title: Strain in fibers of a lumbar disc. Analysis of the role of lifting in producing disc prolapse.
abstract: A three-dimensional nonlinear finite element model has been used to predict the strain in the disc fibers of a lumbar motion segment under various single and combined loads such as those representing symmetric and non-symmetric liftings. A progressive failure analysis also has been performed under loads representing lifting while bending to one side: assuming yield and ultimate fiber strains of 14 and 16%, respectively. Large tensile strains of about 10% in the disc fibers are predicted under the maximum loads simulating symmetric lifting. Addition of lateral bending and twisting significantly increases the maximum fiber strain to more than 20%, and hence augments the risk for disc rupture. The maximum fiber strain occurs in the innermost annulus layer at the posterolateral location. Loss of intradiscal pressure or volume has a marked diminishing effect on the magnitude of maximum fiber strain predicted under flexion loadings. Failure analysis indicates that rupture initiates in the fibers in the innermost layer at the posterolateral location. With a slight increase in the loads, rupture progresses radially to the adjacent outer layer. Further progress of rupture in the fibers toward the annulus outer periphery resulting in complete radial fissure and disc prolapse appears to require additional increase in the loads. In the presence of large intradiscal pressure, the generated partial or complete radial fissure is likely to result in annulus protrusion or disc herniation, respectively. The results of clinical, epidemiologic, and experimental studies support the failure mechanism predicted in the present study.
authors.affiliation: Department of Mechanical Engineering, Ecole Polytechnique de Montrèal, Quebec, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Shirazi-Adl
mesh_terms: D001696:Biomechanical Phenomena; D003198:Computer Simulation; D006801:Humans; D007403:Intervertebral Disc / Q000502:physiology*; D007405:Intervertebral Disc Displacement / Q000209:etiology*; D008954:Models, Biological