Research Review By Gary Maguire©

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Date Posted:

December 2011

Study Title:

New Trends in the Treatment and Management of Myofascial Pain Syndrome

Authors:

Srbely JZ

Author's Affiliations:

Department of Human and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada

Publication Information:

Current Pain & Headache Reports 2010; 14: 346-352.

Background Information:

Myofascial pain syndrome (MPS) is a common, costly, but poorly understood condition. Fortunately, emerging research is revealing the mechanisms and therapeutic approaches for MPS that could have a significant impact on better diagnostic and therapeutic options. The key characteristic of MPS is: the expression of deep, dull, and poorly localized aches or pains localized to myofascial tissues. It also manifests with physiologic and/or clinical conditions such as chronic weakness and fatigue, disturbed sleep and visceral pain syndromes (1). MPS symptoms are often exacerbated by stress, increased activity, cold, exercise and poor posture.

While MPS is considered to be the most common form of musculoskeletal pain, the pathophysiologic mechanisms are poorly understood. This has led to questionable status as a legitimate clinical entity. The crux is that the terms myofascial pain and musculoskeletal pain often are used interchangeably, though the two conditions likely have little in common. Musculoskeletal pain results from overload (either single/acute or multiple/chronic) of musculotendinous units, whereas myofascial pain is a chronic pain condition characterized by the proliferation of myofascial trigger points. While overall the literature remains unclear, there is evidence that trigger points (TrPs) may be initiated by neurogenic mechanisms secondary to central sensitization and not necessarily by local injury.

With an aging population, the impact of MPS on society is an increasing concern. Currently statistics report that musculoskeletal pain affects an overwhelming 85% of the population, with MPS considered a leading cause (2). Fortunately a variety of treatments are currently available in the management of MPS including manual therapy, electrotherapy, exercises and needle therapy (wet and dry). Therapeutic ultrasound is also emerging as a cost effective and noninvasive intervention targeting trigger points. The goal of this paper was to review the existing literature on MPS.

Paper Summary:

Understanding Myofascial Trigger Points in the Study of MPS:
Trigger points within myofascial tissue are defined as “hyperirritable muscular nodules located within taut bands of skeletal muscle that can be classified as both active and latent”. When active, they produce spontaneous local and/or referred pain at rest, in contrast to latent TrPs that do not. Latent TrPs are theorized to be the “dormant” state of the active TrP, producing pain only when directly palpated or irritated.

Acupuncture has played an important role in providing insight into the physiologic mechanisms of TrPs. A significant 71% correlation between TrPs and acupuncture points has been observed when comparing their spatial distributions and pain referral patterns (3). Further evidence of this correlation has recently been supported by using electrophysiologic comparisons of TrPs and acupoint locations. A recent descriptive term has been proposed - secondary hyperalgesic locus. This term is thought to represent the trigger point/acupoint phenomenon (4).

Myofascial Trigger Points and Myofascial Pain Physiologic Mechanisms:
The current viewpoint is that TrPs are caused by local mechanical trauma. However, emerging evidence now suggests that TrPs may be neurogenic manifestations of primary pathologies found elsewhere within the common neurologic segment (also called a neuromeric field). Research has also evolved with an “integrated hypothesis” of TrP formation which states TrPs are “initiated by a local, acute or chronic overload injury of the myotendinous unit, leading to increased motor end plate activity, persistent release of acetylcholine, and focal hypertonicity which is typically present in TrP regions”. If allowed to persist, this process results in hypoxia and subsequent release of vasoactive, inflammatory, and algogenic substances. This causes tissue hypersensitivity as well as local autonomic effects. As this cycle develops it becomes self-sustaining, and unless interrupted, leads to the initiation of an “active” TrP.

While not always a result of local injury, TrPs have also been linked to medical conditions related to musculoskeletal, metabolic, visceral, endocrine, infectious and psychological origin. The question remains whether TrPs are initiated by a local mechanical trauma to the myotendinous unit, or whether they exist as a function of an underlying pathology. TrPs also exist in non-musculoskeletal pathologies – all void of local trauma (e.g. pelvic urogenital syndromes, herpes zoster infection and pyogenic sacroiliitis). It has also been noted that TrPs can occur with non-traumatic conditions such as psychological distress and fibromyalgia.

