Chronic widespread pain presents challenges to patients, clinicians, and researchers in both diagnosing and treating its complex manifestations. As with many pain disorders, clinicians identified a grouping of symptoms, and the scientific community has attempted to develop sensitive and specific diagnostic criteria. This process has evolved recently to reflect an improved understanding of the disease process and the challenge of accurately diagnosing fibromyalgia (FM) in the clinical setting. Moreover, the complex pathophysiology obscures both the etiology and treatment options for this centrally mediated disease. Myofascial pain syndrome (MPS) is frequently found under the same umbrella as FM. They have separately struggled for recognition in the medical arena despite being fairly common in every contemporary society and exacting a moderately severe toll on the patients who suffer from them.
Explanations for this situation are varied but may relate to obscure belief systems on the part of physicians regarding the nature of the conditions themselves. Similarly, FM and MPS are painful and impair the ability of the affected person to function normally. Both are assessed subjectively, with some semi-objective clinical signs. Both can be associated with patient behavior that makes clinicians worry that something is being missed. Neither has a specific laboratory test that unequivocally defines the condition, like many of the disease states along the spectrum of central sensitization. Both seek simple instruments that are robust to change, with clinical improvement. Until relatively recently, neither had medications approved by the U.S. Food and Drug Administration (FDA) specifically indicated for treatment of its symptoms. Both FM and MPS cause mild to moderate dysfunction in the majority of patients, but with new understanding of the pathophysiology and improved diagnostic criteria, there have been changes in the field in the last several years.
Nevertheless, these conditions are easily distinguished from each other on the basis of medical history, physical examination, and even some laboratory findings. Therefore, it is even possible to identify patients who have both conditions at the same time. This chapter attempts to summarize the current status of these disorders with respect to their clinical features, epidemiology, pathogenesis, and management.
Myofascial Pain Syndrome
Diagnostic Criteria
The combined work of Kellgren, Travell, and Simons has influenced the development of proposed criteria for the diagnosis of MPS ( Box 29.1 ). It is described as a painful regional syndrome characterized by the presence of an active trigger point (TrP) in a skeletal muscle. The implications of an active TrP are that the examiner should expect to find spot tenderness with deep palpation over the TrP. Stimulation of these TrPs should result in concordant pain. Moreover, there should be concomitant referral of pain to a zone of reference within the affected muscle. A latent TrP has been defined as one for which there is no passive experience of spontaneous pain but pain is still inducible by manipulating the TrP. Manipulation of the TrP is generally achieved by digital pressure, a flick across the muscle, or penetration by a needle. This stimulation typically induces a “twitch” response, which can be felt as a palpable taut band that restricts normal excursion of the affected muscle.
The strongest examination findings are
- •
A tender spot (trigger point) in an affected muscle
- •
Referral of pain to a zone of reference
- •
Reproducibility of the patient’s usual pain
- •
Poorer reliability was associated with
- •
Eliciting local tenderness
- •
Palpating a taut band
- •
Documenting the local twitch response
- •
The problem for investigators trying to validate diagnostic criteria for MPS has been that experienced clinicians have not been able to demonstrate a high level of agreement when applying the Simons and Travell criteria to serially blinded patients versus disease controls or healthy controls. Moreover, even experienced clinicians need to standardize their examination techniques and approach for proper interpretation of the findings. When this was done immediately before performing blinded examinations, the results were much more reproducible. The most reproducible clinical features from among the Simons and Travell criteria were finding a tender spot (the TrP) in the proximal or distal third of an affected skeletal muscle, referral of pain to a zone of reference, and reproduction of the patient’s usual pain. Much poorer reliability was associated with eliciting local tenderness, palpating a taut band, and documenting the local twitch response.
A telling series of two tables has been provided by Simons and colleagues. The first table summarizes the inter-rater reliability (κ values) from four clinical studies for various critical examination procedures used in diagnosing MPS. The second compares the relative difficulty of performing or interpreting these test procedures versus the relative importance of these tests in diagnosing MPS confidently. The tests considered more important in making the diagnosis are also the ones most difficult to perform or interpret.
