Definition

Myofascial pain syndrome (MPS) is a painful disorder characterized by the presence of myofascial trigger points (MTrPs), distinct sensitive spots in a palpable taut band of skeletal muscle fibers [1] that produce local and referred pain. Thus, MPS is characterized by both a motor abnormality (a taut or hard band within the muscle) and a sensory abnormality (tenderness and referred pain) [2] (Fig. 104.1). In addition to pain, the disorder is accompanied by referred autonomic phenomena as well as by anxiety and depression. The pathophysiologic mechanism of MPS is not clearly understood in part because of the scarcity of reliable valid studies. Moreover, concomitant disorders and frequent behavioral and psychosocial contributing factors in patients with MPS contribute to the complexity of human studies. Symptoms of MPS are generally associated with physical activities that are thought to contribute to “muscle overload,” either acutely by sudden overload or gradually with prolonged repetitive activity [3]. MPS is reported to be prevalent in regional musculoskeletal pain syndromes; however, the syndrome can be classified as regional or generalized. Some authors broaden the definition of myofascial pain to include a regional pain syndrome of any soft tissue origin. Thus, MPS may be considered either a primary disorder causing local or regional pain syndromes or a secondary disorder that occurs as a consequence of some other condition, such as a radiculopathy.

The MTrP is generally considered the hallmark of MPS; therefore, much attention has been given to characteristic features of MTrPs in skeletal muscle [4,5]. One such feature of the MTrP is the so-called twitch response. This local response is considered a characteristic finding of the MTrP. Mechanical stimulation (“snapping” palpation, pressure, or needle insertion) can elicit a local twitch response that frequently is accompanied by referred pain [6]. The twitch response is accompanied by a burst of electrical activity (“end-plate noise”) within the muscle band that contains the activated trigger point, whereas no activity is seen at other muscle bands. End-plate noise is significantly more prevalent in MTrPs than in sites that lie outside of the MTrP but still within the end-plate zone [7]. This observation has been attributed to a spinal reflex [4,6], as the response is abolished by motor nerve ablation or infusion of local anesthetic. Moreover, spinal cord transection above the neurologic level of the MTrP fails to permanently alter the characteristic response.

A number of hypotheses [8,9] have been put forward to explain the findings observed in MTrPs. One theory proposes that MTrPs are found only at the muscle spindle in an attempt to explain beneficial effects of α-adrenergic antagonists. However, this idea does not fully explain the electromyographic findings recorded at the MTrP. Further, there appears to be little evidence that painful muscle areas, such as MTrPs, are associated with any structural changes, such as an alteration in the appearance of the muscle spindle. Another theory is related to excessive release of acetylcholine in abnormal end plates [4], as the electromyographic activity recorded at trigger points resembles findings described at the end-plate region [7]. This idea has led some clinicians to study effects of botulinum toxin injection into MTrPs in an attempt to reduce release of excessive acetylcholine. To date, results of small cohort studies [10] examining effects of botulinum toxin on MTrPs have yielded inconsistent findings.

Central neurologic processes are increasingly viewed as essential factors in chronic pain syndromes. The medial thalamus is the principal relay of nociceptive input to the anterior cingulate cortex, and persistent stimulation of this pathway by pain in peripheral tissues has been demonstrated to change neurons in the cingulate cortex [11]. Thus, persistent pain is associated with long-term changes in the morphology, neurochemistry, and gene expression of the anterior cingulate cortex, which has the most direct connection with autonomic arousal, thereby contributing to the maintenance and exacerbation of pain [12].

Such central sensitization is characterized by an enhanced pain response to normally painful stimuli (hyperalgesia), a decrease in pain threshold to normally nonpainful stimuli (allodynia), and an increase in spontaneous activity (spontaneous pain). This process is clinically seen in MPS as the pain–muscle tension (in response to autonomic arousal and affective distress)–increased pain–increased tension and distress cycle.

