrome is a musculoskeletal disorder that is characterized by local and referred pain and taut bands called trigger points (TrP) within the muscle, along with symptoms of fatigue and weakness. A TrP is defined as a hyperirritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band. The spot is painful on compression and can give rise to characteristic referred pain, referred tenderness, motor dysfunction, and autonomic phenomena.11
While eight types of TrPs have been defined, the active TrP, characterized by a constant and palpable hard band or nodule within the affected muscle that may cause local or referred pain, is often the most referenced clinical feature attributable to the diagnosis of MPS. Muscle weakness without atrophy, restricted range of motion due to the shortening of the contracted taut band, and pain are key TrP manifestations.12 The pain associated with the TrP is often dull, achy, and poorly localized in nature, but it can also mimic radicular or visceral pain.
Gerwin makes a differentiation between TrPs and tender points, which are areas of widespread tenderness that do not have taut bands, do not refer pain to distant sites, and are identified though the application of pressure for the purpose of diagnosing fibromyalgia.13 Gerwin contends that it is by way of this specific feature that chronic MPS, which tends to result in generalized pain, does not change to become fibromyalgia. More recently, The American College of Rheumatology suspended the use of the "tender point test" to diagnose fibromyalgia, and has replaced this form of physical examination with a 24-question survey about a patient's symptoms.14
While the pathogenesis of the TrP is unknown, several theories pertaining to the formation and maintenance of the taut band or nodule have been postulated:
- Latent TrP may be the predecessor to the active TrP, where the latent TrP is a myofascial trigger point that is clinically quiescent with respect to spontaneous pain; it is painful only when palpated. A latent TrP may have all the other clinical characteristics of an active TrP, including a taut band that increases muscle tension and restricts range of motion.15
- Exercise-induced muscle pain, specifically with eccentric contractions, results from the performance of unaccustomed exercise or exercise with an increased intensity or duration. It is reported that selective “damage” to type II muscle fibers in human and animal muscle occurs following eccentric muscle actions, suggesting that during the initial stages of eccentric exercise, fast-twitch glycolytic fibers are instantaneously fatigued and enter a state of rigor, resulting in mechanical disruption.16
- The integrated hypothesis of TrP formation initially postulated by Simons and expanded by Gerwin suggests that an excess of acetylcholine at the motor endplate, modulated by adrenergic modulation of neurotransmitter release, inhibition of acetylcholine esterase, and other modulating factors such as adenosine concentration and by feedback control of neurotransmitter release related to endplate discharge frequency, results in the development of a localized muscle contraction.17
- The core of the TrP is ischemic and the surrounding area is hyperemic,12 which suggests that direct trauma to the soft tissue is a key initializing factor to the formation of a TrP. This coincides with the argument of exercise-induced strain to the muscle in TrP formation. It would also coincide with the biochemichal changes described in affected muscle groups of patients who suffer from chronic whiplash associated disorder (WAD),17 where such points were found to have generalized pressure hypersensitivity and significantly higher levels of interleukin-6 (IL-6) and serotonin (5-HT) in affected muscles. The findings of this study revealed that higher levels of serotonin positively correlated with pain intensity in chronic WAD patients.
Differentiating Fibromyalgia from Myofascial Pain Syndrome
Fibromyalgia is a chronic muscular pain syndrome that may be associated with a number of other symptoms such as:
- Sleep disturbance
- Morning stiffness
- Irritable bowel syndrome
- Interstitial cystitis
- Mood disturbance
Some of these symptoms are manifestations of referred muscle pain from myofascial trigger points (headache, dyspareunia, morning stiffness), and others, such as irritable bowel syndrome and interstitial cystitis, are viscerosomatic pain syndromes18 that occur more frequently in persons with fibromyalgia (up to 70% in fibromyalgia patients) than in those with MPS. Depression may also be a complaint of fibromyalgia patients, but is not more common in those with complaints of fibromyalgia than in the general population.
The clinical picture of MPS includes complaints of musculoskeletal pain, limited mobility, weakness, and referred pain. Clumsiness and in-coordination may also be present. Involvement of the muscles of the head, neck and shoulders may give rise to headache, neck, and shoulder pain. Involvement of the pelvic floor muscles may cause referred pain to the viscera. Pain can be felt at the site of the muscle dysfunction, called the myofascial trigger point, and also in the region of referred pain.
