Lumbar spinal stenosis.

Spinal stenosis was described as early as 1899 by Sachs and Frankel,[1] who described patients with lumbar or lower-extremity pain who walked bent forward and whose symptoms were relieved by laminectomy. Spinal stenosis is caused by narrowing of the spinal canal or the various tunnels through which nerves and other structures communicate with that canal.[2] Narrowing of the spinal canal can be the result of (1) the shape of the canal, (2) degenerative changes that decrease the canal size, or (3) movement of one anatomic segment in relation to another.

The chief complaint of patients with symptomatic spinal stenosis is claudication, an intense pain brought on by walking and usually felt in one or both lower extremities. The pain is often sufficiently intense to force patients to stop walking and to sit in order to seek relief. Claudication may be either vascular or neurogenic. Vascular claudication is brought on by ischemia (usually the result of lower-extremity vascular disease). Neurogenic claudication is the pain associated with impingement of neural structures caused by lumbar spinal stenosis.

Classification

Spinal stenosis is classified as either primary or secondary. In primary stenosis, the spinal canal is constricted due to a congenital abnormality or a disorder in postnatal development.[3] Primary stenosis is extremely rare and will not be discussed further in this update. In secondary stenosis, there is compression of neural elements due to one or more acquired conditions such as degenerative changes of the vertebral bodies, facet joints, and disks.[3] Secondary stenosis also may occur in the late stages of an infection or following a fracture. Iatrogenic stenosis may occur postsurgically (eg, when there is excessive scar tissue or proliferation of bone).

Secondary stenosis is the most common form of stenosis and results from degenerative changes.[3,4] A prevalence rate of 10:1, comparing degenerative and developmental stenosis, has been reported.5,13 Degenerative spinal stenosis is most frequently seen in men in their fifth or sixth decade of life.[3,7]

Pathoanatomy

The three primary structures that contribute to spinal stenosis are the ligamentum flavum, the facet joints, and the disk space. With degenerative changes, the ligamentum flavum and facet joints may hypertrophy, secondary to mechanical stresses. The aging process results in diminished disk height, which if pronounced can allow buckling of the ligamentum flavum into the spinal canal.[5] Ligament hypertrophy, osteophytes, or disk bulging can all encroach on the spinal canal.

The diameter of the spinal canal varies with race, age, and gender and at different levels of the canal[8]; therefore, references to "normal" diameters of the vertebral canal cannot be made. Diagnosis of spinal stenosis may depend less on the size of the canal than on the configuration of the canal or the amount of space available for the thecal sac and nerve roots.[9,10]

Pathophysiology

Symptoms associated with lumbar spinal stenosis have been attributed to arterial obstruction, venous hypertension, pressure, or traction on the sinuvertebral nerves and primary rami.[11] Claudication is believed by some investigators[7] to be due to vascular insufficiency of the nerve roots themselves. On tomograms and myelograms, nerve root impingement appears to increase with extension of the spine and to be reduced by flexion of the spine. These observations support the nerve root compression theory.[12,13]

In patients with spinal stenosis, an abnormally small anteroposterior (AP) diameter of the dural sac is excessively decreased by extension. Sortland et al[13] demonstrated that under normal circumstances, the decrease of dural AP diameter in extension amounted to 9%, whereas in people with severe stenosis, the reduction was 67%. Using tomographic-myelographic studies, Penning and Wilmink[11] and narrowing of the spinal canal in extension and widening of the canal with relief of nerve root involvement in flexion.

Clinical Findings

Lumbar spinal extension, in patients who demonstrate symptoms of lumbar spinal stenosis, will usually reproduce or exacerbate the patients' lower-extremity symptoms (pain, paresthesia).[6,7] People with lumbar spinal stenosis generally have reduced lower-extremity symptoms when their spine is flexed because this posture allows the vertebral foramen to open up, thereby diminishing or eradicating the neural compression.[7,11] Quite often, patients with lumbar spinal stenosis report that they are more comfortable walking uphill than downhill or that they can walk farther if they bend forward while they walk.[14]

Changes in symptoms associated with different positions have been explained by Penning[14] using the "rule of progressive narrowing." This rule states that the more the canal is structurally narrowed by a stenosing process, the more it will be functionally narrowed by additional extension.[14] This progressive narrowing suggests that in severe cases of stenosis, only minimal extension is required to increase the patients' neurogenic symptoms.

