The Effects of an Acute Maximal Seated Lumbar Spine Flexion Exposure on Low Back Mechanical Pain Sensitivity

Viscoelastic creep generated in the lumbar spine following sustained spine flexion may affect the relationship between tissue damage and perceived pain. Two processes supporting this altered relationship include altered neural feedback and inflammatory processes. Our purpose was to determine how low...

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Bibliographic Details
Published in:Journal of applied biomechanics 2022-02, Vol.38 (1), p.12-19
Main Authors: Viggiani, Daniel, Callaghan, Jack P
Format: Article
Language:English
Subjects:
Biomechanical Phenomena
Cross-Sectional Studies
Electromyography
Female
Humans
Low Back Pain
Lumbar Vertebrae
Male
Muscle, Skeletal
Pain
Range of Motion, Articular
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Summary:Viscoelastic creep generated in the lumbar spine following sustained spine flexion may affect the relationship between tissue damage and perceived pain. Two processes supporting this altered relationship include altered neural feedback and inflammatory processes. Our purpose was to determine how low back mechanical pain sensitivity changes following seated lumbar spine flexion using pressure algometry in a repeated-measures, cross-sectional laboratory design. Thirty-eight participants underwent a 10-minute sustained seated maximal flexion exposure with a 40-minute standing recovery period. Pressure algometry assessed pressure pain thresholds and the perceived intensity and unpleasantness of fixed pressures. Accelerometers measured spine flexion angles, and electromyography measured muscular activity during flexion. The flexion exposure produced 4.4° (2.7°) of creep that persisted throughout the entire recovery period. The perception of low back stimulus unpleasantness was elevated immediately following the exposure, 20 minutes before a delayed increase in lumbar erector spinae muscle activity. Women reported the fixed pressures to be more intense than men. Sustained flexion had immediate consequences to the quality of mechanical stimulus perceived but did not alter pressure pain thresholds. Neural feedback and inflammation seemed unlikely mechanisms for this given the time and direction of pain sensitivity changes, leaving a postulated cortical influence.
ISSN:1065-8483
1543-2688
DOI:10.1123/jab.2021-0238