The taut band is the primary identifiable abnormality accessible to physical examination in the muscle, and may be present without tenderness. However, tenderness in MPS is not present without a taut band. The clinical diagnosis is made by physical examination. Identification of the trigger point by physical examination has good inter-rater reliability.20
Guidelines for Clinical Evaluation
The first step in the evaluation of a patient with pain is to diagnose any underlying problem that may be contributing in varying degrees to the symptoms. Muscle pain is a component of all injuries and other conditions; it may be the major source of symptoms or a part of a more significant problem.
Fractures in and of themselves are painful; however muscle contractions to support the injured limb are usually more painful than the bone injury. In such instances, we have learned to help the patient relax, and if applicable, use gentle traction or splinting to allow the muscles to stop contracting and attain significant pain relief, even though the underlying condition has not yet been alleviated.
This is an extremely important concept: In back conditions such as disc herniation, for example, removal of the disc may not always relieve the patient’s pain; the back muscles may continue to contract to protect the spine pathology. This may be mistaken for instability and the surgeon may believe a fusion is required. Again, the pain persists because of the secondary muscle response.
Differential diagnosis is then undertaken to delineate whether contractile tissues are the primary source of the pain, and to localize and identify the site of pain and dysfunction in the muscle. While muscular dysfunction may be associated with muscle pain, it may also be associated with reduced muscle strength and flexibility. This can be evaluated by testing the muscle through its movement arc, as well as muscle contraction against resistance.
Identification and palpation of tender trigger points through digital pressure within the muscle may also reveal dysfunction within the contractile elements. However, this method alone does not adequately address associated muscular dysfunction. Tenderness is frequently elicited when palpating asymptomatic musculotendinous tissues and may also be found in normal functioning muscles. Tenderness to palpation may result from abnormalities that are secondary to underlying or related pathology. Furthermore, pain complaints and TrP tenderness alone do not enable the examiner to fully assess dysfunction within the myofascial elements, which may also manifest altered movement patterns and restricted range of motion.
Therefore, components of the soft tissue evaluation should include:
- Range of motion of a muscle
- Quality and power of concentric and eccentric contraction
- Muscle tone at rest and in midrange
- Muscle play, defined as the accessory mobility between a muscle and its adjacent structures
Reduced joint and muscle end play can be seen in patients with reduced physical activities; they have a role in de-conditioning syndromes that accompany chronic pain. Common causes of reduced muscle play are prolonged spasm, pain, muscle guarding, movement avoidance, and other protective pain behaviors.21
Specific Findings in Patient Populations with Myofascial Pain
The senior author has had the opportunity to evaluate over 30,000 patients with some form of pain condition arising out of motor vehicle or work injuries. On examination of these patients, it has become apparent that they have developed a method of motion designed to protect their spine. This can be noted in the slow and cautious manner in which they perform simple range-of-motion tests, especially forward bending and resisting gravity. Further testing will find that most will be unable to get up from the table without turning sideways, assisting themselves, or asking others for assistance. These are important observations because they demonstrate the de-conditioning of the musculature as well as the patient's anxiety about allowing spontaneous and normal smooth function.
As is the case in the athlete who may have over trained some muscles to the detriment of others, there is a muscular imbalance both from weakness and from the patient’s own input to retrain their muscles to protect their spine and be careful about how it moves. But isn’t that what we, as clinicians, tell our patients in the treatment programs, as in “Be careful how you bend”, “Don’t lift more than 10 pounds,” and so on? Is it any wonder that they change their methods of motion?
Several years ago, isokinetic testing of the quadriceps was initiated to determine the actual strength of this important muscle group in rehabilitation of the knee (Fielden RHN, unpublished data). As an adjunct to this, an isokinetic testing machine was developed for the back muscles. The senior author had the opportunity to evaluate 128 patients with various types of back pain, including healed fractures, post-discectomies, diagnosed but stable disc herniations, spondylolisthesis, degenerative disc changes on plain films, and post-spinal fusion patients. Along with these patient samples were patients in which no underlying pathology was demonstrated clinically or radiologically. All being seen for back pain, and all had to be able flex and extend their spine without spasm or other evidence of clinical limitations while performing specific tests as part of the evaluation.