Part of the problem may have been that there are so many muscles in the body that have the potential to be affected by MPS; examination techniques need to be adapted for each muscle. Clinicians who are skilled in diagnosing MPS must have an adequate knowledge of neuromuscular anatomy and function, plus a high level of manual dexterity and trained sensory discrimination in their hands. In addition, these skills must account for the common distortions in ideal anatomy by patients’ neglect of their physical conditioning and the development of overlying layers of adipose tissue. If every MPS patient had the “ideal body” with well-defined musculature, the anatomic challenge might be less onerous. Some muscles are particularly difficult to evaluate because they are under other muscles (e.g., piriformis deep to the gluteal muscles of the buttocks). The muscles in the lower extremities seem to be more problematic in this regard than those in the trunk and upper extremities.
A study design patterned after that used to develop the 1990 American College of Rheumatology (ACR) research classification criteria for FM has been proposed to validate diagnostic criteria for MPS involving muscles of the upper part of the torso. Application of this protocol by teams of experts (a Delphi and a blinded examiner) at two centers in different countries confirmed the historically observed outcome that there was poor agreement (κ = 0.21 to 0.35) on the diagnosis between pairs of examiners based on the standard examination approaches. Primarily, this discrepancy resulted from examination of the healthy controls by the blinded examiner when a very high proportion exhibited a taut band, an area of tenderness, a local twitch response, a jump sign, and even referral of pain. Moreover, the most specific discriminators of patients with MPS from healthy controls were painfully restricted range of motion, muscle strength limited by pain, the skin rolling test, and the pressure pain threshold according to algometry. A second component of the study involved the use of validated questionnaire instruments that examined subjective pain, dysfunctional sleep, physical function, anxiety, and depression. Significantly, the questionnaire instruments were more consistently effective in distinguishing individuals with MPS from healthy controls than were the examination measures. Of particular interest were the findings of sleep dysfunction, anxiety, and depression in MPS patients, all of which challenge the long-standing notion that myofascial pain is primarily a “peripheral” pain disorder. Further analysis of these data will probably result in recommendation of a combined diagnostic profile for MPS that involves elements from the medical history, validated questionnaire instruments, and musculoskeletal examination.
Although there are certainly critics of the Simons and Travell clinical criteria for the diagnosis of MPS, it is generally agreed by physicians treating patients with musculoskeletal pain that such a condition does exist. A national survey of 1663 American Pain Society members resulted in 403 completed surveys being returned. The participants responded to questions about the legitimacy of MPS as a unique condition, whether they considered it to be distinct from FM, and which signs or symptoms were important for its diagnosis. Of the respondents, 88% indicated that MPS is a legitimate diagnosis and 81% believed that it is distinct from FM. When examined by specialty, the perception of legitimacy ranged from 50% to 100%, with osteopaths and orthopedic surgeons (poorly sampled at only 0.5% and 1.2% of the respondents, respectively) reporting the lowest legitimacy (50% to 60%) and anesthesiologists and physiatrists, who accounted for 67% of the respondents, indicating higher than 90% legitimacy for MPS. The latter groups were generally (83%) convinced that MPS is distinct from FM. When asked about which findings were essential in making the diagnosis of MPS, the respondents showed strong support for regional pain, the presence of TrPs, normal findings on neurologic examination, and pain that decreases with local injection. The respondents considered irrelevant or placed much less importance on finding palpable nodules, a local twitch response, and decreased range of muscle motion.
As advocates of the MPS construct strive for uniformity in their approach to diagnosis, there is also value in striving for uniform and logical terminology. If the essence of the condition is conceptualized, it is the TrP. Many authors have referred to this construct as a “myofascial TrP,” as though there were some other type of TrP. It has been suggested that the term used be simply “TrP” because the term “myofascial” adds nothing of significance. This has already become the editorial policy of the Journal of Musculoskeletal Pain .
Prevalence Estimates
The prevalence of MPS in the general population is uncertain. This information is difficult to obtain because there are as yet no validated diagnostic criteria for the condition. Thus, it has not been possible to confidently seek out the disorder on a large scale with screening survey instruments.
