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Mechanisms of Myofascial Pain.

Jafri MS - Int Sch Res Notices (2014)

Bottom Line: It affects a majority of the general population, impairs mobility, causes pain, and reduces the overall sense of well-being.This is likely due to the complex nature of the disorder which involves the integration of cellular signaling, excitation-contraction coupling, neuromuscular inputs, local circulation, and energy metabolism.Based on new findings linking mechanoactivation of reactive oxygen species signaling to destabilized calcium signaling, we put forth a novel mechanistic hypothesis for the initiation and maintenance of myofascial trigger points.

View Article: PubMed Central - PubMed

Affiliation: Krasnow Institute for Advanced Study, George Mason University, 4400 University Drive, MNS 2A1, Fairfax, VA 22030, USA.

ABSTRACT

Myofascial pain syndrome is an important health problem. It affects a majority of the general population, impairs mobility, causes pain, and reduces the overall sense of well-being. Underlying this syndrome is the existence of painful taut bands of muscle that contain discrete, hypersensitive foci called myofascial trigger points. In spite of the significant impact on public health, a clear mechanistic understanding of the disorder does not exist. This is likely due to the complex nature of the disorder which involves the integration of cellular signaling, excitation-contraction coupling, neuromuscular inputs, local circulation, and energy metabolism. The difficulties are further exacerbated by the lack of an animal model for myofascial pain to test mechanistic hypothesis. In this review, current theories for myofascial pain are presented and their relative strengths and weaknesses are discussed. Based on new findings linking mechanoactivation of reactive oxygen species signaling to destabilized calcium signaling, we put forth a novel mechanistic hypothesis for the initiation and maintenance of myofascial trigger points. It is hoped that this lays a new foundation for understanding myofascial pain syndrome and how current therapies work, and gives key insights that will lead to the improvement of therapies for its treatment.

No MeSH data available.


Related in: MedlinePlus

Hypothesis of how changes to the affected region cause a sustained perturbation yielding a trigged point. Conceptual phase plane diagrams for intracellular [Ca2+] and [ROS]. (a) The [ROS] cline (red) intersects the [Ca2+] cline (blue) at the steady state value for resting [Ca2+] and [ROS] (black dot). (b) With the changes that occur with microtubule proliferation and reduction in the ability of the myocyte to remove ROS, the [ROS] cline shifts to the right higher [ROS] for a given level of [Ca2+] resulting in a higher steady-state [ROS] and [Ca2+].
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Figure 3: Hypothesis of how changes to the affected region cause a sustained perturbation yielding a trigged point. Conceptual phase plane diagrams for intracellular [Ca2+] and [ROS]. (a) The [ROS] cline (red) intersects the [Ca2+] cline (blue) at the steady state value for resting [Ca2+] and [ROS] (black dot). (b) With the changes that occur with microtubule proliferation and reduction in the ability of the myocyte to remove ROS, the [ROS] cline shifts to the right higher [ROS] for a given level of [Ca2+] resulting in a higher steady-state [ROS] and [Ca2+].

Mentions: Considering that the two nociceptors above most likely are involved in the sensation of pain in the environment of trigger points, the question arises—why are some trigger points latent and some active? We hypothesize that pain is likely felt with manipulation of trigger points as the cytoskeleton is being stretched and reactive oxygen species production increased activation of more nociceptors. Some trigger points might be active because the local extracellular reactive oxygen species concentration in the location of the TRPV1 receptors is high enough for their activation. This requires that these receptors be close enough to the trigger point (Figure 3). Shown are three curves for the ROS level (blue), proton concentration (red), and ROS level upon palpation (green). The active trigger points are likely located closer to pain receptor channels so that the receptors see high levels of protons and ROS. Hence both ASIC3 and TRPV1 channels are activated. Latent channels are farther away so that they see lower levels of ROS (which dissipates faster than the pH gradient as ROS are unstable and larger molecules). Experimental studies have indicated that pressing on a cell activates stretch-activated channels causing increases in myoplasmic calcium [123]. This suggests that palpation might also trigger stretch-activated processes such as X-ROS signaling. Therefore, when palpated, the ROS levels might rise resulting in activation of the TRPV1 channels causing pain.