The initial purpose of the machine and the test was to (1) determine the strength of the flexors and extensors of the spine, which include the gluteal muscles; (2) determine if abnormalities in the motion segment could be observed under dynamic load; and (3)if such abnormalities existed, determine whether the findings correlated with the known pathology. The test was considered valid (ie, performed to the best of the patient’s ability) if the patient could perform the motion at least three consecutive times and the computerized data were accepted, provided the coefficient of variance was less that 10%.
The results of the study did not demonstrate significant changes in spinal biomechanical function across the groups of patients tested. However, an interesting finding occurred in approximately 20% of patients: Their motion pattern was one that would strongly suggest a co-contraction of the flexors and extensors in an antagonistic pattern, rather than the normal synergistic cooperation of these muscle groups when performing spinal flexion and extension against resistance — so much so, that this subgroup of patients was unable to achieve 20 pounds of force in either flexion or extension. Clinical observation as well as computer evaluation of this motion pattern revealed aberrant motor findings equivalent to people suffering from tremors. Thus, it was the conclusion of the senior author that these patients had developed a physiologic dysfunction of the postural muscles of their spine, in that any activity in which they engaged would require extensive muscle contraction and energy. This, in fact, was born out by their history and presentation, as all presented with chronic myofascial pain.
Similar findings have been documented and reported in a recent study demonstrating that myofascial TrPs are associated with reduced efficiency of reciprocal inhibition, which may contribute to the delayed and incomplete muscle relaxation following exercise and unbalanced muscle activation. The study concluded that eliminating latent myofascial TrPs and/or preventing latent myofascial TrPs from becoming active may improve motor functions.22
Behaviorists have demonstrated that individuals can be trained to respond to suggestions and change the manner in which they function. This is accomplished through reward for changing the behavior. These are very important findings because as treating practitioners, we can influence and change how patients respond to their stimuli. The patient has learned to react in a dysfunctional way both by pain avoidance and by suggestions to be careful, and their reward comes in many forms:
- They may receive medication which can be addictive.
- They may get help from family so they do not need to do the menial chores of home care.
- They may receive monetary rewards for their pain.
All of this takes away the incentive for patients to change their behavior to a more positive active lifestyle.
If there is no reason to protect the patient from possible harm, there is no reason to constantly treat and suggest to the patient that he/she be careful in his/her activities. Consequently, there is also evidence suggesting that cognitive behavioral therapy is beneficial in the retraining of behavior in patients suffering from chronic pain.23-27
General Treatment Options
The mode(s) of treatment can take many forms. So long as the underlying pathology, or lack of pathology, is understood and the goal of treatment is to increase the ability of the individual to perform their normal daily activities, then the following modalities of care may be used judicially
Acute muscular injuries usually benefit from rest, ice, and compression to relieve associated pain and swelling. Medications such as non-steroidal anti-inflammatory drugs (NSAIDs) may be used for pain relief and to decrease inflammation. As the pain and swelling decrease, a chiropractor or physical therapist can evaluate the patient to address restrictions in range of motion, application of manual therapy, and gradual muscle strengthening through a prescribed physical conditioning regimen.
Cryotherapy is most effective within the first 24 to 48 hours to reduce inflammation and swelling, especially in cases in which hemorrhage or hematoma is present. Ice affects neural circuitry and helps inhibits pain. Caution must be taken when applying ice, as worsening can occur when extreme or prolonged cold is applied to the injured tissue.
Rest may be employed initially to modulate pain control in the acute inflammatory phase, which lasts approximately 1 to 5 days after injury. After resolution of acute inflammation, progressive low- to no-resistance activity is recommended to promote neurophysiologic gating and blood flow to the injured area.
