New perspectives on the development of muscle contractures following central motor lesions. (7th December 2016)

• Record Type: Journal Article
• Authors: Pingel, J.; Bartels, E. M.; Nielsen, J. B.
• Is Part Of: Journal of physiology. Volume 595:Number 4(2017:Feb.)
• Page Start: 1027
• Page End: 1038
• Publication Date: 2016-12-07
• Subjects: contracture -- motor control -- skeletal muscle; Physiology -- Periodicals; 612.005
• DOI: 10.1113/JP272767
• Languages: English
• ISSNs: 0022-3751

Abstract

Abstract : This figure summarizes the current unresolved questions regarding the development of muscle contractures. Central motor lesions cause an adaptation in tissue homeostasis in the neuromuscular–tendon–connective tissue complex. This new state of homeostasis affects several mechanisms in the muscle including growth, atrophy, genetics, epigenetics, chemotransduction, mechanotransduction and vascularization. It is this complex adaptation that we need to understand in order to prevent and treat muscle contractures. Abstract: Muscle contractures are common in patients with central motor lesions, but the mechanisms responsible for the development of contractures are still unclear. Increased or decreased neural activation, protracted placement of a joint with the muscle in a short position and muscle atrophy have been suggested to be involved, but none of these mechanisms are sufficient to explain the development of muscle contractures alone. Here we propose that changes in tissue homeostasis in the neuromuscular–tendon–connective tissue complex is at the heart of the development of contractures, and that an integrated physiological understanding of the interaction between neural, mechanical and metabolic factors, as well as genetic and epigenetic factors, is necessary in order to unravel the mechanisms that result in muscle contractures. We hope thereby to contribute to a reconsideration of how and why muscle contractures develop in a way which will open a window towards new insight in this area in the future.