S E M I N A R S I N NE:URO120C;Y-VO12UME
1 I , NO. 3
Sk,'PTEMBI:'K 1991
Myofascial Pain Syndrome and Fibromyalgia
Chronic ~nyofascialpain is a well-established but not widely known cause of chronic pain and disability. Many patients with myof'ascial pain syndrome (MPS) have seen numerous other physicians, physical therapists, and chiropractors, with none providing lasting relief from their pain. This nonsurgical musculoskeletal pain disorder remains one of the least understood, yet most frequently encountered, problems seen in the outpatient setting. MPS is a common soft tissue disorder that often presents with additional symptoms suggestive of other neurologic disorders. Complaints of localized o r diffuse muscle pain and tenderness, headache, vertigo, visual disturbance, paresthesias, discoordination, and referred pain all demand not only careful neurologic evaluation but also a detailed musculoskeletal examination.' Unfbrtunately, confusion with respect to taxonomy and definition has impeded both research and clinical application in the study of soft tissue pain disorders. Discussions of muscle pain due to palpable, tender bands within symptomatic muscle groups first appeared in the European medical literature during the early 19th century. In 1852, Virchow coined the term "muscular rheumatism" in postulating such palpable changes in muscle, although histologically unsubstantiated, as a complication of' rheumatic fever.' Gowers" first discussed the possibility that a number of' musculoskeletal contlitions, including lumbago, involved muscle inflarnmation, which he termed "fibrositis." Stockman' almost sinlultaneously described connective tissue hyperplasia, which by 19 15 was considered the pri-
mary histopathologic process underlying the fihrositic presentation.' Since such histologic studies were never reproduced on a consistent basis, the term and contlitior~known as "fibrositis" has subsequently assumed a highly controversial place within the 20th century medical lexicon. Kellgren," in 1938, first reported symptoms of referred pain during palpation of tender points in skeletal muscle. His descriptions quite likely constitute the first published observation of'the trigger point phenomenon now considered an essential criterion for the diagnosis of myofascial pain. Janet Travell subsequently clarified the concept of the trigger point and popularized the term "myof'as-
DEFINITIONS Myofascia1 pain syndrome: M PS is now understood to refer to a spectrum of clinical presentations distinct from other n~usculoskeletal conditions such as fibromyalgia (formerly termed "f'ibrositis"), strains, o r sprains. Indeed, much of the confusion and misunderstanding surrounding this entity sterns from the myriad of names used by investigators and clinicians in discussing soft tissue p a i n Muscular rheumatism, myalgia, myogelosis, interstitial myofibrositis, fibrornyositis, and rnyofasciitis have all, in the past, referred to clinical conditions that may have shared some attributes with the more specifically defined MPS. Trigypr points: T h e presence o r absence of trigger points determines whether a clinical presentation qualifies as a MPS. Muscle trigger points are
Center fir Spine Rehabilitation, Spalding Rehabilitation Hospital, and the Colorado Neurological Institute, Englewood, a n d the Department of Rehabilitation Medicine, University of Colorado Health Sciences Center, Denver, Colorado; and Center for Occupational Neurology a n d Neurotoxicology, Neur-o~riuscularDisease PI-ogl-am,Colorado Neur-ological Institute, t:nglcwootl, a ~ the ~ dL)cpartnier~tof'lLledicir~e(Clinical Pharmacology), Ulliver-sit! of Colorado Health Sciences (;enrcl-, 1)enver-, Colorado Reprint requests: Dr. Goldrr~an,Center for Spine Rehabilitation. 125 E. 1la111ptlenAvenue, Englewood, CO 801 10 Copyright O 1991 by .fhieme Medical I'ublisher-s, I I I ~ .381 , Park Avcllue South. New York, N Y 10016. All rights reserved.
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L. Burton Goldmun, M.D., and Nril L. Rosenberg, M.D.
?
7
diagnostic criteria, but also to treatment approach and prognosis. MPS tends to be more acute in onset, more regional in presentation, more amenable to treatment, and characterized by an objective trigger point phenomenon. Fibromyalgia syndrome tends to be more insidious in onset, more global in presentation, more guarded in prognosis, arid characterized by subjective tender points (Table 1). Recently, the criteria required fbr the diagnosis of fibrornyalgia have been defined. T h e American College of Rheumatology in 1990 set criteria for the classification of fibromyalgia that include at least 3 months of widespread pain in the presence of' 11 of 18 specific tender points on palpation.'" However, the locations of many of these classic tender points overlap classic trigger point sites. Moreover, distinguishing between latent trigger points and tender points is often difficult. Patient history and symptom pattern needs to be considered more carefully in such circumstances. Lastly, active trigger points can "metastasize" via activation of satellite o r secondary trigger points, resulting in the gradual transformation from an initial, regional myofascial presentation to a subsequent global fibromyalgic picture. Satellite trigger points become activated because they reside within the pain reference zone of another previously activated trigger point, whereas secondary trigger points occur in synergistic muscle groups outside of the initial trigger point's zone of' reference. 'The mechanism for creation o r activation of secondary trigger points involves an overuse phenomenon to compensate for antecedent guarding and disuse of the muscle groups originally associated with the patient's initial myofascial presentation.