TrPs express unique physiologic properties, suggesting their association with neurogenic mechanisms. TrPs have regional aggregations of multiple “sensitive” and “active” loci which represent sensitized nociceptors and sensitized motor end plates, respectively. The result is a stimulation of sensitive loci which evoke referred pain (which is not evoked by comparable stimulation of adjacent normal tissue). The induction of referred pain from site-specific stimulation of TrPs reveals that TrPs may be networked via sensitized TrP circuits. Within active TrPs are specific sites that produce spontaneous end plate activity (SEA). This SEA is characterized by spontaneous low-amplitude noise combined with intermittent, higher amplitude spikes. The result is an intermittent release of acetylcholine, something that is not seen in a normal end plate.

The neurogenic nature of TrPs is supported by the coexistence of both active and sensitive loci in the TrP region. The anatomical basis is that sensitive loci are sensitized nociceptors linked to afferent pathways, while active loci are sensitized motor end plates positioned at the terminal end of efferent pathways. Due to this coexistence, there exists the possibility that these sensitized pathways may be initiated centrally, within their common spinal segment. It is important to note that stimulation of TrP pain evokes a soothing ache which does not activate a withdrawal reflex. The opposite occurs with acute tissue stimulation which evokes a sharp, noxious and well-demarcated pain as well as the withdrawal reflex. This distinct behavior supports additional evidence that TrPs may not be local acute injury but rather, a neurogenic phenomenon.

Novel Concepts Emerging in the Research of Myofascial Trigger Points and Myofascial Pain:
Observations of the unique anatomic and physiologic characteristics of TrPs have created novel hypotheses, providing new insight into the possible initiating mechanisms of MPS and corresponding TrPs. The underlying foundation is that they are neurogenic expressions and not primarily a result of acute injury:
  • Neurogenic Hypothesis of Trigger Point Formation: Myofascial trigger points are a myofascial expression of central sensitization. Central sensitization creates TrP formations and is evoked by a primary pathology located within the common neurologic segment of the tissue containing the TrP. The resulting observed local anatomic and physiologic changes at the TrP are secondary to neurogenic inflammation triggered by central sensitization.
  • Central Sensitization and Neurogenic Inflammation (The neurophysiologic bases for the neurogenic hypothesis): Central sensitization and neurogenic inflammation provide the cornerstones of the neurogenic hypothesis. While central sensitization is the physiologic increase in the responsiveness of neurons within the CNS (see Related Review below), the mechanism by which it can induce the formation of a TrP is through neurogenic inflammation. This neurogenically mediated inflammation refers to the discharge of inflammatory mediators and neuropeptides (such as substance P or calcitonin gene-related peptide) from the peripheral terminals of nociceptors in tissues (both visceral and somatic) that are neurologically linked to a primary pathology. Sensitization of peripheral nociceptors develops due to a cascade of inflammatory events and biochemical changes. This in turn results in the formation of discrete tender locus characteristics of the TrP region. Autonomic effects to the TrPs are also thought to result from central sensitization.
  • Myofascial Trigger Point Formation can Result from any Pathologic Focus: Formation of MPS and TrPs can occur from either musculoskeletal or non-musculoskeletal pathologies. Evidence suggests that persistent pain of visceral origin has been shown to cause neurogenic plasma extravasation and trophic skin changes in zones of referral. Neurogenic inflammation has also been linked to other nonmusculoskeletal pathologies (e.g. irritable bowel syndrome, cystitis and changes in both uterine and bladder contractility).
  • Trigger Point Formation Follows Segmental Patterns: Evidence supports a segmental relationship between TrPs in muscles that are segmentally linked to primary disc pathology as well as a segmental correlation between central sensitization and TrP sensitivity. When central sensitization is reduced by treating the primary pathology, there is a reduction in TrP sensitivity in segmentally related tissue.
  • Stimulation of TrPs Evoke Systematic Segmental Physiologic Effects by Modulating Central Sensitization: One current hypothesis proposed is that site-specific stimulation of TrPs/acupoints evokes systematic physiologic effects by modulating the level of central sensitization within the common neurosegment of the involved TrP. Research continues to emerge that distinct segmental physiologic effects are evoked by site-specific TrP stimulation. These physiologic responses can occur in ways other than needle stimulation of TrPs. Results have also been attained with the stimulation of acupoints/TrPs with electrical, pressure, magnetic and ultrasound therapeutic modalities. This supports the notion that TrPs are more dependent on site specificity rather than type of modality or intervention applied. This paves the way that functional outcome may be achieved using less invasive, safer and more cost-effective approaches in treating MPS and TrPs.

