Regression of Lumbar Ossification of the Ligamentum Flavum after Indirect Decompression via Full-endoscopic Trans-Kambin's Triangle Lumbar Interbody Fusion: A 3-year Case Report

经全内镜经坎宾三角腰椎椎间融合术间接减压后黄韧带骨化消退:一例3年病例报告

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Abstract

Ossification of the ligamentum flavum is a pathological condition that can cause progressive myelopathy or severe radiculopathy. Standard surgical management involves direct decompression via posterior resection of the ossification. However, there is a substantial risk of complications, including dural tears and iatrogenic instability. We report a rare case of lumbar ossification of the ligamentum flavum with degenerative spondylolisthesis treated solely by full-endoscopic trans-Kambin's triangle lumbar interbody fusion, aiming for indirect decompression and stabilization, without direct resection of the ossification. A 68-year-old woman had progressive low back pain, bilateral lower extremity radiculopathy, and severe neurogenic claudication, limiting ambulation to 100 m. Imaging revealed Meyerding Grade I L4-L5 spondylolisthesis with dynamic instability and significant canal stenosis due to ossification of the ligamentum flavum, measuring 4.06 mm in maximal thickness. She underwent single-level Kambin's triangle lumbar interbody fusion at L4-L5. Postoperatively, rapid improvement was observed (visual analog scale low back pain: 7→1, leg pain: 8→0; Oswestry Disability Index: 52%→10% at 3 years). Follow-up computed tomography/magnetic resonance imaging demonstrated progressive regression of the ossification, from 4.06 mm to 3.2 mm at 1 year and 1.46 mm at 3 years (64.0%). This case suggests that Kambin's triangle lumbar interbody fusion with indirect decompression is an effective surgical option in lumbar ossification of the ligamentum flavum with segmental instability. The remarkable regression of the ossification suggests that spinal stabilization may suppress pathological mechanical stress, shifting bone remodeling toward resorption, and supports a mechanistic hypothesis. Further prospective studies are warranted to validate this pathophysiological mechanism.

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