Table 1. Comparison of Myofascial Pain and Fibromyalgia Myofascial Pain
Fibromyalgia
Sex
Male and female
Predominantly female
Age Pain
All Focal
40-60 years primarily
Mediation
Endorphin
Substance P
Duration
Acute or chronic
Chronic
Twitch response
Present
Absent
Pain areas
Distinct reference zones
Nonradiating
Etiology
Generally mechanical
Internal, environmental
Prognosis
Good with elimination of perpetuating factors
Guarded
DIFFERENTIAL DIAGNOSIS T h e distinctio~ibetween active trigger points and less specific tender points is an important one. More cornrnonly associated with fibroniyalgia syndronle, tender points may be associated with taut banding or nodularity within the muscle, but will not manifest a local twitch response or characteristic pain reference zone on palpation. Subjective in presentation, tender points may be associated with more subtle and global evidence of autonon~ic dysfunction in the context of a fibromyalgia syndrome, without the focality o f a MPS." Likewise, the distinction between MPS and fit~romyalgiais important with respect not only to
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the central elements of' MPS. 'Ii-igger points may be found in a number of anatomic sites, including muscle, skin, joints, and ligaments. They are painful regions and taut bands of muscle that refer pain to distant areas. Skeletal muscle trigger points, which have generally been emphasized in clinical practice because of their accessibility and their research considerations, are characterized by taut bands within the muscle which will manifest a local twitch response on direct palpation. 1,ocal twitch responses represent transient involuntary shortening of the fibrous muscular bands harboring trigger points that may be observed by the trained eye in the more superficial muscle groups. In order to establish a diagnosis of myofascial pain, the clinician must be able to distinguish between the involuntary local twitch response and voluntary contraction of the entire muscle group produced by the patient's guarding. 1rigger points are generally classified as either active or latent. Active trigger points cause ongoing pain arid restricted motion of the muscle in which they abide. Latent trigger points are quiescent and result primary in muscle tightness, shortening, and dysfunction without the presence of persistent pain."' In addition to the local twitch response, active trigger points are also characterized by specific patterns of pain radiation during palpation that depend on the location of the trigger point. These pain reference zones may o r may not mimic more traditionally recognized derrnatomal, myotornal, or- scleratornal referred pain patterns." Focal or regional autonomic dysfunction, including localized vasoconstriction, persistent hyperernia after palpation, diaphoresis, lacrimation, coryza, salivation, and pilomotor activity, is often associated with trigger point presentation. In light of these associated findings, MPS may represent one of the milder variants of the autonon~ically mediated reflex neurovascular syndromes.
Diffuse
275
SEMINARS I N NEUROLOGY
PATHOPHYSIOLOGY
later, may then prohibit closing of the sensory neural circuit. The passive, locally mediated, prolonged contraction of specific muscle filaments in the absence of neuromuscular junction stimulation further consumes ATP and calcium substrates and increases local anaerobic by-products. Actin and myosin filaments initially contracted at the onset of trauma are unable to lengthen to original dimensions once ATP is depleted in this environment of relative ischemia. Ultimate dissolution of the muscle filament into granular ground substance results in localized fibrosis.
Our understanding of the histopathologic basis of trigger points remains incomplete because of lack of muscle biopsy reproducibility in a number of studies and the probability that biopsies of tender points versus trigger points have been conDIFFERENTIAL DIAGNOSIS AND PERPETUATING FACTORS fused in the l i t e r a t ~ r e . 'Indeed, ~ , ~ ~ almost all of the pertinent literature regarding trigger point paSince myofascial pain can mimic a myriad of thology appears to focus primarily on fibrositic or fibromyalgic tender points and not on specific conditions, consideration of the differential diagmyofascial trigger points. Clinical observation of nosis for a given symptom presentation is required trigger point stigmata indicates that the average prior to initiation of any diagnostic workup or single trigger point is less than '/s inch in diame- treatment plan (Table 2). Musculoskeletal and neuter.17 On electromyographic examination, bursts of rologic conditions, visceral diseases, infections, insertional activity have been observed only during neoplasms, and psychogenic conditions must be initial penetration of the trigger point or during considered as possible primary or secondary perdisorders in the presence of trigger manual elicitation of the local twitch r e s p ~ n s e . ' ~petuating ~~~ A current hypothesis based on previous neuro- points. Patient history, physical examination, and physiologic studies and electromyographic docu- clinical suspicion will usually suffice to clarify the mentation of trigger point hyperirritability is that situation. Evaluation and treatment of myofascial myofascial pain is mediated in part through group pain perpetuating factors is crucial if one is to I11 o r group IV free nerve endings or both.20 achieve optimal resolution of trigger point pheTrigger-point-associated pain can be reproduced following bupivacaine neutralization by injecting naloxone, a finding that supports a role for endogTable 2. Differential Diagnosis and Underlying enous opiates in the modulation of myofascial Conditions in Myofascial Pain Syndrome pain, whereas the pain associated with fibromyalI. Musculoskeletal gia is believed to be mediated by substance P (Table
276
Pathophysiologic explanations for the development of trigger points and myofascial pain remain hypothetical. The most popular explanations incorporate principles suggested by MelzackZ2and an initiating Simons and Tra~ell.~Vresumably, event such as direct trauma or cumulative noxious input such as prolonged tension patterns results in disruption of the sarcoplasmic reticulum that stimulates a local contractile cycle mediated by calcium and adenosine triphosphate (ATP). This cycle may exceed local circulatory aerobic support and lead to relative ischemia with increased production of anaerobic by-products and interstitial serotonin, histamine, kinins, and prostaglandins. Noxious stimulation of group I11 and group IV free nerve endings ensues, resulting in a centrally mediated referred pain syndrome via lamina I or lamina V dorsal horn cells. Perpetuating factors, discussed
II.
Ill. IV.
