REVIEW For reprint orders, please contact: [email protected]
Treatment of myofascial pain
Practice Points
Mehul J Desai*1, Matthew C Bean1, Thomas W Heckman1, Dhinu Jayaseelan1, Nick Moats1 & Andrew Nava1 Managing patients with myofascial pain syndrome involves identifying and treating any underlying
etiologies, which may include repetitive activities, inactivity, chronic tension, limb length inequalities, spinal pathologies, or asymmetric joint pain. Physicians should screen for and treat any comorbid behavioral issues (e.g., depression). Treatment modalities may be combined to maximize pain relief. First-line treatment includes NSAIDS (topical or oral; acutely), muscle relaxants (acutely), or topical
anesthetics in conjunction with physical therapy and its associated modalities, such as transcutaneous electric nerve stimulation, myofascial release, spray and stretch, and ischemic compression, with or without laser light therapy. In refractory patients, physicians may consider the use of injectable anesthetics, botox or dry needling
to facilitate physical therapy outcomes.
SUMMARY The objective of this article was to perform a narrative review regarding the treatment of myofascial pain syndrome and to provide clinicians with treatment recommendations. This paper reviews the efficacy of various myofascial pain syndrome treatment modalities, including pharmacological therapy, injection-based therapies and physical therapy interventions. Outcomes evaluated included pain (visual analog scale), pain pressure threshold and range of motion. The evidence found significant benefit with multiple treatments, including diclofenac patch, thiocolchicoside and lidocaine patches. Trigger point injections, ischemic compression therapy, transcutaneous electrical nerve stimulation, spray and stretch, and myofascial release were also efficacious. The authors recommend focusing on treating underlying pathologies, including spinal conditions, postural abnormalities and underlying behavioral issues. To achieve maximum pain reduction and improve function, we recommend physicians approach myofascial pain syndrome with a multimodal plan, which includes a combination of pharmacologic therapies, various physical therapeutic modalities and injection therapies. Myofascial pain syndrome (MPS) is a musculo skeletal condition characterized by regional pain and muscle tenderness associated with the presence of myofascial trigger points (MTrPs).
Clinically, these MTrPs are focally hypersensitive taut bands that produce a local twitch response and a typical referral pattern upon palpation [1,2] . MPS affects up to 95% of patients with
George Washington University Medical Center, The GW Spine & Pain Center, 2131 K Street, NW Suite 600, Washington, DC, USA *Author for correspondence: [email protected] 1
10.2217/PMT.12.78 © 2013 Future Medicine Ltd
Pain Manage. (2013) 3(1), 67–79
part of
ISSN 1758-1869
67
REVIEW Desai, Bean, Heckman, Jayaseelan, Moats & Nava chronic pain disorders and is a common finding in patients at specialty pain medicine centers [3] . It is estimated that the overall prevalence of MPS in middle-aged adults (30–60 years old) is 37% in males and 65% in females, with a prevalence rate approaching 85% in the elderly (>65 years old) [4] . MPS also carries a significant financial burden in the USA, with an estimated cost of US$47 billion per year [5] . Owing to the poorly understood patho physiologic mechanism involved in MPS, a variety of treatment modalities are typically employed, often with varying benefit. Treatments such as pharmacologic management with NSAIDs, physical therapy techniques, dry needling and psychosocial intervention, as well as newer and emerging therapies, are routine strategies for dealing with this complex syndrome. This paper provides a narrative review of the current treatments for MPS, including an overview of its diagnosis and pathophysiology. Diagnosis While diagnostic criteria vary, most researchers investigating MPS, and the authorities they cite, require the following: a painful nodule in a taut band of skeletal muscle and predicted, or recognized, referred pain upon palpation of a MTrP [2,3] . Other frequently used diagnostic criteria include a local twitch response (LTR) upon palpation and limited range of motion (ROM) [6] . LTR is controversial due to low interrater reliability and is thus considered to be the least reliable diagnostic test, according to Simons et al. [2] . Simons et al. consider a predictable pain referral pattern to be nonspecific and instead includes “painful limitation to movement” [2] . Objectively, Fischer characterizes MTrP as a “pressure algometry reading at tender points at least 2 kg/cm2 lower than at nontender points” [7] . To further complicate MPS diagnosis, fibromyalgia (FM) tender points are frequently compared with MPS trigger points. Tender points are typically defined as focally tender, but lacking the LTR and/or referred pain, and are often diagnosed as trigger points [8] . Borg-Stein et al. suggests that MPS and FM may be two points in the same pathologic spectrum [3] . Ge et al. further argues that FM tender points are actually MTrPs [6] and has demonstrated the existence of referred pain in FM patients [9–11] . As a result of the variability in diagnostic criteria, the diagnoses, and thus studies of MPS, are complicated by poor inter-rater reliability [12] .
