You are in: eMedicine Specialties > Orthopedic Surgery > SPINE Spinal StenosisArticle Last Updated: Dec 13, 2007AUTHOR AND EDITOR INFORMATIONAuthor: Amir Vokshoor, MD, Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic and Interventional Spinal Care, St. John's Health Center Amir Vokshoor is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, and American Medical Association Coauthor(s): Ali R Jamali, MD, Assistant Professor of Orthopedic Surgery and Internal Medicine, Department of Orthopedic Surgery, Eastern Virginia Medical School Editors: K Daniel Riew, MD, Professor, Department of Orthopedic Surgery, Washington University School of Medicine; Chief, Cervical Spine Surgery, Department of Orthopedic Surgery, Barnes-Jewish Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; William O Shaffer, MD, Associate Professor & Residency Program Director, Department of Orthopedic Surgery, University of Kentucky at Lexington; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Mary Ann E Keenan, MD, Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania Author and Editor Disclosure Synonyms and related keywords: spondylosis, spinal canal narrowing, neurogenic claudication, myelopathy, focal stenosis, lateral recess syndrome, cervical spondylotic myelopathy, CSM, ligamentum flavum hypertrophy INTRODUCTIONSpinal stenosis refers to the narrowing of the spinal canal anywhere along its axis. Although the disorder often results from acquired degenerative changes (spondylosis), spinal stenosis may also be congenital in nature. In some cases, the patient has acquired degenerative changes that augment a congenitally narrow canal. The canal components that contribute to acquired stenosis include the facets (hypertrophy, arthropathy), ligamentum flavum (hypertrophy), posterior longitudinal ligament (OPLL), vertebral body (bone spurs), the intervertebral disk, and the epidural fat. Congenital stenosis may predispose an individual with mild degenerative changes to become symptomatic earlier in life. Spinal stenosis is most common in the cervical and lumbar areas.1, 2 Stenosis of the central cervical and thoracic spine may result in myelopathy from cord compression.3, 4 Canal stenosis in the lumbosacral region often results in radicular pain, neurogenic claudication, or both. Lateral canal stenosis at any region of the spine may lead to nerve root compression. The patients may experience radicular pain, weakness, and numbness along the distribution of the affected spinal nerve. Lateral recess syndrome in the lumbar spine is a result of such focal stenosis. Treatment can be conservative or surgical. The modes of conservative therapy include rest, physical therapy with strengthening exercises for paraspinal musculature, bracing, use of optimal postural biomechanics, nonsteroidal anti-inflammatory medications, analgesics, and antispasmodics. Surgical decompression is indicated in persons who experience incapacitating pain, claudication, neurologic deficit, or myelopathy.5, 6 Concomitant stabilization is reserved for individuals in whom segmental instability is suspected (ie, patients with spondylolisthesis showing abnormal movement on dynamic studies). For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education articles Back Pain and Lumbar Laminectomy. CERVICAL AND THORACIC STENOSISCongenital stenosis of the cervical spine may predispose an individual to myelopathy as a result of minor trauma or spondylosis.3, 4, 7, 8, 9, 10, 11 Cervical spondylosis refers to age-related degenerative changes of the cervical spine. These changes, which include intervertebral disk degeneration, disk space narrowing, spur formation, and facet and ligamentum flavum hypertrophy, can lead to the narrowing of the cervical spinal canal. Cervical spondylotic myelopathy (CSM) refers to the clinical presentation resulting from these degenerative processes. CSM is the most common cause of spinal cord dysfunction in adults older than 55 years. Degenerative changes of the cervical spine have been observed in as many as 95% of asymptomatic individuals older than 65 years. Myelopathy is believed to develop in up to 20% of individuals with evidence of spondylosis.3, 8, 10, 11, 12, 13 The pathophysiology of spinal stenosis is related to cord dysfunction elicited by a combination of mechanical compression and degenerative instability. With aging, the intervertebral disk degenerates and collapses, leading to spur formation. This most commonly occurs at C5-6 and C6-7. A relative decrease in spinal motion occurs at these levels with a concomitant increase in spinal motion at C3-4 and C4-5. The resultant degeneration and abnormal motion lead to instability with anterolisthesis or retrolisthesis (subluxation of vertebral bodies out of the normal cervical alignment). Therefore, the cord tends to be compressed from spur formation at C5-6 and C6-7 and compressed from listhesis at C3-4 and C4-5. Often, this is accompanied by posterior canal compromise from ligamentum flavum hypertrophy.4, 14 The cord is subject to further injury from repetitive dynamic injury during normal neck movements. These static and dynamic compressive forces on the cord lead to spinal cord injury and the