The "bicycle test" has been advocated to differentiate between vascular claudication and neurogenic claudication attributable to spinal stenosis.[15] This test requires the patient to cycle with the spine first extended and then flexed. The distance cycled under both conditions is the same if the patient has vascular claudication, whereas in patients with neurogenic claudication, the flexed spine allows for greater exercise tolerance.[15] Dong and Porter[15] reported a sensitivity of only 30% using the "bicycle test" to identify patients who have neurogenic claudication.

The "stoop test" has been devised to assess the relationship between claudication-like symptoms (pain, paresthesia in the lower extremity) elicited while standing versus walking.10 The test consists of the patient walking "briskly" while maintaining an upright posture. When the symptoms of claudication become intense, the patient assumes a stooped posture while continuing to walk. The patient is then asked to stop walking and stand upright, at which time the symptoms usually return. The stoop test is considered positive for neurogenic claudication when flexion while walking or stooping relieves the symptoms in the limb.[10] No relationship has been found between the degree of myelographic abnormality and the relief of lower-extremity symptoms by lumbar flexion.[10]

Neurogenic claudication secondary to spinal stenosis is characterized by lower-extremity pain that is poorly localized and sometimes associated with numbness or weakness, exacerbated by walking or standing, and relieved by spinal flexion.[6,11,16] Physical findings (eg, range of motion, sensory or motor deficits) are often minimal and nonspecific, the most common being decreased spinal extension.[3,6] Reflexes at the knee and ankle and straight leg raises are usually normal. Motor or sensory abnormalities may or may not occur. Reexamination after exercise may show findings that differ from those of the original neurological examination.

Katz et al,[17] in a multicenter study of 93 patients, showed a strong association between lumbar spinal stenosis and age, severe lower-extremity pain, and the absence of pain when seated. Associated with stenosis were wide-based gait; abnormal Romberg test (ability to stand in one place with feet together and eyes closed); thigh pain following 30 seconds of lumbar extension; and neuromuscular deficits, including deep tendon (Achilles tendon) reflexes, decreased strength (of the knee flexors and extensors, ankle dorsiflexors and plantar flexors, and extensor hallucis longus muscle), and decreased sensation (pinprick and vibration). In this study, although the sample size was small (N=93), several independent variables (eg, advanced age, absence of pain when seated, wide-based gait, thigh pain following 30 seconds of lumbar extension) were shown to correlate with lumbar spinal stenosis.

Diagnostic imaging

Measurements of bony structures alone cannot be used to reliably identify patients who have spinal stenosis.[6] Measurement of the transverse area of the dural sac, enhanced by contrast in the sac, is the most accurate method for identifying stenosis.[6] Techniques used to diagnose lumbar spinal stenosis are computed tomography, magnetic resonance imaging (MRI), and myelography.[7,9] Computed tomography, however, is usually the method of choice because of its superior ability to image bone and therefore to allow for visualization of the canal.[9] Measurement of the cross-sectional area of the dural sac by computed tomography has been reported to be reliable.[9]

Radiographic abnormalities have been found in people without symptoms due to stenosis. Hitselberger and Witten[18] found a 24% occurrence of myelographic abnormalities in asymptomatic subjects, and Boden et al[19] reported that MRI studies of asymptomatic subjects over 60 years of age showed spinal stenosis in 21% of the subjects.