Mechanisms of Myofascial Pain.

Jafri MS - Int Sch Res Notices (2014)

Hypothesis of how changes to the affected region cause a sustained perturbation yielding a trigged point. Conceptual phase plane diagrams for intracellular [Ca2+] and [ROS]. (a) The [ROS] cline (red) intersects the [Ca2+] cline (blue) at the steady state value for resting [Ca2+] and [ROS] (black dot). (b) With the changes that occur with microtubule proliferation and reduction in the ability of the myocyte to remove ROS, the [ROS] cline shifts to the right higher [ROS] for a given level of [Ca2+] resulting in a higher steady-state [ROS] and [Ca2+].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4285362&req=5

Figure 3: Hypothesis of how changes to the affected region cause a sustained perturbation yielding a trigged point. Conceptual phase plane diagrams for intracellular [Ca2+] and [ROS]. (a) The [ROS] cline (red) intersects the [Ca2+] cline (blue) at the steady state value for resting [Ca2+] and [ROS] (black dot). (b) With the changes that occur with microtubule proliferation and reduction in the ability of the myocyte to remove ROS, the [ROS] cline shifts to the right higher [ROS] for a given level of [Ca2+] resulting in a higher steady-state [ROS] and [Ca2+].
Mentions: Considering that the two nociceptors above most likely are involved in the sensation of pain in the environment of trigger points, the question arises—why are some trigger points latent and some active? We hypothesize that pain is likely felt with manipulation of trigger points as the cytoskeleton is being stretched and reactive oxygen species production increased activation of more nociceptors. Some trigger points might be active because the local extracellular reactive oxygen species concentration in the location of the TRPV1 receptors is high enough for their activation. This requires that these receptors be close enough to the trigger point (Figure 3). Shown are three curves for the ROS level (blue), proton concentration (red), and ROS level upon palpation (green). The active trigger points are likely located closer to pain receptor channels so that the receptors see high levels of protons and ROS. Hence both ASIC3 and TRPV1 channels are activated. Latent channels are farther away so that they see lower levels of ROS (which dissipates faster than the pH gradient as ROS are unstable and larger molecules). Experimental studies have indicated that pressing on a cell activates stretch-activated channels causing increases in myoplasmic calcium [123]. This suggests that palpation might also trigger stretch-activated processes such as X-ROS signaling. Therefore, when palpated, the ROS levels might rise resulting in activation of the TRPV1 channels causing pain.

Bottom Line: It affects a majority of the general population, impairs mobility, causes pain, and reduces the overall sense of well-being.This is likely due to the complex nature of the disorder which involves the integration of cellular signaling, excitation-contraction coupling, neuromuscular inputs, local circulation, and energy metabolism.Based on new findings linking mechanoactivation of reactive oxygen species signaling to destabilized calcium signaling, we put forth a novel mechanistic hypothesis for the initiation and maintenance of myofascial trigger points.

View Article: PubMed Central - PubMed

Affiliation: Krasnow Institute for Advanced Study, George Mason University, 4400 University Drive, MNS 2A1, Fairfax, VA 22030, USA.

ABSTRACT

Myofascial pain syndrome is an important health problem. It affects a majority of the general population, impairs mobility, causes pain, and reduces the overall sense of well-being. Underlying this syndrome is the existence of painful taut bands of muscle that contain discrete, hypersensitive foci called myofascial trigger points. In spite of the significant impact on public health, a clear mechanistic understanding of the disorder does not exist. This is likely due to the complex nature of the disorder which involves the integration of cellular signaling, excitation-contraction coupling, neuromuscular inputs, local circulation, and energy metabolism. The difficulties are further exacerbated by the lack of an animal model for myofascial pain to test mechanistic hypothesis. In this review, current theories for myofascial pain are presented and their relative strengths and weaknesses are discussed. Based on new findings linking mechanoactivation of reactive oxygen species signaling to destabilized calcium signaling, we put forth a novel mechanistic hypothesis for the initiation and maintenance of myofascial trigger points. It is hoped that this lays a new foundation for understanding myofascial pain syndrome and how current therapies work, and gives key insights that will lead to the improvement of therapies for its treatment.

No MeSH data available.


Related in: MedlinePlus