Lumbar Canal Stenosis and Associated Deformities

Degenerative lumbar spinal stenosis results from pathological degeneration of the facet joints, disc herniation, hypertrophy and buckling of the ligamentum flavum, and spondylolisthesis. Degenerative changes in the three-joint complex (the intervertebral disc and two facet joints) explain the fluctuation in symptoms with alterations in posture, load, and duration of load. Lumbar intervertebral disc degeneration represents a cascade of events involving disc herniation, bulging of the disc and ligamentum flavum into the canal, and resulting chronic facet arthrosis, sclerosis, and osteophytic growth. Hypertrophy of the ligamentum flavum is also an important element in the development of spinal stenosis. Lumbar spinal encroachment induces ligamentum flavum hypertrophy, which further aggravates stenosis. Disease of the nerve roots and cord, however, does not typically result directly from compression of the nerves. Rather, the resulting stenosis causes decreased flow of cerebrospinal fluid, which represents approximately 60% of the nutritional supply to the cauda equina, and increased venous pressure. In such a scenario, any concurrent spinal deformities may critically compromise the nerve roots and cord, as well as exacerbate neurological symptoms of lumbar stenosis.

Spondylolisthesis can be caused by congenital, developmental, traumatic, neoplastic, or degenerative conditions. In degenerative spondylolisthesis, the most common type observed with lumbar stenosis, anterior/posterior displacement of a VB results from facet joint erosion and attenuation of the muscular, capsular, and ligamentous structures. Fourfold more common in females than in males, degenerative spondylolisthesis occurs most frequently at the L4-5 and L5-S1 levels.Disc degeneration causes spondylolisthesis with resulting segmental hypermobility, compounded by arthritis in sagittal facet joints.

There are many other spinal deformities associated with the LCS. For the detailed article visit-

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