Surgery

Surgery for spinal stenosis usually consists of decompressive laminectomy or a diskectomy and fusion to relieve the symptoms of neurogenic claudication.[2] Short-term results from spinal surgery appear to be good for most patients, but long-term follow-up indicates some progressive deterioration over time.[2] Long-term follow-up appears to indicate a higher percentage of good-to-excellent outcomes for patients who had fusions than for patients who had surgeries that did not include fusions.[2]

There is a 10% to 15% complication rate for surgery for spinal stenosis, with 50% of the complications considered to be life threatening.[2] The population of patients with lumbar spinal stenosis generally consists of older people who may have various additional health problems, which could affect the surgery complication rate.[2]

Summary

Symptoms for spinal stenosis apparently result from an incongruity between the capacity and contents of the spinal nerve passages. These symptoms are most frequently seen in men in their fifth or sixth decade of life. Spinal extension generally exacerbates the claudication-type symptoms (lower-extremity pain and paresthesia), whereas spinal flexion diminishes these symptoms. Differential diagnosis is needed to rule out vascular claudication due to atherosclerosis. Decisions regarding surgery should be made based not only on diagnostic imaging but also on a thorough history and clinical examination.

References

[1] Sachs B, Frankel V. Progressive and kyphotic rigidity of the spine. J Nerv Ment Dis. 1900;27:1. [2] Bigos S, Bowyer O, Braen G, et al. Acute Low Back Problems in Adults. Clinical Practice Guideline No. 14. Rockville, Md: Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services; 1994. AHCPR Publication No. 95-0642,. [3] Ciricillo SF, Weinstein PR. Lumbar spinal stenosis. West J Med. 1993;158: 171-177. [4] Getty CJM. Lumbar spinal stenosis: the clinical spectrum and results of operations. J Bone Joint Surg [Br]. 1980;62:481-485. [5] Schonstrom NSR, Bolender NF, Spengler DM. The pathomorphology of spinal stenosis as seen on CT scans of the lumbar spine. Spine. 1985;10:806-811. [6] Moreland LW, Lopez-Mendez A, Alarcon GS. Spinal stenosis: a comprehensive review of the literature. Semin Arthritis Rheum. 1989;19:127-149. [7] Howe JW, Yochum TR, Rowe LJ. Diagnostic imaging of spinal stenosis and intervertebral disc disease. In: Yochum TR, Rowe LJ, eds. Essentials of Skeletal Radiology: Volume. 1. Baltimore, Md: Williams & Wilkins; 1987:273-316. [8] McAfee PC, Ullrich CG, Yauan HA, et al. Computed tomography in degenerative spinal stenosis. Clin Orthop. 1981;161:221-234. [9] Bolender NF, Schostrom NSR, Spengler DM. Role of computed tomography and myelography in the diagnosis of central spinal stenosis. J Bone Joint Surg [Am]. 1985;67:240-246. [10] Dyck P. The stoop test in lumbar entrapment radiculopathy. Spine. 1979;4:89-92. [11] Penning L, Wilmink JT. Posture-dependent bilateral compression of L4 or L5 nerve roots in facet hypertrophy: a dynamic CT-myelographic study. Spine. 1987;12:488-500. [12] Kapila A, Chakeres DW. Flexed sitting maneuver for complete lumbar myelography in patients with severe spinal stenosis and apparent block. Radiology. 1986;160:265-267. [13] Soutland O, Magnae B, Hauge T. Functional myelography with metrizamide in the diagnosis of lumbar spinal stenosis. Acta Radiol Suppl. 1977; 355:42-54. [14] Penning L. Functional pathology of lumbar spinal stenosis. Clin Biomech. 1992;7:3-17. [15] Dong GX, Porter RW. Walking and cycling test in neurogenic and intermittent claudication. Spine. 1989;14:965-969. [16] Paine KWE. Clinical features of lumbar spinal stenosis. Clin Orthop. 1976; 115:77-91. [17] Katz JN, Dalgas M, Stucki G, et al. Degenerative lumbar spinal stenosis: diagnostic value of history and physical examination. Arthritis Rheum. 1995;9:1236-1241. [18] Hitselberger WE, Witten RM. Abnormal myelograms in asymptomatic patients. J Neurosurg. 1968;28:204-206. [19] Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects: a positive investigation. J Bone joint Surg [Am]. 1990;72:403-408.