V. VI.
A. Myopathies: polymyositis, dermatomyositis B. Arthritis: osteoarthritic, rheumatoid, gouty, psoriatic C. Tendinitis/bursitis/tenosynovitis Neurologic A. Central: multiple sclerosis, other intracranial pathologic processes B. Peripheral: neuralgias (trigeminal, glossopharyngeal, sphenopalatine), Meniere's disease, torticollis, thoracic outlet syndrome, radiculopathies, polyneuropathies Visceral: ischemic heart disease, peptic ulcer disease, appendicitis Infections A. Viral: Colorado tick fever, arbovirus encephalitis, Omsk hemorrhagic fever, influenza A, psittacosis, Rocky Mountain spotted fever, prodromal smallpox, pleurodynia, herpes simplex B. Bacterial: infectious myositis, cellulitis, leptospirosis, poststreptococcal arthralgia C. Protozoan: trichinosis, filariasis, malaria Neoplasms Psychogenic A. Somatoform, conversion, symptom magnification, or histrionic disorders B. Secondary gain
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Myofascial pain and fibromyalgia need not be considered mutually exclusive conditions in a given patient and the possibility that these two diagnostic entities may represent distinct manifestations within the same continuum of pathologic processes in soft tissue remains a topic for future debate and research. l 4
VOLUME 11, NUMBER 3 SEPTEMBER 1991
MYOFASCIAL PAIN SY NDROME-GOLDMAN,ROSENBERG
I. Mechanical stressors A. Structural asymmetry: leg length discrepancy, small hemipelvis, relatively short humerus B. Poor posture II. Nutritional deficiencies Ill. Metabolic and endocrine abnormalities A. Hypothyroidism B. Hypoglycemia C. Hyperuricemia IV. Secondary psychosocial factors A. Adjustment disorders with depression or anxiety B. Psychosomatic or somatoform disorders C. Secondary gain issues V. Chronic infections VI. Sleep disorders VII. Neurologic disorders A. Radiculopathy B. Entrapment neuropathies C. Peripheral polyneuropathy D. Plexopathy E. Multiple sclerosis VIII. Rheumatologic disorders A. Osteoarthritis 6 . Rheumatoid arthritis C. Systemic lupus erythematosus
nomena. Myofascial perpetuating factors are comprised of a number of relative structural, metabolic, nutritional, psychologic, and infectious conditions that facilitate either reinjury of the affected muscle group or propagation of the neuromuscular feedback loop theorized to result in chronic trigger point manifestation (Table 3). Should a patient's myofascial pain condition prove to be refractory or recurrent after a reasonable trial of specific treatment (generally within 4 to 8 weeks of implementation), exploration of possible concomitant or perpetuating conditions is indicated in order to optimize treatment and clarify prognosis. Although nutritional factors have been cited as important in the development of MPS, the evidence that hypovitaminosis is a significant perpetuating factor in MPS remains anecdotal. Travell and Simons emphasize particular attention to vitamins B,, B,, Bly, folic acid, and C in the treatment of refractory MPS. Evidence for the importance of the other entities listed in Table 3 as perpetuating factors in the development of MPS is also anecdotal. Nevertheless, empirical clinical experience has repeatedly supported the contentions of Travell and Simons in this regard. Recognition of the similarities between many common neurologic pain syndromes and MPS is essential in establishing an accurate diagnosis and treatment plan. These disorders include mixed tension-vascular headaches, thoracic outlet syndrome (TOS), temporomandibular joint (TMJ) dysfunction, and the piriformis syndrome.
Mixed tension-vascular headaches have been associated with trigger points in the sternocleidomastoid, suboccipital, temporalis, posterior cervical, and scalene m u ~ c l e s . ~ - ~ ~ explanation A ~likely for unexpected failures in TOS surgery is the myofascia1 origin of most of the symptoms associated with this syndrome. Trigger points in the scalene and pectoralis minor muscles have been described in association with classic TOS symptoms.29Similarly, the controversy surrounding the diagnosis of TMJ dysfunction is partially precipitated by an early emphasis on questionably correlative internal joint abnormalities resulting in suboptimal surgical outcomes. Clinical experience supports the findings of Fricton et a130that most TMJ conditions are primarily myofascial in origin, with particular trigger point involvement of the temporalis, masseter, posterior cervical, sternocleidomastoid, and medial pterygoid muscles. Lastly, trigger points within the piriformis muscle, resulting in a piriformis syndrome with sciatica, are often overlooked in favor of a more dubious diagnosis of radiculopathy due to a bulging lumbar disc.31
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Table 3. Common Perpetuating Factors in Myofascial Pain Syndromes
TREATMENT OF MYOFASCIAL PAIN SYNDROME Once a trigger point has been identified that stimulates a portion of a patient's pain complaints, and pertinent underlying or perpetuating conditions have been addressed, the clinician may proceed with specific myofascial interventions, including spray and stretch counterstimulation, myofascial massage techniques, and trigger point injections when necessary. Completion of trigger point therapies should be followed by a stretching and restrengthening program in order to restore optimal function to the injured muscle and minimize the risk for reinjury. SPRAY AND STRETCH
Spray and stretch technique in the treatment of muscular pain was first popularized by Hans Kraus in the 1 9 4 0 ~ .T~ h*e stretching component is the most critical aspect of the treatment, with the prior use of a vapocoolant spray seen as a means to facilitate relaxation of the muscle involved. Fluoromethane spray has been found to be most effective in the neutralization of trigger points. Ethyl chloride may result in over-cooling of the dermal and myofascial tissues. For optimal results, the direction of the vapocoolant spray should parallel the course of the muscle fibers harboring the trigger point of interest. Knowledge of the various techniques required to isolate and specifically
277
stretch involved muscle groups is also required for spray and stretch technique to be effective. T h e rate of spray application should approximate 10 cmlsecond to optimize reflex relaxation of the underlying muscle tissue. Passive, not active, stretching of the affected muscle fibers is imperative during and following administration of fluoromethane spray in order to neutralize trigger point phenomena. Hot packs should then be applied to potentiate further muscle relaxation and the patient should be instructed in an active stretching program. Spray and stretch therapies often result in immediate short-term relief of myofascia) pain. Failure to effect either short-term o r long-term relief with this modality may be d u e to: (1) static contracture limiting complete stretching of the involved musculature, (2) poor technique, (3) failure to identity and correct underlying perpetuating factors, (4) substantial fibrotic reaction in chronic trigger points, (5) inadequate patient relaxation o r carryover of active stretching home program, and (6) misdiagnosis (for example, tender point instead of' true trigger point).