clinical myelopathic syndrome.4 Other skeletal conditions that predominantly lead to stenosis or deformity of the cervical spinal canal are rheumatoid arthritis, ankylosing spondylitis, and ossification of posterior longitudinal ligament (OPLL) (see Image 1). Genetic factors play a major role in the geographic prevalence of these conditions. Thoracic spinal stenosis is much more rare and often is associated with focal disease of long-standing nature. Thoracic spinal stenosis may be associated with disk bulging or herniation, hypertrophy of the posterior elements (namely, the facet and ligamentum flavum), and, occasionally, calcification of ligamentum flavum.4 LUMBAR STENOSISNarrowing of the lumbar spinal canal is an increasingly common problem, affecting 1 per 1000 persons older than 65 years. The degeneration of the vertebral motion segment, consisting of the intervertebral disk and the facet joints, is believed to be the pathophysiologic mechanism involved with the development of stenosis.15, 16, 17 The pathophysiology of disk degeneration and facet arthropathy has been investigated extensively, but the nature and etiology of pain generation are still debated. Degeneration of the annulus fibrosis results in radial tears through which a posteriorly migrated nucleus pulposus can herniate. Disk herniation in the typical posterolateral region may cause nerve root impingement (usually of the root passing to the next lower foramen). Lateral recess stenosis is the result of such herniations, leading to radiculopathy. The most common site for this is L5-S1 followed by L4-L5. Central disk bulges or herniations contribute to central canal stenosis. Degeneration of the disk also may lead to changes affecting the stability of the spinal motion segment, which consists of the 2 articular facet joints and the disk. This concept emphasizes that disease in each of the components may affect other components and elicit progressive changes in other segmental units. Osteophytes or spurs form at the endplate-annulus margins, presumably as a result of excessive motion. Associated facet and ligamentum flavum further contribute to central or lateral canal stenosis leading to neurogenic claudication, radiculopathy, or both. Degenerative disk disease itself may contribute to mechanical back pain without causing stenosis of the canal or the lateral recess.14, 18 CLINICAL PRESENTATIONStenosis of the cervical spine causes the clinical syndrome of CSM. Initial symptoms may be subtle loss of hand dexterity and mild proximal lower extremity weakness, often without neck or arm pain. With progression, spastic quadriparesis results. Pathologic reflexes such as the Hoffman sign, clonus, and/or the Babinski reflex may augment the diffuse hyperreflexia. Some patients also have associated ataxia from compression of spinocerebellar tracts.3, 8, 9, 19, 20 If associated cervical root impingement exists, patients may experience sharp radicular pain into the affected arm, with associated paresthesias and weakness referable to the compressed root. Depending on the level, some upper extremity reflexes (biceps, triceps, brachioradialis) may be depressed or absent in such patients. Males older than 55 years most commonly are affected. Up to two thirds of patients with myelopathy have deteriorating or unchanging conditions. They are also at increased risk of spinal cord injury in the setting of minor trauma. Patients with significant lumbar spinal canal narrowing report pain, weakness, numbness in the legs while walking, or a combination thereof. Onset of symptoms during ambulation is believed to be caused by increased metabolic demands of compressed nerve roots that have become ischemic due to stenosis. This is the hallmark of neurogenic claudication. The pain is relieved when the patient flexes the spine by, for example, leaning on shopping carts or sitting. Flexion increases canal size by stretching the protruding ligamentum flavum, reduction of the overriding laminae and facets, and enlargement of the foramina. This relieves the pressure on the exiting nerve roots and, thus, decreases the pain. The most common nerve affected is the L5, with associated weakness of extensor hallucis longus. RADIOLOGIC STUDIESPlain radiographs can reveal a narrow anteroposterior diameter in both congenital and acquired forms of spinal stenosis. Degenerative changes and spondylolisthesis may be found.21, 22 Myelography also can be diagnostic, by revealing a narrow dye column or a complete blockage in advanced forms. Lumbar puncture may be difficult in persons with severe stenosis. Combined computed tomography and myelography provide the most information in both sagittal and axial planes, with good visualization of bony anatomy.23 CT provides general information about canal diameter, spur formation, and foraminal stenosis. When combined with myelography, CT demonstrates central or lateral canal stenosis in both sagittal and axial planes. MRI is most useful in evaluating soft tissues and neural structures. It reveals disk degeneration, ligamentous and facet hypertrophy, malalignment, central or lateral canal stenosis, and intrinsic cord or root abnormalities, such as syrinx or contusion. MRI is not