68
Pain Manage. (2013) 3(1)
Srbely argues that identification of the primary pathology leading to central sensitization is the first step in accurate MPS diagnosis [4] . A complete review of systems along with a physical examination focusing on regions that are neurologically linked to the location of identified MTrPs is crucial to appropriate diagnosis and management [4] . Additionally, physical examination of spine and joint degeneration manifestations, specifically in elderly patients, should be considered [4] . Pathophysiology While the precise pathophysiologic mechanism of MPS is unclear, the characteristics of MTrPs can be adequately characterized by the presence of: palpable nodules; local hyperalgesia upon palpation; and referred pain upon palpation. The nodules of taut muscle bands are believed to be caused by increased acetylcholine (ACh) release at motor end plates, resulting in sustained muscle contraction, which leads to hypoxia, tis sue damage and subsequent release of inflamma tory, vasocative and algogenic substances. These substances include substance P, bradykinin, sero tonin, protons and prostaglandins. The increased concentration of these substances has been con firmed in vivo. The continued presence of these inflammatory mediators may be responsible for persistent local pain associated with MPS [13] . This cascade of events eventually causes periph eral sensitization of local muscle nociceptors, resulting in local hyperalgesia. Dorsal horn sensitization is hypothesized to spread to adjacent myotomes, causing referred pain [10] . Srbely has postulated that active trigger point loci demonstrate spontaneous end plate activity, which results from spontaneous release of ACh [4] . Continuous activation of nociceptors by ACh, along with the convergence of multiple afferent MTrP nociceptors and spontaneous end plateactivated efferent pathways, amplifies the signal in the spinal dorsal horn. This sensitizes second order/central neurons in the spinal cord, resulting in further hyperalgesia and allodynia in adjacent spinal segments [14] . In addition, the supraspinal inhibitory descending pain control pathway may also be impaired, causing a decrease in release of GABA, serotonin and norepinephrine [15] . Finally, a positive feedback loop is created by substance P, bradykinin, serotonin and histamine, which stimulates the autonomic nervous system to further increase motor end plate ACh release (Figure 1) [15] .
future science group
Treatment of myofascial pain Treatment Resolving the pathologic condition of MPS is the primary goal of treatment. Reduction of pain and disability are the secondary treatment goals. The complex pathophysiology requires that multiple therapeutic strategies be utilized, including releasing MTrP nodules and decreasing muscle fatigue, both of which lead to local nociceptor pain relief and a decrease in sensitization. Psychosocial intervention The prevalence of pain and depression comorbidity is approximately 30–50% [16] . Change in depression severity has been shown to correlate with changes in pain symptoms. In
Mechanical or chemical stimulus
REVIEW
a randomized 12‑month longitudinal study of 500 patients with chronic pain, change in pain was a strong (significant) predictor of subsequent depression severity (p
Treatment of myofascial pain
Practice Points
Mehul J Desai*1, Matthew C Bean1, Thomas W Heckman1, Dhinu Jayaseelan1, Nick Moats1 & Andrew Nava1 Managing patients with myofascial pain syndrome involves identifying and treating any underlying
etiologies, which may include repetitive activities, inactivity, chronic tension, limb length inequalities, spinal pathologies, or asymmetric joint pain. Physicians should screen for and treat any comorbid behavioral issues (e.g., depression). Treatment modalities may be combined to maximize pain relief. First-line treatment includes NSAIDS (topical or oral; acutely), muscle relaxants (acutely), or topical
anesthetics in conjunction with physical therapy and its associated modalities, such as transcutaneous electric nerve stimulation, myofascial release, spray and stretch, and ischemic compression, with or without laser light therapy. In refractory patients, physicians may consider the use of injectable anesthetics, botox or dry needling
to facilitate physical therapy outcomes.
SUMMARY The objective of this article was to perform a narrative review regarding the treatment of myofascial pain syndrome and to provide clinicians with treatment recommendations. This paper reviews the efficacy of various myofascial pain syndrome treatment modalities, including pharmacological therapy, injection-based therapies and physical therapy interventions. Outcomes evaluated included pain (visual analog scale), pain pressure threshold and range of motion. The evidence found significant benefit with multiple treatments, including diclofenac patch, thiocolchicoside and lidocaine patches. Trigger point injections, ischemic compression therapy, transcutaneous electrical nerve stimulation, spray and stretch, and myofascial release were also efficacious. The authors recommend focusing on treating underlying pathologies, including spinal conditions, postural abnormalities and underlying behavioral issues. To achieve maximum pain reduction and improve function, we recommend physicians approach myofascial pain syndrome with a multimodal plan, which includes a combination of pharmacologic therapies, various physical therapeutic modalities and injection therapies. Myofascial pain syndrome (MPS) is a musculo skeletal condition characterized by regional pain and muscle tenderness associated with the presence of myofascial trigger points (MTrPs).