ISCHEMIC COMPRESSION MASSAGE
Through her work with Hans Kraus and Janet Travell, Bonnie Prudden popularized the concept of "myotherapy" o r ischemic compression massage as a primary o r adjunctive treatment of myofascial trigger points."" T h e proposed mechanism for this technique's efficacy involves applying a localized force suft'icient to produce a transient, focal ischemia in the tissues surrounding the trigger point (generally 20 to 30 pounds of pressure). Release of' this pressure results in a reactive hyperemia that presumably allows enough oxygen and electrolytes to permeate the trigger point and permit transformation of adenosine diphosphate to ATP, with relaxation of the trigger point in the presence of passive stretching. Ischemic compression is a valuable adjunct to spray - . and stretch, as well as trigger point injection interventions, but many times proves inadequate as the sole means of treatment. Reasons for suboptimal response to this modality are similar to those often associated with spray and stretch failure.
TRZGGER POINT INJECTIONS
278
Trigger point injections may serve as an extremely valuable treatment option in the presence of chronic MPS if carried out judiciously and with careful technique. It is interesting that the mechanism of action is primarily mechanical and inde-
VO1,UME I I , N U M B E K 3
SEPTLMMER 1091
pendent of the d r u g o r drugs used in the injection. T h e mechanism by which trigger point injection presumably works is disruption of the fibrous banding associated with chronic trigger points. T h e key to success with trigger point injections lies in exactly locating arid penetrating relatively small trigger points within a larger muscle mass. Use of i~~jection media may allow for a margin of error with respect to specific puncture of a given trigger point because of hydrostatic separation of' neighboring fibrous bands, when they are present, as well as local relaxation of the muscle by an anesthetic effect. Since it is the mechanical rather than the pharmacologic effect of the injection that causes trigger point neutralization, choice of injectable agents that are least noxious to the muscle membrane, such as 0.5%) procaine. is recommended. Successf'ul trigger point injection technique involves more skill and time on the part of the clinician than a typical intranluscular injection. Triggerpoint injection should not be considered during the acute phase of injury. Delaying trigger point injection by 2 to 4 weeks allows for stabilization of edema and generalized soft tissue disruption. This also allows the clinician time to resolve the patient's rriyofascial pain through less invasive means and assess potential benefit from the procedure. In o u r experience, approximately 75 to 80% of patients presenting with acute o r subacute myofascial pain can be optimally treated without the need for trigger point injection. Contraindications to trigger point injection include known allergy to the injectable agent, uncontrolled bleeding diathesis, and localized infection in the region of the trigger point. Prior to trigger point injection, the patient should be placed in a position that facilitates relaxation of the muscle groups under consideration. Following aseptic preparation of the area, the trigger point must be precisely located. Elicitation o f a strong local twitch response during which the patient reports exact reproduction of his o r her pain symptoms indicates a technically successful irijection. However, neutralization of the trigger point may occur even in the absence of an obvious local twitch response if' the involved muscle fibers are sufficiently separated by the injection ~ n e d i u mand the patient is able t o relax the involved musculature. Spray and stretch, ischemic compression, and warm hydrocollator packs should be applied immediately following the injection in order to niaximize results and minimize postinjection soreness. In particular, riot applying sufficient henios~atic pressure directly following trigger point in,jection to counteract the myoirritant effect of small amounts of bleeding following capillary puncture is a common reason fbr increased postinjection sore-
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SEMINARS IN NEUROLOGY
MYOFASCIAL PAIN SYNDROME-GOI~MAN,ROSENBERG
ADJUNCTIVE PHYSICAL THERAPY
T h e initial treatrnent period for optimal stabilization, if not resolution, of niyofascial pain symptoms is generally 4 to 8 weeks, depending on the complexity of' the pr-esentation. O n occasion, more than 8 weeks is required. This phase oftreatment should be followed by a reconditioning program aimed at restoring strength to the affected n~usculatureas well as maintaining muscle length. and flexibility. As already noted, passive and active stretching exercises specific for the muscle groups involved should be prescribed at the onset of myofascia1 therapies. Early addition of an aerobic conditioning program, utilizing nluscle groups not directly impacted by the myofascial condition, is useful in preventing cardiovascular deconditioning and reinforcing an active role for the patient in rehabilitation. As the patient responds to the more specific myofascial interventions already discussed, gradual addition of first aerobic and then, later, progressive resistive exercises specific f'or the affected muscle groups to the patient's stretching and gener-alized aerobic conditioning program is essential in order to optimize patient function and minimize the risk of recurrence.
TREATMENT OF FIBROMYALGIA Although the treatrnent of MPS often results in a good outcome, such is not the case with fibromyalgia. Numerous treatment modalities, includ. ing those discussed earlier, have been used in the treatment of' fibromyalgia. Physical (aerobic conditioning, acupuncture, transcutaneous nerve stimulation), psychologic (biofeedback, psychotherapy, cognitive-behavioral therapy), medication (antidepressants, nonsteroidal anti-inflammatory
agents), and homeopathic therapies have been used, often with encouraging initial results, but with generally disappointing long-term, clinically meaningful improvement in the majority of patients .~ s - ' iTi h e tricyclics amitriptyline and cyclobenzaprine have been the most extensively studied, and in controlled studies have proven to be more effective than either placebo o r nonsteroidal antiinflam~natoryagents. With prognosis being so different for MPS and fibromyalgia, it is essential to make the correct diagnosis before institution of therapy.
