Lumbar spinal stenosis

Anthony E Chiodo MD (Dr. Chiodo of the University of Michigan Medical School has no relevant financial relationships to disclose.)
Matthew Lorincz MD PhD, editor. (Dr. Lorincz of the University of Michigan has no relevant financial relationships to disclose.)
Originally released September 7, 1999; last updated February 10, 2020; expires February 10, 2023

This article includes discussion of lumbar spinal stenosis, neurogenic claudication, pseudoclaudication, and spinal stenosis. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Lumbar spinal stenosis is a clinical syndrome with a hallmark of radiating leg pain with standing and walking relieved with bending forward or sitting. MRI findings lack specificity in identifying patients with symptomatic lumbar stenosis and do not correlate well with pain. Lumbar paraspinal needle electromyography lacks sensitivity but is highly specific in mild to moderate symptomatic lumbar stenosis, and is highly sensitive and specific in severe symptomatic lumbar stenosis. There is no radiologic or electrophysiologic gold standard at this time. Symptoms are caused by mechanical compression on the neural elements or their blood supply. Neurogenic claudication is classically described as a poorly localized sense of discomfort and aching pain in the lower back, buttocks, and legs that is precipitated by walking and relieved by sitting or leaning forward. The most common operative treatment is decompressive laminectomy with or without fusion or bilateral laminotomy. Minimally invasive lumbar decompression has demonstrated similar results with less cost, complication, and reoperation rates than open decompression. Interspinous process devices add cost and reoperation risk without additional functional or pain benefit. Of patients successfully treated nonsurgically, 15% to 43% will continue to enjoy improvement over a 1- to 5-year follow-up. The occurrence of concurrent asymptomatic lesions in the cervical or thoracic regions is well-known in elderly patients with surgical decompression for lumbar stenosis. This may have significant bearing on otherwise unexplained findings on physical examination, the position of the patient during surgery, and management in general. Lipoprostaglandin E1 and EP4 agonist at high concentrations might be potential therapeutic agents because they are expected to increase blood flow in nerve roots in patients with spinal canal stenosis, although their value has not been demonstrated as better than or additive to pregabalin in a controlled trial.

Key points


• Lumbar spinal stenosis is a very common condition. It is the most common cause of spinal surgery in individuals over 65 years of age.


• Degenerative lumbar spinal stenosis often results in disc space collapse, facet joint hypertrophy, soft-tissue infolding, and osteophyte formation, thus, narrowing the space available for the thecal sac and exiting nerve roots.


• Standard treatment options for patients with lumbar spinal stenosis include nonoperative therapies as well as decompression and fusion surgical procedures.


Epidural steroid therapy during the acute phase does have the potential to offer significant time limited relief from pain.


• In patients with lumbar stenosis without concomitant degenerative spondylolisthesis, symptoms of predominant back pain over leg pain is associated with inferior outcome following spinal fusion in conjunction with decompression for lumbar spinal stenosis. Additional spinal fusion does not offer added clinically significant benefit.

Historical note and terminology

Stenosis of the lumbar spinal canal is most commonly associated with multilevel degenerative spine disease, although commonly worst at the L4-5 level. Such narrowing of the spinal canal may be asymptomatic, associated with low back pain, cause symptoms and signs of focal nerve root injury, or give rise to neurogenic claudication. The reason why some patients develop symptomatic stenosis and others do not is still unknown. When symptomatic, it is caused by mechanical compression on the neural elements or their blood supply. Neurogenic claudication refers to pain and discomfort in the low back, buttocks, and legs that occurs after walking and is relieved by sitting or leaning forward.

In 1803, Portal first made note of lumbar spinal stenosis from autopsies of patients with rickets. Many of these patients had not been symptomatic during life. In 1911, Dejerine distinguished neurogenic from vascular claudication. In 1950, Verbiest suggested that lumbar spinal stenosis might result in compromise of the cauda equina and produce pain in the lower limbs (Verbiest 1954). Kirkaldy-Willis further clarified the pathoanatomic basis of spinal stenosis (Kirkaldy-Willis et al 1974).

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