The Pathogenesis and Pathophysiology of Myofascial Trigger Points (MTrPs) and Their Role in Myofascial Pain Syndrome (MPS). 

History of MPS as a Diagnosis

• Guillaume de Baillous (1538-1616) of France was one of the first to write in detail about muscle pain disorders. 
• In 1816, the British physician Balfour associated “thickenings” and “nodular tumors” in muscle with local and regional muscle pain. 
• Froriep in 1843 coined the term “muskelshwiele” (muscle callouses) to describe what he believed was a “callus” of deposited connective tissue in patients with rheumatic disorders. 
• In 1904, Gowers suggested that inflammation of fibrous tissue (i.e., “fibrositis”), created the hard nodules. 
• Schade (1919) later proposed that the nodules, which he called “myogeloses”, were high viscosity muscle colloids. 
• In the mid 1900s, important work was conducted independently by Michael Gutstein in Germany, Michael Kelly in Australia, and J.H. Kellgren in Britain. By injecting hypertonic saline into various anatomical structures such as fascia, tendon, and muscle in healthy volunteers, Kellgren was able to chart zones of referred pain in neighbouring and distant tissue. 
• U.S. physician Janet Travell, whose work on myofascial pain, dysfunction, and trigger points is arguably the most comprehensive to date. 
• Travell and Rinzler coined the term “myofascial trigger point” in the 1950s, reflecting their finding that the nodules can be present and refer pain to both muscle and overlying fascia. 
• The current use of the term “MPS” implies a specific condition which presents as regional pain, sometimes with referred pain, often accompanied by increased tension and decreased flexibility. 
• MPS has also been associated with other pain conditions including radiculopathies, joint dysfunction, disk pathology, tendonitis, craniomandibular (jaw) dysfunction, migraines, tension type headaches, carpal tunnel syndrome, computer-related disorders, whiplash-associated disorders, spinal dysfunction, pelvic pain and other urologic syndromes, post-herpetic neuralgia, and complex regional pain syndrome.

MPS Is Different To Fibromyalgia

• It is known to coincide with other diseases and syndromes associated with pain, e.g. rheumatic diseases and fibromyalgia.
• Unlike MPS, fibromyalgia is a widespread and symmetrically-distributed pain condition associated with sleep and mood disturbances. 
• The pain of MPS is usually local or regional and may be found in a limited number of select quadrants of the body.
• MPS has traditionally been thought to present independently of mood or sleep abnormalities, recent studies indicate that MPS is associated with both mood and sleep disruptions. 
• The definition and pathogenesis of MPS is still not fully understood, and disagreement persists as to whether MPS is a disease or process, rather than a syndrome.

Diagnosis For MTrPs; Not Straight Forward

• The current gold standard for the diagnosis of MPS is the physical examination as described in The Trigger Point Manual:

1. Palpation of a taut band; Diagnosis of MPS has been tissue specific and anatomically based on palpation of the skeletal muscle for MTrPs.
2. Identification of an exquisitely tender nodule (MTrP) in the taut band. 
3. Reproduction of the patient's symptomatic pain with sustained pressure.

• An MTrP is a common physical finding and often overlooked of non-articular musculoskeletal pain as its pathophysiology (explanation) is not fully understood. 
• Digital palpation has several limitations. For instance, it lacks adequate sensitivity and specificity.
  
• Besides the use of palpation, there are currently no accepted criteria for identifying or describing MTrPs. 
• Further research is needed to determine not only the role of the MTrP, but also its surrounding area.
• Diagnostic criteria are imprecise, and the full impact of MPS on life activity and function is not fully understood. 
• To complicate this issue further, MTrPs are associated clinically with a variety of medical conditions including those of metabolic, visceral, endocrine, infectious, and psychological origin and are present across a wide range of musculoskeletal disorders. 
• If the MTrP is frequently associated with other musculoskeletal pain syndromes, it would make this finding non-specific — if it is not, it would make the MTrP specific for MPS.
• Muscle pain displays unique clinical characteristics compared to cutaneous (skin) and neuropathic pain, the nature of the symptoms are highly dependent upon the individual's perception of its characteristic qualities (e.g., boring, aching, sharp, etc.), intensity, distribution, and duration. 
• Characteristics like the quality of the pain, its distribution, and whether it radiates, have never been required for the diagnosis of MPS.
• Accurate diagnosis depends upon the examiner's clinical acumen, experience, index of suspicion, training, and palpation skills. 

The Role of Muscle and The Cinderella Hyposthesis

• The Cinderella Fiber Hypothesis was first proposed by Hagg (1990) which explains how low level muscle damage could be brought on via low-threshold motor units (MUs) within muscles which are continuously activated during low level static exertions (LLSEs).
• Types of LLSEs or exertions are typically utilized by occupational groups such as office workers, musicians, hair dressers and dentists. 
• "Cinderella" fibers are small low threshold muscle fibres which can become continuously overloaded and more prone to develop into myofascial trigger points since they are activated longer and are more likely to be metabolically exhausted before other fibres.  
• A study by Treaster et al. (2006) supports the Cinderella Hypothesis by demonstrating that low-level, continuous muscle contractions in office workers during 30 minutes of typing induced formation of MTrPs.
• In contrast, larger motor muscle fibers do not work as hard and spend less time being activated.

• The "Cinderella" fiber theory, alone, fails to explain all aspects of injury related to LLSEs. 
• It fails to explain the exact origin and mechanism of muscle pain as evidence suggests that muscle fiber activity and motor unit recruitment may be a consequence of pain rather than a cause. 
• Low-threshold muscle fibers may fatigue and become metabolically exhausted but this does not explain how pain occurs. 

• A more widely accepted hypothesis is that trigger points develop because some initiating event causes an excessive release of acetylocholine (ACh) from the motor endplates resulting in increased fiber tension and localized ischemia. 
  
• The localized ischemia restricts the blood flow and insufficient ATP synthesis which is needed to restore energy. The increased demand and reduced supply of ATP forms the energy crisis and encourages the release of neuroreactive substances and metabolic byproducts (i.e., bradykinin (BK), substance P (SP), serotonin (5-HT)) which causes the peripheral nociceptors to become sensitive.
• Without ATP, the sarcoplasmic reticulum does not function correctly and the muscle sarcomeres remain contracted as the lack of energy (ATP) means that the the actin and myosin cross-bridges cannot disengage or release. 
• ATP is also needed by the calcium (Ca2+) pump to remove calcium (Ca2+) from the muscle binding sites and restore them to the sarcoplasmic reticulum. Calcium (Ca2+) is needed and binds to troponin on the muscle fibers, which makes the muscle fibers contract.
• Localized areas containing "contraction knots" are believed to release sensitizing agents and additional acetylcholine (ACh) that cycles back to cause increased fiber tension. 
• A feedback loop to maintain contraction is created and a self perpetuating cycle is established. 
• Until this positive-feedback loop is interrupted, the muscle sarcomeres at the TrP remain in a shortened state, resulting in a local energy crisis.