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== Definition ==
== Definition ==
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The myofascial pain syndrome is a common clinical problem of muscle pain involving sensory, motor and autonomic symptoms caused by myofascial trigger points. Despite myofascial pain is a commonly found in clinical practice, there are few prevalence studies found in the scientific literature. Skootsky et al.<ref name="prevalence">Skootsky, S. A., Jaeger, B. Oye, R. K. (1989). Prevalence of myofascial pain in general internal medicine practice. Western Journal of Medicine, 151(2), 157.</ref> found that 30% of patients that visited a primary care unit presented myofascial trigger points. In a recent study regarding shoulder pain Bron et al. concluded that all 72 subjects included in their study presented myofascial trigger points in shoulder girdle muscles, mainly in the infraspinatus muscle and upper trapezius.<ref name="shoulder">Bron, C., Dommerholt, J., Stegenga, B., Wensing, M.,
&amp;amp;amp;amp;amp;amp;amp;amp;amp;
Oostendorp, R. A. (2011). High prevalence of shoulder girdle muscles with myofascial trigger points in patients with shoulder pain. BMC musculoskeletal disorders, 12(1), 139.</ref> YOU SAY THIS IS A COMMON PROBLEM>>PLEASE CAN YOU REFErCE AND GIVE STATISTICS TO SUBSTATITAE THIS CLAIM.<br>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.<ref name="simmons">Travell JG, SimmonsDG. Myofascial Pain and Dysfunction: The Trigger Point Manual. 2nd ed. Vol 1. Baltimore, MD: Williams and Wilkins; 1999</ref><br>
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The myofascial pain syndrome is a common clinical problem of muscle pain involving sensory, motor and autonomic symptoms caused by myofascial trigger points. Despite myofascial pain is a commonly found in clinical practice, there are few prevalence studies found in the scientific literature. Skootsky et al.<ref name="prevalence">Skootsky, S. A., Jaeger, B. Oye, R. K. (1989). Prevalence of myofascial pain in general internal medicine practice. Western Journal of Medicine, 151(2), 157.</ref> found that 30% of patients that visited a primary care unit presented myofascial trigger points. In a recent study regarding shoulder pain Bron et al. concluded that all 72 subjects included in their study presented myofascial trigger points in shoulder girdle muscles, mainly in the infraspinatus muscle and upper trapezius.<ref name="shoulder">Bron, C., Dommerholt, J., Stegenga, B., Wensing, M., Oostendorp, R. A. (2011). High prevalence of shoulder girdle muscles with myofascial trigger points in patients with shoulder pain. BMC musculoskeletal disorders, 12(1), 139.</ref> YOU SAY THIS IS A COMMON PROBLEM>>PLEASE CAN YOU REFErCE AND GIVE STATISTICS TO SUBSTATITAE THIS CLAIM.<br>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.<ref name="simmons">Travell JG, SimmonsDG. Myofascial Pain and Dysfunction: The Trigger Point Manual. 2nd ed. Vol 1. Baltimore, MD: Williams and Wilkins; 1999</ref><br>
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When the pain resulting from an active trigger point becomes persistant the patient may develop satellite trigger points. A satellite trigger point is localized in the referral zone of the primary trigger point (i.e. the active trigger point that was originaly activated), usualy in an overloaded synergist muscle<ref name="simmons" />. This referal zone corresponds to the pain pattern described by the patient, it is often described as a difuse pain, usualy distant to the active trigger point location. This is explained by the effects of [[Central sensitization]] and each trigger point has its own referal zone. PLEASE CAN YOU EXPLAIN THE TERMs 'REFRERAL ZONE & PRIMARY TRIGGER POINT'
When the pain resulting from an active trigger point becomes persistant the patient may develop satellite trigger points. A satellite trigger point is localized in the referral zone of the primary trigger point (i.e. the active trigger point that was originaly activated), usualy in an overloaded synergist muscle<ref name="simmons" />. This referal zone corresponds to the pain pattern described by the patient, it is often described as a difuse pain, usualy distant to the active trigger point location. This is explained by the effects of [[Central sensitization]] and each trigger point has its own referal zone. PLEASE CAN YOU EXPLAIN THE TERMs 'REFRERAL ZONE & PRIMARY TRIGGER POINT'
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Another interesting clinical characteristic is the spontaneous electrical activity (SEA) recorded in myofascial trigger point sites with needle electromyography<ref name="sea">Hubbard, D. R., Berkoff, G. M. (1993). Myofascial trigger points show spontaneous needle EMG activity. Spine, 18(13), 1803-1807.</ref>. 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. HOW IS THIS MEASURED< IS IT DETECTABLE IN CLNICAL PRACTCIE?