REFERENCES 1. .li.avcll ,I
1 I , NO. 3
Sk,'PTEMBI:'K 1991
Myofascial Pain Syndrome and Fibromyalgia
Chronic ~nyofascialpain is a well-established but not widely known cause of chronic pain and disability. Many patients with myof'ascial pain syndrome (MPS) have seen numerous other physicians, physical therapists, and chiropractors, with none providing lasting relief from their pain. This nonsurgical musculoskeletal pain disorder remains one of the least understood, yet most frequently encountered, problems seen in the outpatient setting. MPS is a common soft tissue disorder that often presents with additional symptoms suggestive of other neurologic disorders. Complaints of localized o r diffuse muscle pain and tenderness, headache, vertigo, visual disturbance, paresthesias, discoordination, and referred pain all demand not only careful neurologic evaluation but also a detailed musculoskeletal examination.' Unfbrtunately, confusion with respect to taxonomy and definition has impeded both research and clinical application in the study of soft tissue pain disorders. Discussions of muscle pain due to palpable, tender bands within symptomatic muscle groups first appeared in the European medical literature during the early 19th century. In 1852, Virchow coined the term "muscular rheumatism" in postulating such palpable changes in muscle, although histologically unsubstantiated, as a complication of' rheumatic fever.' Gowers" first discussed the possibility that a number of' musculoskeletal contlitions, including lumbago, involved muscle inflarnmation, which he termed "fibrositis." Stockman' almost sinlultaneously described connective tissue hyperplasia, which by 19 15 was considered the pri-
mary histopathologic process underlying the fihrositic presentation.' Since such histologic studies were never reproduced on a consistent basis, the term and contlitior~known as "fibrositis" has subsequently assumed a highly controversial place within the 20th century medical lexicon. Kellgren," in 1938, first reported symptoms of referred pain during palpation of tender points in skeletal muscle. His descriptions quite likely constitute the first published observation of'the trigger point phenomenon now considered an essential criterion for the diagnosis of myofascial pain. Janet Travell subsequently clarified the concept of the trigger point and popularized the term "myof'as-
DEFINITIONS Myofascia1 pain syndrome: M PS is now understood to refer to a spectrum of clinical presentations distinct from other n~usculoskeletal conditions such as fibromyalgia (formerly termed "f'ibrositis"), strains, o r sprains. Indeed, much of the confusion and misunderstanding surrounding this entity sterns from the myriad of names used by investigators and clinicians in discussing soft tissue p a i n Muscular rheumatism, myalgia, myogelosis, interstitial myofibrositis, fibrornyositis, and rnyofasciitis have all, in the past, referred to clinical conditions that may have shared some attributes with the more specifically defined MPS. Trigypr points: T h e presence o r absence of trigger points determines whether a clinical presentation qualifies as a MPS. Muscle trigger points are
Center fir Spine Rehabilitation, Spalding Rehabilitation Hospital, and the Colorado Neurological Institute, Englewood, a n d the Department of Rehabilitation Medicine, University of Colorado Health Sciences Center, Denver, Colorado; and Center for Occupational Neurology a n d Neurotoxicology, Neur-o~riuscularDisease PI-ogl-am,Colorado Neur-ological Institute, t:nglcwootl, a ~ the ~ dL)cpartnier~tof'lLledicir~e(Clinical Pharmacology), Ulliver-sit! of Colorado Health Sciences (;enrcl-, 1)enver-, Colorado Reprint requests: Dr. Goldrr~an,Center for Spine Rehabilitation. 125 E. 1la111ptlenAvenue, Englewood, CO 801 10 Copyright O 1991 by .fhieme Medical I'ublisher-s, I I I ~ .381 , Park Avcllue South. New York, N Y 10016. All rights reserved.
Downloaded by: University of British Columbia. Copyrighted material.
L. Burton Goldmun, M.D., and Nril L. Rosenberg, M.D.
?
7
diagnostic criteria, but also to treatment approach and prognosis. MPS tends to be more acute in onset, more regional in presentation, more amenable to treatment, and characterized by an objective trigger point phenomenon. Fibromyalgia syndrome tends to be more insidious in onset, more global in presentation, more guarded in prognosis, arid characterized by subjective tender points (Table 1). Recently, the criteria required fbr the diagnosis of fibrornyalgia have been defined. T h e American College of Rheumatology in 1990 set criteria for the classification of fibromyalgia that include at least 3 months of widespread pain in the presence of' 11 of 18 specific tender points on palpation.'" However, the locations of many of these classic tender points overlap classic trigger point sites. Moreover, distinguishing between latent trigger points and tender points is often difficult. Patient history and symptom pattern needs to be considered more carefully in such circumstances. Lastly, active trigger points can "metastasize" via activation of satellite o r secondary trigger points, resulting in the gradual transformation from an initial, regional myofascial presentation to a subsequent global fibromyalgic picture. Satellite trigger points become activated because they reside within the pain reference zone of another previously activated trigger point, whereas secondary trigger points occur in synergistic muscle groups outside of the initial trigger point's zone of' reference. 'The mechanism for creation o r activation of secondary trigger points involves an overuse phenomenon to compensate for antecedent guarding and disuse of the muscle groups originally associated with the patient's initial myofascial presentation.
