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Lumbar spinal stenosis: Treatment and prognosis

Kerry Levin, MD
Section Editors
Michael J Aminoff, MD, DSc
Steven J Atlas, MD, MPH
Deputy Editor
Janet L Wilterdink, MD


Lumbar spinal stenosis (LSS) refers to an anatomic condition that includes narrowing of the intraspinal (central) canal, lateral recess, and/or neural foramena. Spondylosis, or degenerative arthritis affecting the spine, is the most common cause of LSS and typically affects individuals over the age of 60 years [1].

LSS is a cause of disability in the aging population [2,3]. Treatment approaches are often not straightforward and require careful consideration of potential risks and benefits.

This topic will discuss the prognosis and treatment of LSS, focusing on lumbar spondylosis. Other topics discuss more general issues related to the evaluation and treatment of low back pain, and also the pathophysiology, clinical features, and diagnosis of lumbar spinal stenosis. (See "Evaluation of low back pain in adults" and "Subacute and chronic low back pain: Nonsurgical interventional treatment" and "Subacute and chronic low back pain: Nonpharmacologic and pharmacologic treatment" and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis".)


The natural history of lumbar spinal stenosis (LSS) due to degenerative spondylosis is relatively benign. Among 32 patients with symptoms and neuroimaging consistent with LSS who were followed for a mean 49 months without surgical intervention, symptoms remained unchanged in 70 percent, improved in 15 percent, and worsened in 15 percent [4]. However, LSS causes discomfort, often limiting activities of daily living, and can lead to progressive disability.

Radiographic studies suggest that over time adjacent spinal segments also become affected in almost half of patients [5,6]. Some data indicate that this phenomenon may be a more frequent occurrence in those who undergo surgical fusion and contribute to re-operation rates.

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Literature review current through: Nov 2017. | This topic last updated: Oct 15, 2014.
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