Myofascial Pain

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Definition

The myofascial pain syndrome is a common clinical problem of muscle pain involving sensory, motor and autonomic symptoms caused by myofascial trigger points.
A myofascial trigger point is defined as a hyperirritable spot, usually within a taut band of skeletal muscle wich is painful on compression and can give rise to characteristic referred pain, motor dysfunction and autonomic phenomena.

Classification and Clinical Presentation

Myofascial trigger points are classified into active and latent trigger points. An active trigger point is one with spontaneous pain or pain in response to movement that can trigger local or referred pain. A latent trigger point is a sensitive spot with pain or discomfort only elicited in response to compression.

The myofascial trigger points (active or latent) follow common clinical characteristics such as:

• Pain on compression. This may elicit local pain and/or referred pain that is similar to a patient's usual clinical complaint or may aggravate the existing pain.
• Local twitch response. Snapping palpation (compression across the muscle fibers rapidly) may elicit a local twitch response, which is a quick contraction of the muscle fibers in or around the taut band.
• Muscle tightness. Restricted range of stretch, and increased sensitivity to stretch, of muscle fibers in a taut band may cause tightness of the involved muscle.
• Local myasthenia. The muscle with a trigger point may be weak, but usually no atrophy can be noticed.
• Patients with trigger points may have associated localized autonomic phenomena, including vasoconstriction, pilomotor response and hypersecretion.

Spontaneous electrical activity (SEA) has also been recorded in myofascial trigger point sites. The  site of this electrical activity is called "active locus". SEA consists of continuous, noise-like action potentials that can range from 5 to 50 µV, with intermittent large amplitude spikes up to 600 µV. This abnormal endplate potential is caused by an excessive release of acetylcholine at the motor endplate. The magnitude of SEA is related to the pain intensity in patients with myofascial trigger points.

Etiology

Several possible mechanisms can lead to the development of trigger points, including :

• Prolonged muscle contractures: Initially the taut band formation can reflect a muscle contracture. Prolonged contractures are likely to lead to the formation of latent trigger points, which can eventually evolve into active trigger points.
• Low-level muscle contractions or Cinderella hypothesis: Myofascial trigger point pain can be caused by selective overloading of the earliest recruited and last derecruited motor units ("Henneman's size principle"). Smaller motor units are recruited before and de-recruited after larger ones; as a result, the smaller type I fibers are continuously activated during prolonged motor tasks, wich in turn it can result in metabolically overloaded motor units with a subsequent activation of autogenic destructive processes and muscle pain.
• Postural stress.
• Direct trauma.
• Eccentric contractions in unconditioned or unaccustomed muscle
• Maximal or submaximal concentric contractions.

Pathophysiology

The initial change in muscle that is associated with the myofascial pain, and therefore, with trigger points seems to be the development of the taut band, wich is in term a motor abnormality. Several mechanisms have been hypothesied to explain this motor abnormality, the most accepted one is the "Integrated Hypothesis" first developed by Simmon and later expanded by Gerwin.

Simmons' integrated hypothesis is a six-link chain that starts with the abnormal release of acetylcholine. This triggers an increase in muscle fiber tension (formation of taut band). The taut band is thought to constrict blood flow that leads to local hypoxia. The reduced oxygen disrupts mitochondrial energy metabolism reducing ATP and leads to tissue distress and the release of sensitizing substances. These sensitizing substances lead to pain by activation of nociceptors and also lead to autonomic modulation that then potentiates the first step: abnormal acetylcholine release.

Gerwin expanded this hypothesis by adding more specific details. He stated that sympathetic nervous system activity augments acetylcholine release and that local hypoperfusion caused by the muscle contraction (taut band) resulted in muscle ischemia or hypoxia leading to an acidification of the pH. The prolonged ischemia also leads to muscle injury resulting in the release of potassium, bradykinins, cytokines, ATP, and substance P which might stimulate nociceptors in the muscle. The end result is the tenderness and pain observed in myofascial trigger points. Depolarization of nociceptive neurons causes the release of calcitonin gene-related peptide (CGRP). CGRP inhibits acetylcholine esterase, increases the sensitivity of acetylcholine receptors and release of acetylcholine resulting in SEA (stated above).

In recent studies Shah et al. confirmed the presence of these substances using microdyalisis techniques at trigger point sites. Elevations of substance P, CGRP, bradykinin, serotonin, and cytokines were found in active trigger points compared to normal muscle or even latent trigger points. The pH of the active trigger point region was decreased to pH 4 (normal pH value is 7.4) causing muscle pain and also a decrease in acetylcholinesterase activity resulting in a prolonged muscle contraction.

References

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