The Pharmacologic Treatment of Muscle Pain Steven P
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Ⅵ REVIEW ARTICLE David C. Warltier, M.D., Ph.D., Editor Anesthesiology 2004; 101:495–526 © 2004 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. The Pharmacologic Treatment of Muscle Pain Steven P. Cohen, M.D.,* Rohan Mullings, M.D.,† Salahadin Abdi, M.D., Ph.D.‡ MYOFASCIAL pain is a significant source of discomfort two main types, active TPs and latent TPs, the latter of in individuals with regional pain symptomatology. The which is more common. Depending on the pain condi- prevalence of myofascial pain ranges from around 20% in tion, and even within certain subgroups of soft tissue patients with chronic low back pain (LBP)1 to 30% in disorders, muscle pain may be associated with TPs, in- patients with regional pain complaints seen in primary creased muscle tension, or various combinations of care clinics2 to upward of 85% in patients presenting to these pathologic processes. Common clinical conditions specialized pain management centers.3 in which muscle pain is caused primarily by spasm To understand the origin of myofascial pain, it is first include torticollis, trismus, and nocturnal leg cramps. A necessary to possess a fundamental understanding of painful condition that is defined by the presence of two related concepts, muscle tension and trigger points active TPs is myofascial pain syndrome (MPS). Tension (TPs). Muscle tension is the product of two distinct headache and temporomandibular disorder (TMD) are factors: viscoelastic tone and contractile activity.4 Vis- conditions that may be associated with both increased coelastic tone can be classified into two parts, elastic muscle tone and TPs. stiffness and viscoelastic stiffness. Both of these can be Other mechanisms and physiologic processes can con- quantified only in the absence of electromyographic tribute to muscle pain in addition to tone and TPs. These activity. Elastic stiffness is a function of distance moved, include but are not limited to increased metabolism or whereas viscoelastic stiffness considers the effect of diminished perfusion leading to local ischemia, periph- velocity. eral and central sensitization, and autonomic hyperactiv- Contractile activity is composed of three different sub- ity.5,6 Not infrequently, psychogenic factors are found to units: contracture (no electromyographic activity), elec- play a role in soft tissue disorders.7,8 trogenic spasm (pathologic), and electrogenic stiffness Although local anesthetic TP injections have been ad- (normal). Contractures originate endogenously within vocated in the treatment of a wide variety of myofascial muscle fibers independent of electromyographic activ- pain disorders including tension headache, MPS, TMD, ity. Electrogenic spasm refers to involuntary, pathologic and LBP,9 these injections are beyond the scope of this contractions arising from the electrical activity occurring review article. Fibromyalgia, which shares some charac- in alpha motor neurons and motor endplates. Electro- teristics with myofascial pain but which the authors genic stiffness refers to muscle tension that derives from consider a disorder of sensory processing,10 will also not electrogenic muscle contraction in individuals who are be considered. MPS is considered to be a distinct disor- not relaxed. The latter two terms are associated with der with major and minor diagnostic criteria, and the measurable electromyographic activity. authors will limit the use of this term to the syndrome Trigger points are defined as taut bands of muscle that outlined by Simons.11 The term myofascial pain is used produce pain in characteristic reference zones. These more broadly and refers to soft tissue pain of unclear taut bands of contracted muscle can be classified into etiology. *Visiting Associate Professor of Anesthesiology, Pain Management Centers, Departments of Anesthesiology and Critical Care Medicine, Johns Hopkins Study Populations, Limitations, and Search School of Medicine, and Walter Reed Army Medical Center. † Fellow, Depart- ment of Anesthesiology, ‡ Professor of Anesthesiology, University of Miami Pain Methods Center, University of Miami School of Medicine. Received from the Departments of Anesthesiology and Critical Care Medicine There are several inherent limitations in a review of at Johns Hopkins Medical Institutions, Baltimore, Maryland; Walter Reed Army the pharmacologic management of muscle pain. First, Medical Center, Washington, D.C.; and the University of Miami School of Medi- cine, Miami, Florida. Submitted for publication July 24, 2003. Accepted for myofascial pain represents a heterogeneous group of publication April 29, 2004. Support was provided solely from institutional and/or disorders, each characterized by its own unique