Clinical Application & Conclusions:

Clinicians need to be aware of MPS as a potential diagnosis, particularly when TrPs predominate the clinical picture. TrPs can be initiated by local trauma or overuse injury and there is accumulating evidence that TrP formation also may be secondary to neurogenic expressions of central sensitization. Both mechanisms may contribute to the pathophysiology.

While there is currently a variety of treatment approaches for myofascial pain (manual therapy, medication, electrotherapy, biofeedback, ischemic compression therapy and cryo/heat therapy), TrP needling (both wet injection and dry needle) is still one of the most popular and widely used treatments. The problem is that these interventions assume that the TrP is the primary site of pathology. When managing this condition, we must also consider the possibility that MSP is a neurogenic condition.

Treatment and Management of MPS:
  • Identify the Primary Pathology That Causes Central Sensitization: Differential diagnostics are necessary in the identification of the primary pathology contributing to central sensitization and its relationship to TrP involvement. Therapeutic intervention for MPS is then focused on treatment of both the symptomatic TrPs as well as the underlying pathology.
  • Treatment Must Focus on Management of Central Sensitization: It is important to note that myofascial pain is not equivalent to musculoskeletal pain and that an important factor in the treatment of MPS is modulation of central sensitization. TrP stimulation is an important component in intervention as well, with emphasis on site specificity (most important factor), segmental stimulation and modality selection. Inconsistent site specificity leads to discrepancies and unfavorable results. Future research should aim to standardize treatment protocols for TrP/acupoints to allow comparison of results. A neurosegmental paradigm is also necessary to correlate TrPs with acupoints (meridians have been shown to follow referral patterns quite closely).
  • The Potential Role of Therapeutic Ultrasound: While the precise physiologic mechanism and validity of ultrasound (US) is still in question, it is emerging as a promising modality in the treatment of MPS. Recent research involving ultrasound suggests a potential role as a neuromodulator in pain management. US has shown promise for creating antinociceptive effects versus needle stimulation for TrP treatment. Overall, more research is required.
Future research should focus on the management of MPS and TrPs. Key concepts include site specificity of interventions and standardized treatment protocols for consistency between studies to advance treatment and management of MPS. Due to a growing elder patient population afflicted with MPS (prevalence of 85% with elderly > 65 yoa), elucidating the mechanisms of MPS and advancing treatment remain high priorities.

Study Methods:

This was a narrative literature review. No conflicts of interest reported by the author or any individuals in control of the content of this article.<>

Study Strengths / Weaknesses:

This review provides a very strong, well written report on emerging trends in the treatment and management of myofascial pain syndrome. The author, an expert in TrPs, provides a clear outline regarding the role central sensitization plays in MPS as well as to providing a greater understanding of TrP mechanisms. One area that was limited was the management portion of the review which primarily focused on the use of ultrasound as a treatment modality. Further information should have been included about current research available such as the outcome studies of manual therapy, medication, electrotherapy, acupuncture or ischemic compression therapy in addressing MPS and the treatment of TrPs.

Additional References:

  1. Gerwin RD. A review of myofascial pain and fibromyalgia—factors that promote their persistence. Acupuncture Medicine 2005; 23: 121-134.
  2. Staud R. Future perspectives: pathogenesis of chronic muscle pain. Best Pract Res Clin Rheumatol 2007; 21: 581-596.
  3. Melzack R, Stillwell D, Fox E. Trigger points and acupuncture points for pain: correlations and implications. Pain. 1977; 3: 3-23.
  4. Srbely J, Dickey J, Lee D, Lowerison M. Needle stimulation of a myofascial trigger point causes segmental antinociceptive effects. Journal of Rehabilitation Medicine 2010; 42: 463–468.