The spine journal : official journal of the North American Spine Society
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Lumbar lordosis (LL) correlates with pelvic morphology, and it has been demonstrated that as LL increases, the inflection point and apex of lordosis move cranially. This suggests that each segment of the lumbar spine relates to pelvic morphology in a unique way. ⋯ Pelvic incidence can predict segmental angulation. Although the majority of LL is produced at the L4 and L5 motion segments, cephalad lumbar segments sequentially become increasingly important as PI increases. This describes a continuum where the L1 and L2 motion segments crucially fine-tune total LL according to PI. This allows segmental abnormalities to be identified when compensation in adjacent segments maintain normal total LL. It also paves the way for anatomical segmental reconstruction in degenerative adult deformity based on pelvic morphology.
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Cervical spine segmental contributions to motion may reveal movement abnormalities associated with whiplash, disc herniation, disc arthroplasty, or fusion. ⋯ Cervical motion segment contributions to head motion change over the full ROM and cannot be accurately characterized solely from endpoint data. The continuously changing segmental contributions suggest that the compressive and shear loads applied to each motion segment also change over the ROM. The clinical implication of increased contributions from the inferior motions segments near the end ROM is that the clinician may advise the patient to avoid end ROM positions to lessen the demand on the discs of inferior motion segments.
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Chronic low back pain is debilitating and difficult to treat. Depending on the etiology, responses to treatments vary widely. Although chronic low back pain is frequently related to intervertebral disc degeneration, the relationship between disc degeneration severity and clinical symptoms are still poorly understood. In humans, studies investigating the relationship between disc degeneration severity and low back pain are limited by the difficulty of obtaining disc samples from well-characterized patients and pain-free controls. We have previously described the secreted protein, acidic, rich in cysteine (SPARC)-null mouse model of chronic low back pain. SPARC is a matricellular protein involved in regulating the assembly and composition of extracellular matrix. The SPARC-null mice develop age-dependent disc degeneration of increasing severity accompanied by behavioral signs suggestive of axial low back pain, radiating leg pain, and motor impairment. The existence of this model allows for examination of the relationships between clinical symptoms in vivo and pathological signs of disc degeneration ex vivo. ⋯ These data suggest that internal disc disruption contributes to axial low back pain and motor impairment but not to radiating leg pain. These results have implications for the optimization of mechanism-based treatments strategies.