Valerie Phelps, PT ScD OCS FAAOMPT and Vicente Mauri-Stecca, PT ScD COMT

Myofascial pain can be complicated to assess, however specific pain generator(s) can often be identified clinically.  Classification according to specific characteristics facilitates the examination and interpretation process, thereby guiding selection of management strategies specific to the problem. Duration, location, quality and potential etiology of muscle pain are important factors to consider within the clinical reasoning process.

Duration. Muscle pain duration can be classified as acute/subacute, recurrent, or chronic. Generally, acute and subacute duration encompasses a timeframe of less than 3 months, whereas recurrent relates to a condition that is acute/subacute but occurs repeatedly for months to years. Finally, chronic describes both a duration – over 3 months – and involves heightened activity of the central and autonomic nervous systems. For example, transition of acute localized myofascial pain to chronic widespread myofascial pain involves several mechanisms underlying deep-tissue hyperalgesia, temporal summation, referred pain and altered descending control.(1)

Location. Transition from acute/subacute to recurrent to widespread chronic pain generally coincides with myofascial pain location. Here the pain can be categorized as localized, regional, or widespread pain, respectively. Regional pain is characterized by localized tenderness with referred pain, such as in the instance of active myofascial trigger points. Myofascial trigger points, a key component of myofascial pain syndrome, are witnessed in various recurrent pain conditions such as tension-type headache and orofacial pain as well as recurrent back, neck and shoulder pain. (1) Thus, these conditions could fall in the myofascial pain category. In these conditions affected muscles can be painful during movement and cause subjective weakness, increased fatigability, stiffness and a slightly restricted range of motion that is unrelated to joint restriction. Widespread musculoskeletal pain is generally observed bilaterally, both above and below the waistline, and involves axial structures. Syndromes involving widespread pain can additionally fall in the chronic category, such as fibromyalgia and chronic fatigue syndrome.

Quality. Muscle pain (myalgia) is often diffuse and more likely to reproduce referred pain.(2) (3) (4) ‘‘Cramping’’, ‘‘aching’’ and ‘‘tearing’’ are terms commonly used to describe muscle pain.(5) (6)

Etiology. Acute musculoskeletal pain occurs in response to stimulation of deep-tissue polymodal nociceptors related to Aδ and C afferent fibers that release sensitizing neuropeptides, thus leading to nociceptor sensitization and secondary hyperalgesia (peripheral sensitization). Spontaneous pain from a damaged muscle can be explained by the release of algesic substances from the lesion, which directly excite the nociceptors. Peripheral sensitization, if persistent, can trigger a central sensitization response. As a consequence, ongoing nociceptor activity further sensitizes neurons in the dorsal horn, expanding receptor fields and leading to enhanced responsiveness to both noxious and non-noxious stimuli (central sensitization).(5) (7) (8) (1) Not only are receptor fields enlarged by persistent skeletal muscle nociceptor activity, new receptor fields have been found to develop that would lead to a mislocation of the pain source.(9)

Patients suffering from fibromyalgia and chronic fatigue syndrome exhibit central sensitization, lending to their chronic symptomology. In conditions of central sensitization, central integrative mechanisms are upregulated, resulting in facilitated temporal summation of nociceptive signals. Several studies support the involvement of central sensitization in chronic myofascial pain, based on findings of facilitated temporal summation in patients suffering from this disorder. (1) (10) (11) Interestingly, when central sensitization was antagonized in patients with fibromyalgia by using the anesthetic ketamine, the expanded referred pain distribution was reduced and partially normalized.(4)

In a literature review by Queme LF et al., published in 2017, various authors have hypothesized that peripheral perfusion anomalies are also major contributors to painful symptoms present in widespread chronic pain conditions like fibromyalgia.(6) Evidence shows that these conditions are characterized by the impaired perfusion within the painful areas of the body, which is consistent with decreased blood flow response during static and dynamic contractions. (6) The peripheral perfusion anomaly manifests in the phenomenon of experiencing worse pain with exercise; the clinician should be very aware of the fact that exercised muscles in a patient with fibromyalgia experience less blood flow, and therefore decreased pain thresholds (resulting in flare up).

Descending pain control refers to the maintenance of the excitability along the neuro-axis; the manifestation of central sensitization may be due to an imbalance between descending inhibition and facilitation of pain. (1) Indeed Jensen et al (2009) demonstrated reduced activation of the rostral cingulate cortex in patients with fibromyalgia compared to healthy subjects; this brain area is likely essential in the control of descending pain modulation, suggesting a compromise in this patient population. (12)

Understanding how muscle pain may arise from peripheral or central sensitization across various conditions and injury types, and how it can be clinical assessed are important key characteristics for increasing the efficacy of specific pain management approaches.

  • Part 2: Differentiation of acute, from recurrent, from chronic myofascial pain: clinical signs and symptoms related to acute muscle tear, versus trigger points, versus fascial pain, versus ischemia reperfusion injury.
  • Part 3: Management strategies specific to the pathology


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  2. Bonica, JJ. The Management of Pain. Philadelphia : Lea and Febiger, 1954. Vol. First Edition.
  3. Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation . Mense, S, et al. 6, 2003, J Apple Physiol, Vol. 94, pp. 2494-2501.
  4. Ketamine reduces muscle pain, temporal summation, and referred pain in fibromyalgia patients. Graven-Nielsen, T, et al. 2000, Pain, Vol. 85, pp. 483-491.
  5. Nociception from skeletal muscle in relation to clinical muscle pain. Mense, S. 1993, Pain, Vol. 54, pp. 241-289.
  6. Peripheral Mechanisms of Ischemic Myalgia. Queme, LF, Ross, JL and Jankowski, MP. 419, 2017, Fron Cell Neurosc, Vol. 11, p. doi: 10.3389/fncel.2017.00419.
  7. Melzack, R and Wall, PD. The Challenge of Pain. London : Penguin Books, 1996.
  8. Recent advances in the neurophysiology of chronic pain. Baker, K. 2005, Emergency Medicine of Australasia, Vol. 17, pp. 65-72.
  9. Appearance of new receptive fields in rat dorsal horn neurons following noxious stimulation of skeletal muscle: a model for referral of muscle pain? Hoheisel, U, et al. 1993, Neurosci Lett, Vol. 153, pp. 9-12.
  10. Temporal summation of pain from mechanical stimulation of muscle tissue in normal controls and subjects with fibromyalgia syndrome. Staud, R, et al. 2003, Pain, Vol. 102, pp. 1078-1089. 87-95.
  11. Brain activity associated with slow temporal summation of C-fiber evoked pain in fibromyalgia patients and healthy controls. Staud, R, et al. 2008, Eur J Pain, Vol. 12, pp. 1078-1089.
  12. Evidence of dysfunctional pain inhibition in fibromyalgia reflected in rACC during provoked pain. Jensen, K, et al. 2009, Pain, Vol. 144, pp. 95-100.