Table 1. Comparison of Myofascial Pain and Fibromyalgia Myofascial Pain
Fibromyalgia
Sex
Male and female
Predominantly female
Age Pain
All Focal
40-60 years primarily
Mediation
Endorphin
Substance P
Duration
Acute or chronic
Chronic
Twitch response
Present
Absent
Pain areas
Distinct reference zones
Nonradiating
Etiology
Generally mechanical
Internal, environmental
Prognosis
Good with elimination of perpetuating factors
Guarded
DIFFERENTIAL DIAGNOSIS T h e distinctio~ibetween active trigger points and less specific tender points is an important one. More cornrnonly associated with fibroniyalgia syndronle, tender points may be associated with taut banding or nodularity within the muscle, but will not manifest a local twitch response or characteristic pain reference zone on palpation. Subjective in presentation, tender points may be associated with more subtle and global evidence of autonon~ic dysfunction in the context of a fibromyalgia syndrome, without the focality o f a MPS." Likewise, the distinction between MPS and fit~romyalgiais important with respect not only to
Downloaded by: University of British Columbia. Copyrighted material.
the central elements of' MPS. 'Ii-igger points may be found in a number of anatomic sites, including muscle, skin, joints, and ligaments. They are painful regions and taut bands of muscle that refer pain to distant areas. Skeletal muscle trigger points, which have generally been emphasized in clinical practice because of their accessibility and their research considerations, are characterized by taut bands within the muscle which will manifest a local twitch response on direct palpation. 1,ocal twitch responses represent transient involuntary shortening of the fibrous muscular bands harboring trigger points that may be observed by the trained eye in the more superficial muscle groups. In order to establish a diagnosis of myofascial pain, the clinician must be able to distinguish between the involuntary local twitch response and voluntary contraction of the entire muscle group produced by the patient's guarding. 1rigger points are generally classified as either active or latent. Active trigger points cause ongoing pain arid restricted motion of the muscle in which they abide. Latent trigger points are quiescent and result primary in muscle tightness, shortening, and dysfunction without the presence of persistent pain."' In addition to the local twitch response, active trigger points are also characterized by specific patterns of pain radiation during palpation that depend on the location of the trigger point. These pain reference zones may o r may not mimic more traditionally recognized derrnatomal, myotornal, or- scleratornal referred pain patterns." Focal or regional autonomic dysfunction, including localized vasoconstriction, persistent hyperernia after palpation, diaphoresis, lacrimation, coryza, salivation, and pilomotor activity, is often associated with trigger point presentation. In light of these associated findings, MPS may represent one of the milder variants of the autonon~ically mediated reflex neurovascular syndromes.
Diffuse
275
SEMINARS I N NEUROLOGY
PATHOPHYSIOLOGY
later, may then prohibit closing of the sensory neural circuit. The passive, locally mediated, prolonged contraction of specific muscle filaments in the absence of neuromuscular junction stimulation further consumes ATP and calcium substrates and increases local anaerobic by-products. Actin and myosin filaments initially contracted at the onset of trauma are unable to lengthen to original dimensions once ATP is depleted in this environment of relative ischemia. Ultimate dissolution of the muscle filament into granular ground substance results in localized fibrosis.
Our understanding of the histopathologic basis of trigger points remains incomplete because of lack of muscle biopsy reproducibility in a number of studies and the probability that biopsies of tender points versus trigger points have been conDIFFERENTIAL DIAGNOSIS AND PERPETUATING FACTORS fused in the l i t e r a t ~ r e . 'Indeed, ~ , ~ ~ almost all of the pertinent literature regarding trigger point paSince myofascial pain can mimic a myriad of thology appears to focus primarily on fibrositic or fibromyalgic tender points and not on specific conditions, consideration of the differential diagmyofascial trigger points. Clinical observation of nosis for a given symptom presentation is required trigger point stigmata indicates that the average prior to initiation of any diagnostic workup or single trigger point is less than '/s inch in diame- treatment plan (Table 2). Musculoskeletal and neuter.17 On electromyographic examination, bursts of rologic conditions, visceral diseases, infections, insertional activity have been observed only during neoplasms, and psychogenic conditions must be initial penetration of the trigger point or during considered as possible primary or secondary perdisorders in the presence of trigger manual elicitation of the local twitch r e s p ~ n s e . ' ~petuating ~~~ A current hypothesis based on previous neuro- points. Patient history, physical examination, and physiologic studies and electromyographic docu- clinical suspicion will usually suffice to clarify the mentation of trigger point hyperirritability is that situation. Evaluation and treatment of myofascial myofascial pain is mediated in part through group pain perpetuating factors is crucial if one is to I11 o r group IV free nerve endings or both.20 achieve optimal resolution of trigger point pheTrigger-point-associated pain can be reproduced following bupivacaine neutralization by injecting naloxone, a finding that supports a role for endogTable 2. Differential Diagnosis and Underlying enous opiates in the modulation of myofascial Conditions in Myofascial Pain Syndrome pain, whereas the pain associated with fibromyalI. Musculoskeletal gia is believed to be mediated by substance P (Table
276
Pathophysiologic explanations for the development of trigger points and myofascial pain remain hypothetical. The most popular explanations incorporate principles suggested by MelzackZ2and an initiating Simons and Tra~ell.~Vresumably, event such as direct trauma or cumulative noxious input such as prolonged tension patterns results in disruption of the sarcoplasmic reticulum that stimulates a local contractile cycle mediated by calcium and adenosine triphosphate (ATP). This cycle may exceed local circulatory aerobic support and lead to relative ischemia with increased production of anaerobic by-products and interstitial serotonin, histamine, kinins, and prostaglandins. Noxious stimulation of group I11 and group IV free nerve endings ensues, resulting in a centrally mediated referred pain syndrome via lamina I or lamina V dorsal horn cells. Perpetuating factors, discussed
II.
Ill. IV.