Clinically, these MTrPs are focally hypersensitive taut bands that produce a local twitch response and a typical referral pattern upon palpation [1,2] . MPS affects up to 95% of patients with
George Washington University Medical Center, The GW Spine & Pain Center, 2131 K Street, NW Suite 600, Washington, DC, USA *Author for correspondence: [email protected] 1
10.2217/PMT.12.78 © 2013 Future Medicine Ltd
Pain Manage. (2013) 3(1), 67–79
part of
ISSN 1758-1869
67
REVIEW Desai, Bean, Heckman, Jayaseelan, Moats & Nava chronic pain disorders and is a common finding in patients at specialty pain medicine centers [3] . It is estimated that the overall prevalence of MPS in middle-aged adults (30–60 years old) is 37% in males and 65% in females, with a prevalence rate approaching 85% in the elderly (>65 years old) [4] . MPS also carries a significant financial burden in the USA, with an estimated cost of US$47 billion per year [5] . Owing to the poorly understood patho physiologic mechanism involved in MPS, a variety of treatment modalities are typically employed, often with varying benefit. Treatments such as pharmacologic management with NSAIDs, physical therapy techniques, dry needling and psychosocial intervention, as well as newer and emerging therapies, are routine strategies for dealing with this complex syndrome. This paper provides a narrative review of the current treatments for MPS, including an overview of its diagnosis and pathophysiology. Diagnosis While diagnostic criteria vary, most researchers investigating MPS, and the authorities they cite, require the following: a painful nodule in a taut band of skeletal muscle and predicted, or recognized, referred pain upon palpation of a MTrP [2,3] . Other frequently used diagnostic criteria include a local twitch response (LTR) upon palpation and limited range of motion (ROM) [6] . LTR is controversial due to low interrater reliability and is thus considered to be the least reliable diagnostic test, according to Simons et al. [2] . Simons et al. consider a predictable pain referral pattern to be nonspecific and instead includes “painful limitation to movement” [2] . Objectively, Fischer characterizes MTrP as a “pressure algometry reading at tender points at least 2 kg/cm2 lower than at nontender points” [7] . To further complicate MPS diagnosis, fibromyalgia (FM) tender points are frequently compared with MPS trigger points. Tender points are typically defined as focally tender, but lacking the LTR and/or referred pain, and are often diagnosed as trigger points [8] . Borg-Stein et al. suggests that MPS and FM may be two points in the same pathologic spectrum [3] . Ge et al. further argues that FM tender points are actually MTrPs [6] and has demonstrated the existence of referred pain in FM patients [9–11] . As a result of the variability in diagnostic criteria, the diagnoses, and thus studies of MPS, are complicated by poor inter-rater reliability [12] .
68
Pain Manage. (2013) 3(1)
Srbely argues that identification of the primary pathology leading to central sensitization is the first step in accurate MPS diagnosis [4] . A complete review of systems along with a physical examination focusing on regions that are neurologically linked to the location of identified MTrPs is crucial to appropriate diagnosis and management [4] . Additionally, physical examination of spine and joint degeneration manifestations, specifically in elderly patients, should be considered [4] . Pathophysiology While the precise pathophysiologic mechanism of MPS is unclear, the characteristics of MTrPs can be adequately characterized by the presence of: palpable nodules; local hyperalgesia upon palpation; and referred pain upon palpation. The nodules of taut muscle bands are believed to be caused by increased acetylcholine (ACh) release at motor end plates, resulting in sustained muscle contraction, which leads to hypoxia, tis sue damage and subsequent release of inflamma tory, vasocative and algogenic substances. These substances include substance P, bradykinin, sero tonin, protons and prostaglandins. The increased concentration of these substances has been con firmed in vivo. The continued presence of these inflammatory mediators may be responsible for persistent local pain associated with MPS [13] . This cascade of events eventually causes periph eral sensitization of local muscle nociceptors, resulting in local hyperalgesia. Dorsal horn sensitization is hypothesized to spread to adjacent myotomes, causing referred pain [10] . Srbely has postulated that active trigger point loci demonstrate spontaneous end plate activity, which results from spontaneous release of ACh [4] . Continuous activation of nociceptors by ACh, along with the convergence of multiple afferent MTrP nociceptors and spontaneous end plateactivated efferent pathways, amplifies the signal in the spinal dorsal horn. This sensitizes second order/central neurons in the spinal cord, resulting in further hyperalgesia and allodynia in adjacent spinal segments [14] . In addition, the supraspinal inhibitory descending pain control pathway may also be impaired, causing a decrease in release of GABA, serotonin and norepinephrine [15] . Finally, a positive feedback loop is created by substance P, bradykinin, serotonin and histamine, which stimulates the autonomic nervous system to further increase motor end plate ACh release (Figure 1) [15] .
future science group
Treatment of myofascial pain Treatment Resolving the pathologic condition of MPS is the primary goal of treatment. Reduction of pain and disability are the secondary treatment goals. The complex pathophysiology requires that multiple therapeutic strategies be utilized, including releasing MTrP nodules and decreasing muscle fatigue, both of which lead to local nociceptor pain relief and a decrease in sensitization. Psychosocial intervention The prevalence of pain and depression comorbidity is approximately 30–50% [16] . Change in depression severity has been shown to correlate with changes in pain symptoms. In
Mechanical or chemical stimulus
REVIEW
a randomized 12‑month longitudinal study of 500 patients with chronic pain, change in pain was a strong (significant) predictor of subsequent depression severity (p
