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      Mechanisms of Myofascial Pain

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      International scholarly research notices

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          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.

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          Most cited references142

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          FAK-Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly.

          Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration.
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            Health-enhancing physical activity and sedentary behaviour in children and adolescents.

            We provide a wide-ranging review of health-related physical activity in children and adolescents using a behavioural epidemiology framework. In contrast to many other reviews, we highlight issues associated with true sedentary behaviours alongside physically active behaviours. Specifically, we review the evidence concerning the links between physical activity and cardiovascular disease, overweight and obesity, psychosocial measures, type II diabetes, and skeletal health. Although the evidence is unconvincing at times, several factors lead to the conclusion that promoting physical activity in youth is desirable. A review of the prevalence of physical activity and sedentary behaviours shows that many young people are active, but this declines with age. A substantial number are not adequately active for health benefits and current trends in juvenile obesity are a cause for concern. Prevalence data on sedentary behaviours are less extensive but suggest that total media use by young people has not changed greatly in recent years. Most children and adolescents do not exceed recommended daily hours of TV viewing. Physical activity is unrelated to TV viewing. We also identified the key determinants of physical activity in this age group, highlighting demographic, biological, psychological, behavioural, social and environmental determinants. Interventions were considered for school, family and community environments. Finally, policy recommendations are offered for the education, governmental, sport and recreation, health, and mass media sectors.
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              Exercise-induced oxidative stress in humans: cause and consequences.

              The observation that muscular exercise is associated with oxidative stress in humans was first reported over 30 years ago. Since this initial report, numerous studies have confirmed that prolonged or high-intensity exercise results in oxidative damage to macromolecules in both blood and skeletal muscle. Although the primary tissue(s) responsible for reactive oxygen species (ROS) production during exercise remains a topic of debate, compelling evidence indicates that muscular activity promotes oxidant production in contracting skeletal muscle fibers. Mitochondria, NADPH oxidase, PLA₂-dependent processes, and xanthine oxidase have all been postulated to contribute to contraction-induced ROS production in muscle but the primary site of contraction-induced ROS production in muscle fibers remains unclear. Nonetheless, contraction-induced ROS generation has been shown to play an important physiological function in the regulation of both muscle force production and contraction-induced adaptive responses of muscle fibers to exercise training. Although knowledge in the field of exercise and oxidative stress has grown markedly during the past 30 years, this area continues to expand and there is much more to be learned about the role of ROS as signaling molecules in skeletal muscle. Copyright © 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                101641951
                43181
                Int Sch Res Notices
                Int Sch Res Notices
                International scholarly research notices
                2356-7872
                2 November 2014
                18 August 2014
                2014
                06 January 2015
                : 2014
                : 523924
                Affiliations
                Krasnow Institute for Advanced Study, George Mason University, 4400 University Drive, MNS 2A1, Fairfax, VA 22030, USA
                Author notes
                Correspondence should be addressed to M. Saleet Jafri; sjafri@ 123456gmu.edu
                Article
                NIHMS638318
                10.1155/2014/523924
                4285362
                25574501
                4e135b35-3704-4c06-b873-357467b1fe7a
                Copyright © 2014 M. Saleet Jafri.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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