Fibromyalgia (see Chapter 101), a chronic musculoskeletal pain condition that predominantly affects women, is characterized by diffuse muscle pain, fatigue, sleep disturbance, depression, and skin sensitivity [13]. Fibromyalgia may fit the classification of MPS as the diagnosis includes the presence of 11 of 18 tender points [14]. Furthermore, treatment of MPS and fibromyalgia is similar as evidence supports the role of exercise, cognitive-behavioral therapy, education, and social support in the management of both fibromyalgia and chronic MPS. However, there is controversy as to whether fibromyalgia and MPS represent specific pathologic processes or are descriptive terms of clinical conditions. Objective evidence of muscle abnormalities in fibromyalgia has been demonstrated by histologic studies showing disorganization of Z bands and abnormalities in the number and shape of muscle mitochondria. Biochemical studies and magnetic resonance spectroscopy have also shown inconstant abnormalities of adenosine triphosphate and phosphocreatine levels. It is unclear whether these abnormalities are a result of physical deconditioning or if abnormalities are due to problems in energy metabolism. There are no clear biochemical markers that distinguish patients with fibromyalgia. Thus, whereas the pathogenesis is still unknown, there has been evidence of increased corticotropin-releasing hormone and substance P in the cerebrospinal fluid of fibromyalgia patients as well as increased substance P and interleukins 6 and 8 in their serum [14]. One hypothesis supports the idea that fibromyalgia is an immunoendocrine disorder in which increased release of corticotropin-releasing hormone and substance P from neurons triggers local mast cells to release proinflammatory and neurosensitizing molecules. This hypothesis fits well with recent discoveries of neuropeptides found in the muscles of patients with active MTrPs [15].

Symptoms

The patient with MPS generally complains about dull or achy pain, sometimes poorly localized, particularly occurring during repetitive activities or during activities requiring sustained postures. Symptoms are exacerbated with digital pressure over tender areas of muscle with reproduction of the patient’s usual pain. Symptoms are relieved with rest or cessation of repetitive activities. In contrast, the patient with fibromyalgia typically presents with sleep disturbances, depressed mood, and fatigue.

Physical Examination

The most important part of the physical examination is generally considered to be finding and localizing MTrPs to provide an accurate diagnosis of MPS. Travell & Simons’ Myofascial Pain and Dysfunction: The Trigger Point Manual [16] is considered the criterion standard reference on locating and treating MTrPs. Active MTrPs, attributed to cause pain, exhibit marked localized tenderness and may refer pain to distant sites, disturb motor function, or produce autonomic changes. Specific clinical training is required to become adept at identifying MTrPs as evidence suggests that “non-trained” clinicians do not reliably detect the taut band and local twitch response [17]. To clinically identify MTrPs, the clinician palpates a localized tender spot in a nodular portion of a taut, rope-like band of muscle fibers. Manual pressure over a trigger point should elicit pain at that area and may also elicit pain at a distant site (referred pain) from the point under the fingertip (Fig. 104.2). MTrPs, when palpated, should also elicit pain that mirrors the patient’s experience. Applied pressure often reproduces the pain. Insertion of a needle, abrupt palpation, or even a brisk tap with the fingertip directly over the trigger point may induce a brief muscle contraction detectable by the examiner. This rapid contraction of muscle fibers of the ropy taut band is termed a local twitch response [3]. In muscles that move a relatively small mass or are large and superficial (such as the finger extensors or the gluteus maximus), the response is easily seen and may cause the limb to visibly move when the examiner introduces a needle into the trigger point. Localized abnormal response from the autonomic nervous system may cause piloerection, localized sweating, or even regional temperature changes in the skin attributed to altered blood flow [8,18,19].

Regional Examination of the Lower Extremity for Piriformis Syndrome

To evaluate individuals for piriformis syndrome [20], their usual buttock, hip, and lower limb pain may be reproduced during the following maneuvers: palpation over a point midway between the sacrum and greater trochanter of the femur, active hip abduction in the lateral recumbent position, and rectal palpation of the ipsilateral side of the involved limb [21,22]. Beatty described a maneuver [23,24] performed with the patient’s lying with the painful side up, the painful leg flexed, and the knee resting on the table. Buttock pain is produced when the patient lifts and holds the knee several inches off the table. A positive finding in at least two of the preceding maneuvers is sufficient to confirm a diagnosis of piriformis syndrome, provided other potential causes have been eliminated from the differential diagnosis.

Diagnostic Studies

No definitive laboratory test or imaging method is diagnostic of MPS. Thus, diagnosis is made primarily by history and physical examination. Whereas no specific laboratory tests confirm (or refute) a diagnosis of MPS [25,26], some tests can be helpful in looking for predisposing conditions, such as hypothyroidism, hypoglycemia, and vitamin deficiencies. Specific tests that may be helpful include complete blood count, chemistry profile, erythrocyte sedimentation rate, and levels of vitamins C, B₁, B₆, B₁₂, and folic acid. If clinical features of thyroid disease are present, an assay for thyrotropin may be indicated [27].