In a study designed to document the prevalence of MPS in a general internal medicine practice, Skootsky and coworkers screened 201 patients and more thoroughly evaluated 172 who visited an academic health care center for various reasons; 54 patients whose symptoms included musculoskeletal pain were retained for additional testing. Patients with pain conditions clearly unrelated to MPS were eliminated. The remaining patients underwent a detailed TrP examination guided by body pain diagrams that had been completed by the patients. When a muscle was found to contain a TrP, it was digitally compressed for 5 to 20 seconds to see whether that maneuver would intensify the pain. The diagnosis of MPS was made when the patient exhibited regional pain intensified by digital pressure and the referral pattern corresponded with established referral maps. Sixteen patients (30% of 54, 8% of 201) in this academic general internal medicine practice satisfied criteria for the diagnosis of MPS. As shown in Figure 29.1 B , this would be slightly higher than the reported prevalence of FM (about 6%) in an academic internal medicine practice.
Related Syndromes
MPS taxonomy encompasses target areas of dysfunction as well. Specifically, two areas of the body that deserve special attention are the muscles of mastication and the muscles of the pelvis.
Dentists typically diagnose and manage temporomandibular joint disorder, now considered part of the spectrum of temporomandibular disorders; it is also referred to by some as myofascial pain dysfunction (MPD) syndrome. Fricton’s classic study of MPD identified 164 patients with this condition from among 296 with pain in the head and neck. In the patients with MPD, there was tenderness in at least one muscle of mastication, referral of the pain to an expected zone of reference, and frequent comorbid conditions such as postural or emotive factors. In most cases (66%) the symptoms emerged gradually, but in others there was a history of antecedent dental work or a motor vehicle accident.
The muscles of the pelvis can contribute to pain that can be confused with low back pain or with female organ pathology that can be manifested as urethral pain, vulvodynia, or dyspareunia. Pelvic area muscles with MPS (e.g., piriformis, iliopsoas, obturator internus) can refer pain to pelvic structures and cause dysfunction, or they can compress nerves (sciatic nerve, pudendal nerve), which then results in the symptoms.
Proposed Pathogenesis
Even though many theories on the etiology of MPSs have been proposed, researchers have not yet developed a definitive pathway. Briefly, it has been suggested that predisposing factors, such as body asymmetry and poor posture, can conspire with mechanical stressors, radiculopathy, nutritional inadequacies, endocrine dysfunction, or anger or other psychological factors to initiate the symptoms of MPS.
Exploration of the TrP via needle electromyography in a rabbit model of MPS and in symptomatic humans has led to the finding of spontaneous electrical activity (SEA). In a controlled research study, an electromyographer found this SEA phenomenon significantly more often when probing with an electromyographic needle in the location of a human TrP site than in the location of a control site. When researchers demonstrated that local infusion of phentolamine eliminated this SEA phenomenon and the pain, it was speculated that the TrP had the characteristic adrenergic dependency of the muscle spindle. Others have argued that the TrP is anatomically located at a neuromuscular junction. Thus, the evidence seems to support a spinal reflex that could involve the spindle and neuromuscular junction within the muscle, the spinal cord, and the radicular nerves that connect the muscle to the cord.
The most dramatic demonstration of objective abnormalities in MPS has come from microanalysis of interstitial fluid samples obtained from human skeletal muscle TrPs. The concentrations of proteins, bradykinin, calcitonin gene–related peptide, substance P (SP), tumor necrosis factor-α, interleukin-1β (IL-1β), serotonin, and norepinephrine were found to be significantly higher in this fluid. Local ischemia is suggested by a lower than normal pH in the region of the TrP ( P < 0.01).
Management Approaches
The trend of therapeutic recommendations for MPSs favors the use of a systematic, comprehensive, multidisciplinary approach to treatment. It has been emphasized that important components of such a program should include the services of an experienced provider who has made an accurate diagnosis, has identified predisposing and perpetuating factors, and makes strategic use of both physical modalities and medications of proven efficacy. These recommendations appear to be surprisingly confident interventions for a condition whose very diagnosis is plagued by uncertainty.
