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Erschienen in: European Spine Journal 5/2006

01.05.2006 | Original Article

A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction

verfasst von: Manohar M. Panjabi

Erschienen in: European Spine Journal | Ausgabe 5/2006

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Abstract

Clinical reports and research studies have documented the behavior of chronic low back and neck pain patients. A few hypotheses have attempted to explain these varied clinical and research findings. A new hypothesis, based upon the concept that subfailure injuries of ligaments (spinal ligaments, disc annulus and facet capsules) may cause chronic back pain due to muscle control dysfunction, is presented. The hypothesis has the following sequential steps. Single trauma or cumulative microtrauma causes subfailure injuries of the ligaments and embedded mechanoreceptors. The injured mechanoreceptors generate corrupted transducer signals, which lead to corrupted muscle response pattern produced by the neuromuscular control unit. Muscle coordination and individual muscle force characteristics, i.e. onset, magnitude, and shut-off, are disrupted. This results in abnormal stresses and strains in the ligaments, mechanoreceptors and muscles, and excessive loading of the facet joints. Due to inherently poor healing of spinal ligaments, accelerated degeneration of disc and facet joints may occur. The abnormal conditions may persist, and, over time, may lead to chronic back pain via inflammation of neural tissues. The hypothesis explains many of the clinical observations and research findings about the back pain patients. The hypothesis may help in a better understanding of chronic low back and neck pain patients, and in improved clinical management.
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Metadaten
Titel
A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction
verfasst von
Manohar M. Panjabi
Publikationsdatum
01.05.2006
Erschienen in
European Spine Journal / Ausgabe 5/2006
Print ISSN: 0940-6719
Elektronische ISSN: 1432-0932
DOI
https://doi.org/10.1007/s00586-005-0925-3

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