Lumbar spinal stenosis

Tarakad S Ramachandran MD (Dr. Ramachandran of SUNY Upstate Medical University has no relevant financial relationships to disclose.)
Matthew Lorincz MD PhD, editor. (Dr. Lorincz of the University of Michigan receives salary support from Wilson Therapeutics AB for performing UWDRS examinations in a clinical trial.)
Originally released September 7, 1999; last updated April 4, 2016; expires April 4, 2019

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.

Overview

Lumbar spinal stenosis may be asymptomatic, associated with low back pain, cause symptoms and signs of focal nerve root injury, or give rise to neurogenic claudication. When symptomatic, it is 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. The most common operative treatment is decompressive laminectomy with fusion or bilateral laminotomy. Of patients 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 the unexplained finding on the 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. The nerve root sedimentation sign (SedSign) is a recently described new diagnostic test for lumbar spinal stenosis.

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 decompressive laminectomy.

 

• Steroid therapy during the acute phase does have the potential to offer significant relief from pain.

 

• Lumbar laminectomy appears to be the most cost-effective treatment strategy for patients with symptomatic lumbar spinal stenosis.

 

• By preserving the posterior ligament complex integrity, spinoplasty is a good alternative to long-segment fusion to enable desired decompression and, at the same time, avoid iatrogenic instability.

 

• 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. 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.

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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