A simple physical intervention that is often at least temporarily effective involves repeatedly applying a cold spray over the TrP in line with the involved muscle fibers, followed by gentle massage of the TrP and stretching of the affected muscle. Observing dramatic therapeutic success with this procedure had the effect of generating belief in the MPS concept on a broader scale. It is also potentially educational for patients as a technique to abort progression of future attacks at an early stage by applying their own local stretch and massage. On the other hand, it is acknowledged that this approach is more readily applied to a superficial muscle, such as the trapezius fibers around the neck, than to a more deeply positioned muscle, such as the piriformis or iliopsoas muscles of the pelvis.
The skills of an experienced physical therapist can be used to teach better posture, body mechanics, and relaxation techniques and to provide TrP massage, postisometric relaxation, reciprocal inhibition, and other manual modalities.
A more invasive approach to therapy is local injection or dry needling of the TrP. Even though the pain of MPS in a given muscle can be eliminated by local anesthesia of the relevant sensory and motor nerves, this approach provides only temporary relief. The more lasting approach is referred to as TrP injection. After the symptomatic (active) TrP has been identified, small amounts of local anesthetic can be injected into the muscle via short jabs of the needle into the location of the TrP.
It is believed that local anesthetic offers no long-term benefit but does make the procedure less uncomfortable. Many practitioners argue in favor of dry needling because the overall results are similar and the patient is not placed at risk of being sensitized to an adverse reaction from the anesthetic. The effectiveness of the needling procedure is explained by local structural damage to the TrP as a result of repeated passes of the needle. It is less clear whether scar tissue formation in the area represents an impediment to recurrence or a nidus favoring it. Typically, several local needling applications over a period of weeks or months are needed to achieve a cure. The required course is recognized to be substantially longer when MPS is complicated by the comorbidity of FM. Some have found additional usefulness in the injection of botulinum toxin, but others have failed to demonstrate a significant effect in controlled clinical trials.
Therefore, it seems likely that MPS is a legitimate clinical construct that has not been fully elucidated, partly because MPS is challenging to diagnose but more importantly because diagnostic criteria have not yet been validated. This is not likely to change until experts in the field feel the need for validated criteria and put their collective efforts to the task so that the results will be more universally accepted. Until this is accomplished, MPS will remain in a form of clinical and scientific limbo. Once validated diagnostic criteria are developed, the next steps would be possible—to conduct epidemiologic, pathologic, and therapeutic studies. The outcomes of such studies would substantially advance the field, both scientifically and in the arena of public opinion.
Fibromyalgia
Diagnostic Criteria
The ACR developed research criteria for the classification of FM syndrome based on the results of a multicenter research study in 1990 ( Table 29.1 ). The scientific community quickly accepted these criteria with a broad application for epidemiologic, biologic, and therapeutic studies. The ACR research classification required only two components for diagnosis: a history of widespread pain (i.e., located in all four quadrants of the body and axial) for at least 3 months and allodynia in response to digital pressure (defined as pain with 4 kg of pressure) at 11 or more of the 18 anatomically defined tender points ( Table 29.2 ). The research diagnostic criteria demonstrated moderate sensitivity (88.4%) and specificity (81.1%) for FM against control patients. The study design included pain-free individuals and patients with other painful conditions as the control groups.
Criterion | Description |
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1. History | Chronic, widespread (four quadrants) soft tissue pain for 3 mo |
2. Examination | Pain (1+ or greater in severity) induced by 4 kg of digital palpation pressure at 11 of 18 anatomically defined tender points (see Table 29.2 ) |
3. 1 and 2 are true | When 1 and 2 are true, sensitivity and specificity for FMS >80% |
Number | Official American College of Rheumatology Bilateral Tender Point Sites |
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1, 2 | Occiput—suboccipital muscle insertions |
3, 4 | Low cervical—anterior aspects of the C5-7 intertransverse spaces |
5, 6 | Trapezius—midpoint of the upper border |
7, 8 | Supraspinatus—origins above the scapular spine, near the medial border |
9, 10 | Second rib—upper lateral surface of the second costochondral joint |
11, 12 | Lateral epicondyle—2 cm distal to the epicondyles |
13, 14 | Gluteal—upper outer aspect of the buttock, anterior fold of the muscle |
15, 16 | Greater trochanter—posterior to the trochanteric prominence |
17, 18 | Knees—medial fat pad, just proximal to the medial condyle |
The tender points in FM are conceptually and anatomically different from the TrPs that define MPS. FM tender points are symmetrically distributed throughout the body, whereas TrPs have a more random distribution. In contrast to MPS, these tender points are not limited to muscular locations but also include other soft tissue structures and do not refer or radiate pain to other locations. The ACR’s research criteria unknowingly created several problems. Researchers developed these criteria to standardize research identification of FM. The research classification identified 18 anatomically defined tender points (see Table 29.2 ) where patients with FM have allodynia in response to digital pressure. Unfortunately, clinicians appropriated these criteria for clinical diagnosis. Many providers did not follow the intent or structure of the criteria, which made the diagnosis of FM even more complicated.