Prolonged immobilization should be discouraged because of harmful effects on the length of the sarcomere; unnecessary immobilization may contribute to abnormal sarcomere length, as well as hypomobility of neighboring tissues and joints and flawed remodeling of pathologic and normal connective tissues. Prolonged or flawed immobilization may also alter the biomechanical properties of the musculotendinous unit, causing the muscle to fail at lower-than-normal biomechanical loads. Early tensile loading of the muscle and other connective tissues is necessary to stimulate appropriate collagen fiber growth and realignment. Furthermore, early motion aligns new collagen to form optimal tensile strength and inhibits the formation of adhesions or collagen cross-links between the healing muscle and adjacent tissues, which restrict muscle play and range of motion.
In cases of chronic muscular injury or recurrent strain injuries, exercise has been shown to reduce both the number and intensity of myofascial TrPs and to strengthen the muscles while reducing pain and dysfunction. Because de-conditioned muscles are more susceptible to recurrent injury, pain, and dysfunction, an optimal exercise program prescribed early following evaluation of a patient should be performed on an ongoing basis for the purpose of improving strength, flexibility, endurance, and aerobic capacity — which will serve as a good preventive measure for future risk of re-injury.
Treatment of myofascial pain requires the inactivation of TrPs, the restoration of normal muscle length, and the elimination or correction of the factors that initially created or perpetuated the trigger points. Modalities that have proven effective include:
- Manual TrP compression
- Myofascial release technique, in which digital compression is applied to the muscle to stretch the fascia, moving over the skin away from the trigger point
- Stretching the associated muscle(s)
Trigger points may also be inactivated by inserting a needle into the trigger zone or point. This can be done with (wet) or without (dry) the injection of local anaesthetic.28
Modest benefit is noted with growth hormone replacement in fibromyalgia patients who have demonstrated deficiency of growth hormone or insulin-growth-factor-1. Thyroid hormone replacement is likewise beneficial in those patients who have demonstrated hypothyroidism, but there is no hard evidence to suggest that hypothyroidism is more common in fibromyalgia patients than in the general population. Graded, progressive exercise programs have been shown to provide both short- and long-term improvement in fibromyalgia patients.
Postural correction is also important. Proper instruction and correction of posture will reduce the risk of injury by avoiding prolonged misalignment of the muscles and joints of patients who remain static in compromising positions for prolonged periods of time. Employing proper posture may combat the wear and tear of cumulative overload, hence reducing muscular injury and repetitive strain of contractile tissues.
Pharmacologically, the use of amitriptyline at bedtime has been shown to provide initial improvement in symptoms, but has not been shown to be sustained more than 6 months.19 Antidepressant treatment improves sleep, fatigue, pain, and mental well-being, but does not reduce tender point pain on palpation. Review of the literature suggests that tricyclic antidepressant therapy showed no greater effectiveness than that of placebo.
Cognitive therapy is effective when combined with exercise. A committee of the American Pain Society reviewed the evidence for effectiveness of currently available treatments recommended for fibromyalgia and found strong evidence to support the use of low-dose tricyclic antidepressants and cylcobenzaprine, cardiovascular exercise, cognitive behavioral therapy, and patient education.11 Moderate evidence also exists for the efficacy of strength training, acupuncture, hypnotherapy, biofeedback, massage, and warm water baths.
There are many modes of therapy that have shown to be efficacious in the treatment of MPS. While most modalities are passive in nature, our assertion is that a comprehensive exercise regimen aimed at improving muscle function and strength, as well as the overall physical conditioning of a patient suffering from myofascial pain, is perhaps the single most important modality in restoring normal physical function. A key barrier to realizing the benefits of exercise in this respect is patient motivation.
Iatrogenesis by way of offering suggestions that may limit the patient’s activity without specific reasons of possible harm is a significant contributor to the development of chronic pain and pain-focused behavior. This calls for greater patient education and perhaps cognitive behavioral therapy to encourage a patient to adopt an active role toward his/her health and well-being and maintain this motivation to remain consistent with exercise therapy — not only for the treatment of MPS but also for the overall improvement of physical condition.
- Fricton JR, Kroening R, Haley D, Siegert R. Myofascial pain syndrome of the head and neck: a review of clinical characteristics of 164 patients. Oral Surg Oral Med Oral Pathol 1985; 60: 615-23.
