Aetiology
In nearly all patients, lumbar stenosis is the consequence of degenerative changes in the lumbar spine. With normal ageing, the intervertebral disc loses proteoglycans and water, leading to diminished disc height and circumferential disc bulging. This results in altered biomechanical stress on the facet joints leading to facet hypertrophy and thickening of the ligamentum flavum, along with collagen and calcium deposition.[7][8][9][10][11]
These changes reduce the diameter of the spinal canal and neural foramina and the space available for the dural sac and exiting nerve roots. Intrusion of the disc anteriorly within the spinal canal and of the hypertrophied facets and ligamentum flavum laterally and posteriorly creates a characteristic triangular or trefoil appearance on cross-section of the canal.
Pathophysiology
Degenerative disease of the lumbar spine may reduce the diameter of the spinal canal and may also produce narrowing of the lateral recess and neural foramina. Bony and ligamentous hypertrophy, intervertebral disc protrusion, and spondylolisthesis all contribute to the stenosis. Ensuing leg symptoms result from the compression of the cauda equina, exiting nerve roots, or both. The reduction of the sagittal diameter of the central canal is responsible for symptoms of claudication, but stenosis of the lateral recess and neural foramina produces compression of exiting nerve roots and radicular symptoms.
Stenosis results from a cascade of micro-degenerative changes. Mild disc degeneration alters the mechanics of the intervertebral disc and the two facet joints. As the disc loses water and the ability to withstand axial and translational forces, greater load is placed on the facet joints and they begin to undergo arthritic changes leading to synovitis, articular cartilage degeneration, and articular surface enlargement. Facet degeneration places further stress on the disc, causing internal disc disruption and eventual development of osteophytes. In many asymptomatic patients, x-ray, computed tomography, or magnetic resonance imaging shows degenerative changes. Radiculopathy and neurogenic claudication may be attributed to direct mechanical compression or indirect vascular insufficiency from inadequate blood flow and oxygenation of the nerve roots or cauda equina. Standing and walking transiently increase lordosis, thus accentuating stenosis and symptoms. In contrast, forward flexion and sitting reverses lordosis, opens the canal, improves blood flow, and relieves symptoms.
Degenerative disease of the lumbar spine is an inevitable part of ageing. The degenerative process starts in people aged 20-29 years, and 80% of women and 95% of men over 65 years have radiographical evidence of changes.[12]
Spondylolisthesis is commonly seen in patients with lumbar stenosis because degeneration of the posterior elements allows for anterior slippage of the superior vertebral body.[13] This anterolisthesis occurs most often at the L4-L5 level and serves to exacerbate underlying canal stenosis. Unlike other types of spondylolisthesis, degenerative vertebral slippage, which is more common in women, seldom produces gross mechanical instability and rarely progresses to higher grades.
These degenerative changes within the disc and facets may cause low back pain. Symptomatic lumbar stenosis is most common at L4-L5, then L3-L4, L2-L3, and lastly L5-S1.[14]
Classification
Lumbar spinal stenosis and nerve root entrapment syndromes[1]
Congenital stenosis
Achondroplasia
Idiopathic narrow spinal canal
Acquired stenosis
Degenerative
Combined degenerative and congenital
Post-traumatic
Iatrogenic (after laminectomy or fusion)
Spondylolisthetic
Metabolic (Paget's disease, acromegaly, calcifications of ligamentum flavum).
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