Primary care physicians diagnose the majority of cases of FM rather than subspecialists. Consequently, many physicians either rigidly (and inappropriately) applied the research criteria or simply rejected their face validity. Accordingly, few providers consistently identified and applied 4 kg of pressure to all 18 designated areas. They used symptom-based diagnostic criteria that focused on fatigue, cognitive impairment, and somatic symptoms, which were excluded in the original research criteria. Moreover, an additional problem with the criteria is that patients with improved symptoms and examination findings no longer met the classification.
Twenty years after the initial research classification was developed, the FM research community recognized the growing need for clinical diagnostic criteria that reflect the spectrum of FM and practical components of clinical diagnosis. The objective was to develop a screening tool with wide applicability that could be used to diagnose and assess the severity of the FM symptoms. Researchers evaluated patients in whom FM was previously diagnosed by using the widespread pain index (WPI) and categorical scales. The new criteria used these categorical scales to assess patients’ cognitive symptoms, unrefreshing sleep, fatigue, and other somatic symptoms. The ACR used these categorical scales to develop a severity scale. Finally, they combined the severity scale with the WPI to stratify disease severity in patients with FM ( Box 29.2 ).
Criteria
A patient satisfies the diagnostic criteria for fibromyalgia if the following three conditions are met:
- 1.
Widespread pain index (WPI) score >7 and symptom severity (SS) scale score >5 or WPI score of 3 to 6 and SS scale score >9
- 2.
Symptoms present at a similar level for at least 3 months
- 3.
No disorder present that would otherwise explain the pain
Ascertainment
- 1.
WPI: note the number of areas in which the patient has had pain over the last week. In how many areas has the patient had pain? The score will be between 0 and 19:
Shoulder girdle, left hip (buttock, trochanter), left jaw, left upper part of back
Shoulder girdle, right hip (buttock, trochanter), right jaw, right lower part of back
Upper part of arm, left upper part of leg, left side of chest or neck
Upper part of arm, right upper part of leg, right side of abdomen
Left lower part of arm, left lower part of leg
Right lower part of arm, right lower part of leg
- 2.
SS scale score:
Fatigue
Waking unrefreshed
Cognitive symptoms
For the each of the three symptoms above, indicate the level of severity over the past week according to the following scale:
0= No problem
1= Slight or mild problems, generally mild or intermittent
2= Moderate: considerable problems, often present and/or at a moderate level
3= Severe: pervasive, continuous, life-disturbing problems
Considering somatic symptoms in general, indicate whether the patient has the following ∗
∗ Somatic symptoms that might be considered are muscle pain, irritable bowel syndrome, fatigue or tiredness, difficulty thinking or remembering, muscle weakness, headache, pain or cramps in the abdomen, numbness or tingling, dizziness, insomnia, depression, constipation, pain in the upper part of the abdomen, nausea, nervousness, chest pain, blurred vision, fever, diarrhea, dry mouth, itching, wheezing, Raynaud’s phenomenon, hives or welts, ringing in the ears, vomiting, heartburn, oral ulcers, loss of or change in taste, seizures, dry eyes, shortness of breath, loss of appetite, rash, sun sensitivity, hearing difficulty, easy bruising, hair loss, frequent urination, painful urination, and bladder spasms.
:
0= No symptoms
1= Few symptoms
2= Moderate number of symptoms
3= Great deal of symptoms
The SS scale score is the sum of the severity of the symptoms (fatigue, waking unrefreshed, cognitive symptoms) plus the extent (severity) of somatic symptoms in general. The final score is between 0 and 12.