V. VI.
A. Myopathies: polymyositis, dermatomyositis B. Arthritis: osteoarthritic, rheumatoid, gouty, psoriatic C. Tendinitis/bursitis/tenosynovitis Neurologic A. Central: multiple sclerosis, other intracranial pathologic processes B. Peripheral: neuralgias (trigeminal, glossopharyngeal, sphenopalatine), Meniere's disease, torticollis, thoracic outlet syndrome, radiculopathies, polyneuropathies Visceral: ischemic heart disease, peptic ulcer disease, appendicitis Infections A. Viral: Colorado tick fever, arbovirus encephalitis, Omsk hemorrhagic fever, influenza A, psittacosis, Rocky Mountain spotted fever, prodromal smallpox, pleurodynia, herpes simplex B. Bacterial: infectious myositis, cellulitis, leptospirosis, poststreptococcal arthralgia C. Protozoan: trichinosis, filariasis, malaria Neoplasms Psychogenic A. Somatoform, conversion, symptom magnification, or histrionic disorders B. Secondary gain
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Myofascial pain and fibromyalgia need not be considered mutually exclusive conditions in a given patient and the possibility that these two diagnostic entities may represent distinct manifestations within the same continuum of pathologic processes in soft tissue remains a topic for future debate and research. l 4
VOLUME 11, NUMBER 3 SEPTEMBER 1991
MYOFASCIAL PAIN SY NDROME-GOLDMAN,ROSENBERG
I. Mechanical stressors A. Structural asymmetry: leg length discrepancy, small hemipelvis, relatively short humerus B. Poor posture II. Nutritional deficiencies Ill. Metabolic and endocrine abnormalities A. Hypothyroidism B. Hypoglycemia C. Hyperuricemia IV. Secondary psychosocial factors A. Adjustment disorders with depression or anxiety B. Psychosomatic or somatoform disorders C. Secondary gain issues V. Chronic infections VI. Sleep disorders VII. Neurologic disorders A. Radiculopathy B. Entrapment neuropathies C. Peripheral polyneuropathy D. Plexopathy E. Multiple sclerosis VIII. Rheumatologic disorders A. Osteoarthritis 6 . Rheumatoid arthritis C. Systemic lupus erythematosus
nomena. Myofascial perpetuating factors are comprised of a number of relative structural, metabolic, nutritional, psychologic, and infectious conditions that facilitate either reinjury of the affected muscle group or propagation of the neuromuscular feedback loop theorized to result in chronic trigger point manifestation (Table 3). Should a patient's myofascial pain condition prove to be refractory or recurrent after a reasonable trial of specific treatment (generally within 4 to 8 weeks of implementation), exploration of possible concomitant or perpetuating conditions is indicated in order to optimize treatment and clarify prognosis. Although nutritional factors have been cited as important in the development of MPS, the evidence that hypovitaminosis is a significant perpetuating factor in MPS remains anecdotal. Travell and Simons emphasize particular attention to vitamins B,, B,, Bly, folic acid, and C in the treatment of refractory MPS. Evidence for the importance of the other entities listed in Table 3 as perpetuating factors in the development of MPS is also anecdotal. Nevertheless, empirical clinical experience has repeatedly supported the contentions of Travell and Simons in this regard. Recognition of the similarities between many common neurologic pain syndromes and MPS is essential in establishing an accurate diagnosis and treatment plan. These disorders include mixed tension-vascular headaches, thoracic outlet syndrome (TOS), temporomandibular joint (TMJ) dysfunction, and the piriformis syndrome.
Mixed tension-vascular headaches have been associated with trigger points in the sternocleidomastoid, suboccipital, temporalis, posterior cervical, and scalene m u ~ c l e s . ~ - ~ ~ explanation A ~likely for unexpected failures in TOS surgery is the myofascia1 origin of most of the symptoms associated with this syndrome. Trigger points in the scalene and pectoralis minor muscles have been described in association with classic TOS symptoms.29Similarly, the controversy surrounding the diagnosis of TMJ dysfunction is partially precipitated by an early emphasis on questionably correlative internal joint abnormalities resulting in suboptimal surgical outcomes. Clinical experience supports the findings of Fricton et a130that most TMJ conditions are primarily myofascial in origin, with particular trigger point involvement of the temporalis, masseter, posterior cervical, sternocleidomastoid, and medial pterygoid muscles. Lastly, trigger points within the piriformis muscle, resulting in a piriformis syndrome with sciatica, are often overlooked in favor of a more dubious diagnosis of radiculopathy due to a bulging lumbar disc.31
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Table 3. Common Perpetuating Factors in Myofascial Pain Syndromes
TREATMENT OF MYOFASCIAL PAIN SYNDROME Once a trigger point has been identified that stimulates a portion of a patient's pain complaints, and pertinent underlying or perpetuating conditions have been addressed, the clinician may proceed with specific myofascial interventions, including spray and stretch counterstimulation, myofascial massage techniques, and trigger point injections when necessary. Completion of trigger point therapies should be followed by a stretching and restrengthening program in order to restore optimal function to the injured muscle and minimize the risk for reinjury. SPRAY AND STRETCH
Spray and stretch technique in the treatment of muscular pain was first popularized by Hans Kraus in the 1 9 4 0 ~ .T~ h*e stretching component is the most critical aspect of the treatment, with the prior use of a vapocoolant spray seen as a means to facilitate relaxation of the muscle involved. Fluoromethane spray has been found to be most effective in the neutralization of trigger points. Ethyl chloride may result in over-cooling of the dermal and myofascial tissues. For optimal results, the direction of the vapocoolant spray should parallel the course of the muscle fibers harboring the trigger point of interest. Knowledge of the various techniques required to isolate and specifically
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stretch involved muscle groups is also required for spray and stretch technique to be effective. T h e rate of spray application should approximate 10 cmlsecond to optimize reflex relaxation of the underlying muscle tissue. Passive, not active, stretching of the affected muscle fibers is imperative during and following administration of fluoromethane spray in order to neutralize trigger point phenomena. Hot packs should then be applied to potentiate further muscle relaxation and the patient should be instructed in an active stretching program. Spray and stretch therapies often result in immediate short-term relief of myofascia) pain. Failure to effect either short-term o r long-term relief with this modality may be d u e to: (1) static contracture limiting complete stretching of the involved musculature, (2) poor technique, (3) failure to identity and correct underlying perpetuating factors, (4) substantial fibrotic reaction in chronic trigger points, (5) inadequate patient relaxation o r carryover of active stretching home program, and (6) misdiagnosis (for example, tender point instead of' true trigger point).