- Fishbain DA, Goldberg M, Meagher BR, Steele R, Rosomoff H. Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain 1986; 26: 181-97.
- Skootsky SA, Jaeger B, Oye RK. Prevalence of myofascial pain in general internal medicine practice. West J Med 1989; 151: 157-60.
- Cakit BD, Taskin S, Nacir B, Unlu I, Genc H, Erdem HR. Comorbidity of fibromyalgia and cervical myofascial pain syndrome. Clin Rheumatol 2010; 29: 405-11.
- Moon CW. Myofascial pain syndrome. Korean J Pain 2004; 17(Suppl): 36-44.
- Marcus NJ. Failure to diagnose pain of muscular origin leads to unnecessary surgery. Pain Med 2002; 3: 161-6.
- Ceneviz C, Maloney G, Mehta N. Myofascial pain may mimic trigeminal neuralgia. Cephalalgia 2006; 26: 899-901.
- Facco E, Ceccherelli F. Myofascial pain mimicking radicular syndromes. Acta Neurochir Suppl 2005; 92: 147-50.
- Guyton & Hall – Textbook of Medical Physiology. 10th Ed. P.67.
- Noonan TJ, Garrett WE: Muscle strain injury: diagnosis and treatment. J Am Acad Orthop Surg 1999, 7:262--269.
- Simons DG, Travell JG, Simons LS. Myofascial Pain and Dysfunction: The Trigger Point Manual. 2nd edition. Baltimore, Lippincott, Williams & Wilkins;1999.
- Gerwin R: Myofascial Pain Syndrome: Here We Are, Where Must We Go? Journal of Musculoskeletal Pain Vol. 18(4), 2010.
- Wolfe et al: The American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity. Arthritis Care & Research Vol. 62, No. 5, May 2010, pp 600--610.
- Simons DG, Travell JG, Simons LS: Myofascial Pain and Dysfunction: The Trigger Point Manual, vol 1, edn 2. Baltimore: Lippincott Williams & Wilkins; 1999
- Byrne et al: Neuromuscular Function After Exercise-Induced Muscle Damage: Theoretical and Applied Implications. Sports Medicine Vol 34, No 1, 2004 , pp. 49-69.
- Gerwin RD, Dommerholt J, Shah J: An expansion of Simons’ integrated hypothesis of trigger point formation. Current Pain and Headache Reports 8: 468--475,2004.
- Gerdle et al. European Journal of Pain 12 (2008) 82--93.
- Heymann RE, Helfenstein M, Feldman D. (2001). A double blind, randomized, controlled study of amitriptyline, nortriptyline and placebo in patients with fibromyalgia. An analysis of outcome measures. Clin Exp Rheumatol 2001;19(6):697-702.
- Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA 2004;292(19):2388-95.
- Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz R. Interrater reliability in myofascial trigger point examination. Pain 1997;69(1-2):65-73.
- Wheeler, A.H., Aaron, G.W.: Muscle Pain Due to Injury. Current Pain and Headache Reports 2001, 5:441-446.
- Ibarra et al. Latent myofascial trigger points are associated with an increased antagonistic muscle activity during agonist muscle contraction. JPain. 2011 Dec;12(12):1282-8.
- Dunne RL, Kenardy J, Sterling M. A Randomized Controlled Trial of Cognitive-behavioral Therapy for the Treatment of PTSD in the Context of Chronic Whiplash. Clin J Pain.2011 Dec 30.
- Pato et al. Comparison of randomized treatments for late whiplash. Neurology.2010 Apr 13;74(15):1223-30.
- Andersson et al. Chronic pain in older adults: a controlled pilot trial of a brief cognitive-behavioural group treatment. Behav Cogn Psychother. 2012 Mar;40(2):239-44.
- Glombiewski et al. Two psychological interventions are effective in severely disabled, chronic back pain patients: a randomised controlled trial. Int J Behav Med. 2010 Jun;17(2):97-107.
- Roland et al. Patient centred CBT for chronic pain. Aust Fam Physician. 2004 May;33(5):339-44
- Cummings TM, White A. Needling therapies in the management of myofascial trigger point pain: a systematic review. Arch Phys Med Rehabil 2001;82(7):986-92.