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Another interesting clinical characteristic is the spontaneous electrical activity (SEA) recorded in myofascial trigger point sites with needle electromyography<ref name="sea">Hubbard, D. R., Berkoff, G. M. (1993). Myofascial trigger points show spontaneous needle EMG activity. Spine, 18(13), 1803-1807.</ref>. 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
. In clinical practice, there is no benefit in using needle electromyography and its utility is limited to research studies
. HOW IS THIS MEASURED< IS IT DETECTABLE IN CLNICAL PRACTCIE?
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THIS SECTION IS A LITTLE CONFUSING. YOU MENTION ON SEVERL OCCASSIONS THERE IS NO AGREED CONCENSUS ON SEVERAL ASECTS OF THE ETIOLOGY..I WOULD LIKE SOME OF THESE TO BE EXPLORED TO GIVE A CRITICAL ELEMENT TO THE ARTICLE.
THIS SECTION IS A LITTLE CONFUSING. YOU MENTION ON SEVERL OCCASSIONS THERE IS NO AGREED CONCENSUS ON SEVERAL ASECTS OF THE ETIOLOGY..I WOULD LIKE SOME OF THESE TO BE EXPLORED TO GIVE A CRITICAL ELEMENT TO THE ARTICLE.
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Several possible mechanisms can lead to the development of myofascial trigger points, including low-level muscle contractions, muscle contractures, direct trauma, unaccustomed eccentric contractions, eccentric contractions in unconditioned muscle, and maximal or submaximal concentric contractions.<ref name="simmons" /><ref name="fernandez" /><ref name="gerwin4">Gerwin, R. D. (2001). Classification, epidemiology, and natural history of myofascial pain syndrome. Current pain and headache reports, 5(5), 412-420.</ref><ref name="bron2">Bron, C.,
&amp;
Dommerholt, J. D. (2012). Etiology of myofascial trigger points. Current pain and headache reports, 16(5), 439-444.</ref><br>
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Several possible mechanisms can lead to the development of myofascial trigger points, including low-level muscle contractions, muscle contractures, direct trauma
, muscle overload, postural stress
, unaccustomed eccentric contractions, eccentric contractions in unconditioned muscle, and maximal or submaximal concentric contractions.<ref name="simmons" /><ref name="fernandez" /><ref name="gerwin4">Gerwin, R. D. (2001). Classification, epidemiology, and natural history of myofascial pain syndrome. Current pain and headache reports, 5(5), 412-420.</ref><ref name="bron2">Bron, C., Dommerholt, J. D. (2012). Etiology of myofascial trigger points. Current pain and headache reports, 16(5), 439-444.</ref><br>
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<u>Low level muscle contractions</u>: <br> Low-level muscle contractions involve a selective overload of the earliest recruited and last derecruited motor units ("Henneman's size principle"<ref name="henneman">Enoka, R. M. Stuart, D. G. (1984). Henneman's ‘size principle’: current issues. Trends in neurosciences, 7(7), 226-228.</ref>). Smaller motor units are recruited before and derecruited 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, this is also known as the Cinderella hypothesis<ref name="thorn">Thorn, S., Forsman, M., Zhang, Q. Taoda, K. (2002). Low-threshold motor unit activity during a 1-h static contraction in the trapezius muscle. International Journal of Industrial Ergonomics, 30(4), 225-236.</ref><ref name="kallenberg">Kallenberg, L. A., Hermens, H. J. (2006). Motor unit action potential rate and motor unit action potential shape properties in subjects with work-related chronic pain. European journal of applied physiology, 96(2), 203-208.</ref>.
