Show simple item record

dc.contributor.authorQuirk, David Adam
dc.date.accessioned2019-08-27T18:21:58Z
dc.date.available2019-08-27T18:21:58Z
dc.date.issued2019-08-27T18:21:58Z
dc.identifier.urihttp://hdl.handle.net/10222/76321
dc.description.abstractIn the early 1990’s Panjabi proposed a theoretical model suggesting one risk of low back pain is a spinal instability event theorizing a deficit to any spinal system (active, passive and neural) could represent a risk. However, the interplay between systems allows for compensation in the event of a deficit. Despite this theory being used for the treatment of low back pain, there is limited supporting empirical evidence. The overarching purpose of this dissertation was to investigate this compensation theory. Study one compared two populations (older adults and those recovered from a low back injury) suspected of having deficits in all three spinal systems with a young asymptomatic control group. The objective was to determine whether both groups had different muscle activation patterns compared to controls. Both deficit groups had higher agonist and antagonist activation amplitudes and evidence of reduced responsiveness of trunk muscles to changing external moments. While the direction of adaptations observed in both deficit groups, suggests that these adaptations were in response to common spinal system deficits, the magnitude differed. Thus, it was unknown if adaptations were unique to a deficit in any singular spinal system or a result of recent pain. To investigate these limitations, three studies compared those with high or low function of the active, passive, and neural systems and whether recent low back pain modified these adaptations. These comparisons identified that lower function within any single spinal system had different trunk muscle activation patterns that interacted with recent pain. Adaptations included increased agonist and antagonist amplitudes and different (increased or decreased) responsiveness to changing external moments. Muscle adaptations were specific to the measured spinal system to produce higher relative muscle force (active) or increase the general stiffness of the spine (passive and neural). Collectively these findings were consistent with Panjabi’s theoretical model that trunk muscle activation patterns adapt to dysfunction within spinal systems. While cross-sectional data cannot infer causation, a rigorous methodology was employed, contributing to a broader understanding of the interrelationships between individual spinal system function, neuromuscular control during dynamic tasks and the modifying effect of recent pain.en_US
dc.language.isoenen_US
dc.subjectElectromyographyen_US
dc.subjectLow Back Painen_US
dc.subjectAgingen_US
dc.subjectBiomechanicsen_US
dc.subjectLumbar Spineen_US
dc.titleTRUNK MUSCLE ACTIVATION PATTERNS ADAPT TO DEFICITS IN INDIVIDUAL SPINAL SYSTEMSen_US
dc.date.defence2019-08-20
dc.contributor.departmentDepartment of Biomedical Engineeringen_US
dc.contributor.degreeDoctor of Philosophyen_US
dc.contributor.external-examinerDr. Stephen Brownen_US
dc.contributor.graduate-coordinatorDr. Jeremy Brownen_US
dc.contributor.thesis-readerDr. John Kozeyen_US
dc.contributor.thesis-readerDr. Derek Rutherforden_US
dc.contributor.thesis-readerDr. Shaun Boeen_US
dc.contributor.thesis-supervisorDr. Cheryl Hubley-Kozeyen_US
dc.contributor.ethics-approvalReceiveden_US
dc.contributor.manuscriptsYesen_US
dc.contributor.copyright-releaseYesen_US
 Find Full text

Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record