Study DesignCross-sectional study.PurposeTo investigate the relationship between ligamentum flavum (LF) thickening and lumbar segmental instability and disc degeneration and facet joint osteoarthritis.Overview of LiteraturePosterior spinal structures, including LF thickness, play a major role in lumbar spinal canal stenosis pathogenesis. The cause of LF thickening is multifactorial and includes activity level, age, and mechanical stress. LF thickening pathogenesis is unknown.MethodsWe examined 419 patients who underwent computed tomography (CT) myelography and magnetic resonance imaging after complaints of clinical symptoms. To investigate LF hypertrophy, 57 patients whose lumbar vertebra had normal disc heights at L4–5 were selected to exclude LF buckling as a hypertrophy component. LF thickness, disc space widening angulation in flexion, segmental angulation, presence of a vacuum phenomenon, and lumbar lordosis at T12–S1 were investigated. Disc and facet degeneration were also evaluated. Facet joint orientation was measured via an axial CT scan.ResultsThe mean LF thickness in all patients was 4.4±1.0 mm at L4–5. There was a significant correlation between LF thickness and disc degeneration; LF thickness significantly increased with severe disc degeneration and facet joint osteoarthritis. There was a tendency toward increased LF thickness in more sagittalized facet joints than in coronalized facet joints. Logistic regression analysis showed that LF thickening was influenced by segmental angulation and facet joint osteoarthritis. Patient age was associated with LF thickening.ConclusionsLF hypertrophy development was associated with segmental instability and severe disc degeneration, severe facet joint osteoarthritis, and a sagittalized facet joint orientation.
Study DesignRetrospective cross-sectional study.PurposeTo investigate the relationship between ligamentum flavum (LF) hypertrophy and lumbar segmental motion.Overview of LiteratureThe pathogenesis of LF thickening is unclear and whether the thickening results from tissue hypertrophy or buckling remains controversial.Methods296 consecutive patients underwent assessment of the lumbar spine by radiographic and magnetic resonance imaging (MRI). Of these patients, 39 with normal L4–L5 disc height were selected to exclude LF buckling as one component of LF hypertrophy. The study group included 27 men and 12 women, with an average age of 61.2 years (range, 23–81 years). Disc degeneration and LF thickness were quantified on MRI. Lumbar segmental spine instability and presence of a vacuum phenomenon were identified on radiographic images.ResultsThe distribution of disc degeneration and LF thickness included grade II degeneration in 4 patients, with a mean LF thickness of 2.43±0.20 mm; grade III in 10 patients, 3.01±0.41 mm; and grade IV in 25 patients, 4.16±1.12 mm. LF thickness significantly increased with grade of disc degeneration and was significantly correlated with age (r=0.55, p<0.01). Logistic regression analysis identified predictive effects of segmental angulation (odds ratio [OR]=1.55, p=0.014) and age (OR=1.16, p=0.008).ConclusionsAge-related increases in disc degeneration, combined with continuous lumbar segmental flexion-extension motion, leads to the development of LF hypertrophy.
The D-dimer assay was useful in predicting DVT development. A D-dimer level of ≥10 μg/mL is considered to be a risk factor for thromboembolic disease after spinal surgery. False-positive cases of thromboembolic disease preclude the use of this assay as a stand-alone test for DVT diagnosis. CT venography and CT pulmonary angiography are recommended to confirm thromboembolic disease.
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