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<u>Low level muscle contractions</u>:<br> Low-level muscle contractions involve a selective overload of the earliest recruited and last derecruited motor units ("Henneman's size principle"<ref name="henneman">Enoka, R. M. Stuart, D. G. (1984). Henneman's ‘size principle’: current issues. Trends in neurosciences, 7(7), 226-228.</ref>). Smaller motor units are recruited before and derecruited 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, this is also known as the Cinderella hypothesis<ref name="thorn">Thorn, S., Forsman, M., Zhang, Q. Taoda, K. (2002). Low-threshold motor unit activity during a 1-h static contraction in the trapezius muscle. International Journal of Industrial Ergonomics, 30(4), 225-236.</ref><ref name="kallenberg">Kallenberg, L. A., Hermens, H. J. (2006). Motor unit action potential rate and motor unit action potential shape properties in subjects with work-related chronic pain. European journal of applied physiology, 96(2), 203-208.</ref>.
<u>Muscle contractures:</u><br> Prolonged contractures are likely to lead to the formation of taut bands inside muscle fibres. The taut band is the first sign of the muscular response to biomechanical stress. This can lead to the formation of latent trigger points, which can eventually evolve into active trigger points<br>
<u>Muscle contractures:</u><br> Prolonged contractures are likely to lead to the formation of taut bands inside muscle fibres. The taut band is the first sign of the muscular response to biomechanical stress. This can lead to the formation of latent trigger points, which can eventually evolve into active trigger points<br>
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Other mechanisms
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<u>Direct trauma
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</u><br> Direct trauma may create a vicious cycle of events wherein damage to the sarcoplasmic reticulum or the muscle cell membrane may lead to an increase of the calcium concentration, a subsequent activation of actin and myosin, a relative shortage of adenosine triphosphate (ATP), and an impaired calcium pump, which in turn will increase the intracellular calcium concentration even more, completing the cycle. As a result taut bands inside muscle may be developed and lead to the formation of active or latent myofascial trigger points.<br>
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*Muscle overload.
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Maximal or submaximal concentric contractions
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During maximal or submaximal concentric contractions high amounts of energy (ATP) are required. When the demands of exercise begin to exceed the ability of the muscle cells to produce ATP, anaerobe glycolysis will begin consuming more and more of the available intracellular ATP. The muscle will eventually run out of ATP and sustained muscle contractions may occur, starting the development of trigger points
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*Postural stress.
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*Direct trauma.
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*Eccentric contractions in unconditioned or unaccustomed muscle
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Maximal or submaximal concentric contractions
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== Pathophysiology ==
== Pathophysiology ==
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Gerwin expanded this hypothesis by adding more specific details<ref name="gerwin" />. 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. <br> 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. <br> Depolarization of nociceptive neurons causes the release of calcitonin gene-related peptide (CGRP). <br> CGRP inhibits acetylcholine esterase, increases the sensitivity of acetylcholine receptors and release of acetylcholine resulting in SEA.<br> In recent studies Shah et al.<ref>Shah, J. P., Danoff, J. V., Desai, M. J., Parikh, S., Nakamura, L. Y., Phillips, T. M., & Gerber, L. H. (2008). Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Archives of physical medicine and rehabilitation, 89(1), 16-23.</ref> confirmed the presence of these substances using microdyalisis techniques at trigger point sites. Elevations of substance P, protons (H+), CGRP, bradykinin, serotonin, norepinephrine, TNF, interleukines, 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 as low as pH 4 (normal pH value is 7,4) causing muscle pain and tenderness as well as a decrease in acetylcholine esterase activity resulting in sustained muscle contractions.<br>
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Gerwin expanded this hypothesis by adding more specific details<ref name="gerwin" />. 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. <br> 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. <br> Depolarization of nociceptive neurons causes the release of calcitonin gene-related peptide (CGRP). <br> CGRP inhibits acetylcholine esterase, increases the sensitivity of acetylcholine receptors and release of acetylcholine resulting in SEA.<br> In recent studies Shah et al.<ref>Shah, J. P., Danoff, J. V., Desai, M. J., Parikh, S., Nakamura, L. Y., Phillips, T. M., &
amp;amp;
amp; Gerber, L. H. (2008). Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Archives of physical medicine and rehabilitation, 89(1), 16-23.</ref> confirmed the presence of these substances using microdyalisis techniques at trigger point sites. Elevations of substance P, protons (H+), CGRP, bradykinin, serotonin, norepinephrine, TNF, interleukines, 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 as low as pH 4 (normal pH value is 7,4) causing muscle pain and tenderness as well as a decrease in acetylcholine esterase activity resulting in sustained muscle contractions.<br>
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<references />
<references />
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[[Category:Pain]] [[Category:PPA_Project]]
[[Category:Pain]] [[Category:PPA_Project]]