Spinal StenosisDz

Last updated: October 31, 2014

ICD-9 Code: Unspecified, 724.0; lumbar, 724.02; thoracic, 724.01; cervical, 723.0.

Definition: Spinal stenosis refers to a narrowing of the lumen of the spinal canal. It occurs most commonly in the lumbar region but can also occur in the cervical spine. The characteristic clinical symptom of spinal stenosis is neurogenic claudication. Although it may be related in rare cases to developmental bony anomalies, the most common cause of spinal stenosis is degenerative change in the vertebrae (these nonspecific degenerative changes are also known as spondylosis).

Pathology: In most patients, a combination of factors contributes to the narrowing of the spinal canal. Anteriorly, degenerative changes of the intervertebral disc cause disc protrusion and extrusion into the spinal canal. Posteriorly, osteoarthritic changes of the facet (apophyseal) joints impinge directly on the spinal cord. Facet joint arthritis, very common among older persons, is also associated with hypertrophy of the ligamentum flavum, which is normally thin and lines the spinal canal. This further diminishes the area of the spinal canal. Degenerative changes of the facet joints may result in laxity and movement of one vertebral body in relation to others, either unilaterally (spondylolysis) or bilaterally (spondylolisthesis). This may result in further impingement of neural structures.

Demographics: Spinal stenosis is most common among the elderly, with a mean age at onset of approximately 60 years of age. Men are affected about twice as frequently as women. Many patients experience symptoms for months or even years before the correct diagnosis is established.

Cardinal Findings: Symptoms of neurogenic claudication (or pseudoclaudication) occur in >90% of patients. It is commonly described as an aching pain in the buttocks, posterior thigh, or calf (>90%) and is often provoked or aggravated by walking. However, it may also be described as numbness (~65%) or weakness (~40%) and is bilateral in ~70% of patients. Of note, the area of the lumbar spinal canal and neural foramina change with position. This space increases with flexion, and patients with spinal stenosis often report relief of symptoms when their backs are flexed (e.g., sitting, bending over, or sleeping in the fetal position). This may provide a useful clue to differentiating vascular from neurogenic claudication. Patients with vascular claudication are limited in their walking by vascular supply. Symptoms are relieved by stopping walking, and patients do not necessarily need to sit down or change position. In contrast, patients with neurogenic claudication find relief by sitting down or bending over. They may also have similar pain by standing erect without walking, and they can walk without limit if their spines are flexed (e.g., pushing a shopping cart or lawnmower).

On physical examination, most patients experience pain on straight leg raising. Many also have depressed lower extremity deep tendon reflexes. Muscle weakness or sensory defects are not common. Pulses are generally easily palpable, another potential point distinguishing neurogenic from vascular claudication.

Diagnostic Testing: Hematologic, chemical, and serologic studies are of no value in evaluating patients with spinal stenosis. Electrodiagnostic studies (e.g., nerve conduction velocity testing) may provide useful information. Such tests may exclude other conditions (e.g., neuropathies) and document the severity and extent of neurologic involvement from spinal stenosis.

Imaging: Plain radiographs are commonly used to evaluate patients with back pain, but their utility may be limited, particularly in spinal stenosis. Radiographs typically show degenerative changes of the lumbar spine. However, such changes provide no information regarding neurologic impingement and do not correlate with the severity of symptoms. Bony abnormalities and narrowing of the spinal canal are easily visualized by CT. However, CT must be combined with myelography for clear definition of bony impingement on the spinal cord or nerve roots. MRI, which allows definition of bone as well as soft and nerve tissue, is now the imaging procedure of choice for patients with spinal stenosis.

Differential Diagnosis: Vascular insufficiency, inflammatory SpA (e.g., AS), spinal metastases, disc disease, and Paget’s disease should be considered.

Therapy: The most appropriate therapy depends on the extent and progression of symptoms. Conservative measures include physiotherapy (e.g., optimizing low back mechanics, muscle strengthening, enhancing flexibility) and analgesic medications.

Surgery: Patients with cauda equina syndrome (loss of bowel or bladder function, “saddle” [perineal] anesthesia) may require surgical decompression of the stenosed canal. Patients with progression of either neurologic defects (e.g., radiculopathy) or intractable pain likewise may benefit from surgical intervention. The type of surgery depends on the specific pathologic changes considered most responsible for the patient’s symptoms. In most patients, laminectomy is the procedure of choice, although a few patients may benefit from foraminectomy or discectomy. Surgery is not required for all patients, and in some series, patients appear to have similar long-term outcomes with or with- out surgery.

Prognosis: The course of spinal stenosis is variable. For many patients, it is a chronic condition that may improve with intervention. Some patients experience relatively rapid progression from intermittent pain to excruciating persistent pain to neurologic defect.

Hall S, Bartleson JD, Onofrio BM, et al. Lumbar spinal stenosis. Ann Intern Med 1985;103:271–275.PMID:3160275
Moreland LW, Lopez-Mendez A, Alarcon GS. Spinal stenosis: a comprehensive review of the literature. Semin ArthritisRheum 1989;19:127–149. PMID:2683093
Swezey RL. Outcomes for lumbar stenosis. J Clin Rheumatol 1996;2:129–133.PMID:19078047


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