Lumbar spinal stenosis

Can be defined as a decrease in the size of the dural sac and spinal canal caused by arthritic changes of the facet joints, disc herniation combined with osteophytes, and spinal nerve root compression.

Developmental lumbar spinal stenosis is a maldevelopment of the dorsal spinal elements involving short pedicles and a trefoil bony spinal canal that increases the likelihood of neural compression at an earlier age.

The clinical definition includes “buttock or lower extremity pain, which may occur with or without low back pain, associated with diminished space available for the neural and vascular elements in the lumbar spine“ 1).

● caused by hypertrophy of facets and ligamentum flavum, may be exacerbated by bulging disc or spondylolisthesis, may be superimposed on congenital narrowing

● most common at L4–5 and then at L3–4

● symptomatic stenosis produces gradually progressive back and leg pain with standing and walking that is relieved by sitting or lying (neurogenic claudication)

● symptoms differentiated from vascular claudication which is usually relieved at rest regardless of position

● usually responds to decompressive surgery (sometimes with fusion) or interspinous spacer

Lumbar spinal stenosis (LSS) is a chronic degenerative disease with pain in the back, buttocks and legs aggrevated by walking and relieved after rest without associated vascular disease of lower extremities observed in patients between 50 and 60 years.

Lumbar spinal stenosis (LSS) and low-grade degenerative spondylolisthesis are frequently associated with facet joint degeneration, considered the main cause of low back pain.

The evidence available in the literature regarding the causes, diagnosis and treatment of lumbar spine stenosis can be confusing, as no level I recommendations can be provided yet based on current data 2).

Elsberg 3) described the successful decompression of lumbar spinal stenosis in 1911.

In 1949, Henk Verbiest first proposed the concept of stenosis in spinal canal, lumbar intervertebral foramen; that is, lumbar spinal stenosis (LSS) 4) 5).

In 1973, Epstein identified lateral recess stenosis as another cause of canal narrowing 6). It was not until 1975 with the evolution of cross-sectional imaging and 1980's advances in CT and later MRI, that it became apparent that the soft tissue ligaments were a major cause of primary and also secondary stenosis.

Growth in the facet joints, ligamentum flavum hypertrophy, disc degeneration, osteophytes and spondylolisthesis, all impinging on the spinal canal and intervertebral foramen cause the spinal canal to narrow down, and consequently result in spinal cord and nerve root compression 7).

A narrow spinal canal or spinal lateral stenosis can compress the central canal spinal cord, cauda equina, or nerve root, causing axonal disruption as a result of the pressure, neurohormone function disorders, and expansion of nerve sheath, resulting in the obstruction of blood flow, venous restriction, tissue hypoxia, and localized stasis, which stimulate the nerve endings and generate the symptoms of low back pain.

Although lumbar spinal stenosis often presents as a degenerative condition, some patients present with symptoms from lifelong narrowing of the spinal canal. These patients have congenital stenosis (CS) and present with symptoms of stenosis at a younger age. CS patients often have a distinct pathophysiology with fewer degenerative changes but present with multi-level involvement. In the setting of neurological symptoms, decompression-alone while preserving stability, has been proposed for both patient populations.

A 60-year-old Japanese man diagnosed with acromegaly at 28 years old had difficulty walking due to worsening back pain. He had been treated with somatostatin analog since 57 years old, but his pain and numbness continued to worsen. Lumbar magnetic resonance imaging showed disc bulging at L3/4 and 4/5, and he was diagnosed with lumbar spinal canal stenosis due to hypertrophy of the yellow ligament. Patients with acromegaly may complain of osteoarthropathy, so we must pay attention to the symptoms of spinal canal stenosis in collaboration with orthopedic specialists 8)

Watters W, Baisden J, Gilbert T, Kreiner D, Resnick D, Bono C, et al. Evidence Based Clinical Guidelines for Multidisciplinary Spine Care: Diagnosis and Treatment of Degenerative Lumbar Spinal Stenosis. Burr Ridge: North American Spine Society; 2007. pp. 19–121.
Bagley C, MacAllister M, Dosselman L, Moreno J, Aoun S, El Ahmadieh T. Current concepts and recent advances in understanding and managing lumbar spine stenosis. F1000Res. 2019 Jan 31;8. pii: F1000 Faculty Rev-137. doi: 10.12688/f1000research.16082.1. eCollection 2019. Review. PubMed PMID: 30774933; PubMed Central PMCID: PMC6357993.
Elsberg CA. Observations upon a series of forty-three laminectomies. Ann Surg. 1912;55:217–26.
Verbiest H. Primary stenosis of the lumbar spinal canal in adults, a new syndrome. Ned Tijdschr Geneeskd. 1950;94:2415–2433.
VERBIEST H. A radicular syndrome from developmental narrowing of the lumbar vertebral canal. J Bone Joint Surg Br. 1954 May;36-B(2):230-7. PubMed PMID: 13163105.
Lumbar nerve root compression at the intervertebral foramina caused by arthritis of the posterior facet. Epstein JA, Epstein BS, Lavine LS, et al. J Neurosurg. 1973;39:362–369.
Arbit E, Pannullo S: Lumbar stenosis: A clinical review. Clin Orthop 384:137-143, 2001
Yoshizawa M, Nagai K, Asano S, Hori T, Takagawa K, Shimatsu A. Lumbar Spinal Canal Stenosis in Acromegaly: A Case Report and Literature Review. Intern Med. 2022 Dec 7. doi: 10.2169/internalmedicine.0763-22. Epub ahead of print. PMID: 36476548.
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