ISCHEMIC COMPRESSION MASSAGE
Through her work with Hans Kraus and Janet Travell, Bonnie Prudden popularized the concept of "myotherapy" o r ischemic compression massage as a primary o r adjunctive treatment of myofascial trigger points."" T h e proposed mechanism for this technique's efficacy involves applying a localized force suft'icient to produce a transient, focal ischemia in the tissues surrounding the trigger point (generally 20 to 30 pounds of pressure). Release of' this pressure results in a reactive hyperemia that presumably allows enough oxygen and electrolytes to permeate the trigger point and permit transformation of adenosine diphosphate to ATP, with relaxation of the trigger point in the presence of passive stretching. Ischemic compression is a valuable adjunct to spray - . and stretch, as well as trigger point injection interventions, but many times proves inadequate as the sole means of treatment. Reasons for suboptimal response to this modality are similar to those often associated with spray and stretch failure.
TRZGGER POINT INJECTIONS
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Trigger point injections may serve as an extremely valuable treatment option in the presence of chronic MPS if carried out judiciously and with careful technique. It is interesting that the mechanism of action is primarily mechanical and inde-
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pendent of the d r u g o r drugs used in the injection. T h e mechanism by which trigger point injection presumably works is disruption of the fibrous banding associated with chronic trigger points. T h e key to success with trigger point injections lies in exactly locating arid penetrating relatively small trigger points within a larger muscle mass. Use of i~~jection media may allow for a margin of error with respect to specific puncture of a given trigger point because of hydrostatic separation of' neighboring fibrous bands, when they are present, as well as local relaxation of the muscle by an anesthetic effect. Since it is the mechanical rather than the pharmacologic effect of the injection that causes trigger point neutralization, choice of injectable agents that are least noxious to the muscle membrane, such as 0.5%) procaine. is recommended. Successf'ul trigger point injection technique involves more skill and time on the part of the clinician than a typical intranluscular injection. Triggerpoint injection should not be considered during the acute phase of injury. Delaying trigger point injection by 2 to 4 weeks allows for stabilization of edema and generalized soft tissue disruption. This also allows the clinician time to resolve the patient's rriyofascial pain through less invasive means and assess potential benefit from the procedure. In o u r experience, approximately 75 to 80% of patients presenting with acute o r subacute myofascial pain can be optimally treated without the need for trigger point injection. Contraindications to trigger point injection include known allergy to the injectable agent, uncontrolled bleeding diathesis, and localized infection in the region of the trigger point. Prior to trigger point injection, the patient should be placed in a position that facilitates relaxation of the muscle groups under consideration. Following aseptic preparation of the area, the trigger point must be precisely located. Elicitation o f a strong local twitch response during which the patient reports exact reproduction of his o r her pain symptoms indicates a technically successful irijection. However, neutralization of the trigger point may occur even in the absence of an obvious local twitch response if' the involved muscle fibers are sufficiently separated by the injection ~ n e d i u mand the patient is able t o relax the involved musculature. Spray and stretch, ischemic compression, and warm hydrocollator packs should be applied immediately following the injection in order to niaximize results and minimize postinjection soreness. In particular, riot applying sufficient henios~atic pressure directly following trigger point in,jection to counteract the myoirritant effect of small amounts of bleeding following capillary puncture is a common reason fbr increased postinjection sore-
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SEMINARS IN NEUROLOGY
MYOFASCIAL PAIN SYNDROME-GOI~MAN,ROSENBERG
ADJUNCTIVE PHYSICAL THERAPY
T h e initial treatrnent period for optimal stabilization, if not resolution, of niyofascial pain symptoms is generally 4 to 8 weeks, depending on the complexity of' the pr-esentation. O n occasion, more than 8 weeks is required. This phase oftreatment should be followed by a reconditioning program aimed at restoring strength to the affected n~usculatureas well as maintaining muscle length. and flexibility. As already noted, passive and active stretching exercises specific for the muscle groups involved should be prescribed at the onset of myofascia1 therapies. Early addition of an aerobic conditioning program, utilizing nluscle groups not directly impacted by the myofascial condition, is useful in preventing cardiovascular deconditioning and reinforcing an active role for the patient in rehabilitation. As the patient responds to the more specific myofascial interventions already discussed, gradual addition of first aerobic and then, later, progressive resistive exercises specific f'or the affected muscle groups to the patient's stretching and gener-alized aerobic conditioning program is essential in order to optimize patient function and minimize the risk of recurrence.
TREATMENT OF FIBROMYALGIA Although the treatrnent of MPS often results in a good outcome, such is not the case with fibromyalgia. Numerous treatment modalities, includ. ing those discussed earlier, have been used in the treatment of' fibromyalgia. Physical (aerobic conditioning, acupuncture, transcutaneous nerve stimulation), psychologic (biofeedback, psychotherapy, cognitive-behavioral therapy), medication (antidepressants, nonsteroidal anti-inflammatory
agents), and homeopathic therapies have been used, often with encouraging initial results, but with generally disappointing long-term, clinically meaningful improvement in the majority of patients .~ s - ' iTi h e tricyclics amitriptyline and cyclobenzaprine have been the most extensively studied, and in controlled studies have proven to be more effective than either placebo o r nonsteroidal antiinflam~natoryagents. With prognosis being so different for MPS and fibromyalgia, it is essential to make the correct diagnosis before institution of therapy.
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