patho- departmental sources. Address reprint requests to Dr. Cohen: Johns Hopkins Medical Institutions, physiology. There are considerable differences in the Departments of Anesthesiology and Critical Care Medicine, Blalock 1415, 600 mechanisms underlying acute muscle injury such as oc- North Wolfe St., Baltimore, Maryland 21287. Address electronic mail to: [email protected]. Indiviual article reprints may be purchased through the curs with muscle tears and succinylcholine-induced my- Journal Web site, www.anesthesiology.org. algia and those responsible for chronic conditions in Anesthesiology, V 101, No 2, Aug 2004 495 496 COHEN ET AL. which muscles play a role, such as MPS and TMD. Sec- a relative lack of basic science and clinical data available ond, different mechanisms of nociception may exist for deep tissue pain, which is more clinically relevant. even within a particular subgroup. For example, in TMD, Muscle pain is generally described as a deep, achy, the primary source of pain is myogenous in some pa- cramping-like sensation in contrast to the sharp, local- tients and arthrogenous in others. Many clinical investi- ized characteristics of cutaneous pain. This pain is often gators have not or perhaps could not distinguish be- poorly localized by patients. Convergent afferent input tween different pain generators. Other examples of from skin, joints, and viscera to the spinothalamic tract disorders for which this problem exists include LBP and and other ascending pain pathways may cause misinter- tension-type/muscle contraction headaches. Third, be- pretation of information arising from A␦- and C-fiber cause the category of muscle pain itself so broad, so too polymodal muscle nociceptors, as is the case with other are the drugs used to treat it. For some agents, such as types of referred pain. topical nonsteroidal antiinflammatory drugs (NSAIDs) Pain in response to muscle injury is transmitted by the and quinine, the indications for use are relatively nar- same basic pathways as those involved for other somatic row, but for drug classes that act on a broad range of structures. After a noxious stimulus, an inflammatory systems, such as antidepressants, their antinociceptive response occurs, which results in the accumulation of effects are not limited to myofascial pain. Unfortunately, neuropeptides and inflammatory cells via chemotaxis. most clinical studies are not capable of distinguishing Release of these peptides results in altered excitability of between pain relief that results from central analgesic sensory and sympathetic nerve fibers and the release of effects and those that are due to peripheral mechanisms. chemical mediators. These substances act to sensitize The evidence for involvement (or lack thereof in the high-threshold nociceptors, a phenomenon known as case of fibromyalgia) of muscle pain in the most com- peripheral sensitization. This manifests as spontaneous mon medical conditions mentioned in this article is re- pain and tenderness after acute muscle injury. viewed in the appendix. These include fibromyalgia, Just as prolonged stimulation of nociceptors can lead tension-type headache, MPS, TMD, LBP, and muscle to altered pain states (peripheral sensitization), so too cramps. The studies evaluated were obtained via a can repetitive stimulation of second- and higher-order MEDLINE search from 1966 through March 2004 using neurons (central sensitization). In a study by Wright et the limit clinical trial and a bibliographic review of al.12 assessing the temporal summation of painful stimuli these articles. Only human studies in which muscle in skin, joint, and muscle, summation was most pro- seemed to play a significant role in the pathogenesis of nounced in muscle tissue, illustrating the underappreci- pain were considered. Heterogeneous and variable, the ated role deep tissues play in the development and study populations for each cited article are outlined in maintenance of central sensitization. Hyperalgesia may the accompanying tables. For drugs in which there was be more likely to occur in small rather than large mus- a lack of controlled trials for muscle pain, uncontrolled cles, which may explain why TMD is so common.13 studies were considered. This review is neither quanti- Central sensitization may also be responsible for referred tative (statistical pooling) nor qualitative (best evidence pain. Hoheisel et al.14 found that the injection of brady- synthesis). Evidence for the efficacy of each drug class in kinin into one muscle in rats unmasked receptive fields muscle pain was classified as strong, moderate, limited, in other muscles. These findings may partially explain conflicting, or no evidence. Finally, it must be remem- the phenomenon of referred pain after muscle injury. bered that pharmacologic treatment is best considered Peripheral