optimal for visualization of bony details (ie, spurs).24 NATURAL HISTORY AND CONSERVATIVE MEASURESCervical stenosis progresses in as many as one third of affected individuals. Among the symptoms are a propensity for initial deterioration, followed by a period of stability (may require years), and subsequent progression of myelopathy. Unfortunately, late treatment of myelopathy by decompression does not always reverse the neurologic deficit, and thus, individuals with severe cervical stenosis should undergo close neurologic follow-up.8 The natural history of lumbar spinal stenosis is not well understood. A slow progression appears to occur in all affected individuals. Even with significant narrowing, such persons are very unlikely to develop an acute cauda equina syndrome in the absence of significant disk herniation. Slow progression of dysfunction in the lumbar spine often leads to a feeling of heaviness in the legs that is only relieved by periods of rest. Infrequently, a facet joint synovial cyst will lead to severe canal stenosis and the development of subacute radiculopathy, often characterized by pain and mild weakness. This may develop as a result of trauma or arthritic changes in the facet joint.7, 25 Nonsurgical measures are aimed at symptomatic relief: analgesics, anti-inflammatory agents (including judicious use of steroids), and antispasmodics can provide relief during acute exacerbations.7 Epidural steroids have been used for stenosis; however, their success rate has been low. Physical therapy with traction and strengthening exercises helps relieve associated symptoms or muscular spasms and mechanical back pain. Unfortunately, most of these approaches only provide temporary relief. Decompression and inversion tables have also been utilized with great initial success and varying amounts of lasting benefit.26 SURGICAL TREATMENTSurgery for stenosis is indicated in persons with significant myelopathy, radiculopathy, and/or neurogenic claudication. The choice of the decompressive approach depends on the spinal region, the spinal alignment, and the anatomic nature of the compressive elements (ie, spurs vs ligamentum flavum). Controversy exists regarding the need for concomitant stabilization, which is generally reserved for cases of gross instability (eg, unstable spondylolisthesis).5, 27, 28, 29, 30, 31, 32 In the cervical spine, debate is ongoing about the superiority of anterior versus posterior approaches. Posterior decompressive laminectomy is mainly advantageous with multilevel disease and congenital stenosis. However, posterior laminectomy alone can lead to instability and kyphotic (swan neck) deformity. Some surgeons prefer the use of laminoplasty (typically used in younger patients) to preserve the integrity of the posterior elements and motion. The use of concomitant arthrodesis and fixation (ie, lateral mass fixation) reduces the risk of postoperative instability and deformity but limits flexibility and can predispose the higher levels to rapid degeneration. The posterior approach is not recommended as the sole approach for the kyphotic cervical spine.32, 33, 34, 35 The anterior approach for cervical decompression addresses the pathology from disk herniation and spur formation. This approach can be used with almost any spinal alignment, but associated risks of morbidity exist. Single-level diskectomies can be performed with or without concomitant fusion with good results, but most surgeons, including the authors, believe the risk of collapse is present without the placement of an interbody graft, spacer, cage, or disc replacement device.; thus, most surgeons advocate the use of a biomechanical device or bone in the disk space.7, 8, 36 An anterior fixation plate is not always needed in single-level disease ; however, in persons in whom multilevel diskectomies or corpectomies (vertebrectomies) are needed, concomitant anterior fixation should be strongly considered. The risk of complications is higher when corpectomies are performed on 3 or more levels. Some surgeons prefer to augment their multilevel anterior decompression and fusion with posterior stabilization. Debate is ongoing regarding the advantages and disadvantages of partial corpectomies (anterior) versus multilevel laminectomy/laminoplasties (posterior) in the treatment of severe multilevel spondylosis. The overriding factor in the decision-making algorithm is the alignment of the spine, the nature of the compressive element, and the surgeon's preference.34, 36, 37, 38, 39, 40, 41, 42, 43, 44 In the lumbar spine, the mainstay of decompressive surgery is single or multilevel laminectomy for canal decompression and foraminotomy for nerve root decompression.33 Depending on the compressive pathology, partial or complete facetectomies and diskectomy may be needed. In general, the techniques of microdecompression in the lateral recess with the use of hemilaminotomies instead of complete laminectomies preserve the biomechanical integrity of the posterior tension band and avoid potential instability or postlaminectomy flat-back syndrome. In persons in whom bilateral total facetectomies (Gill procedures) are performed, some chance of postoperative instability exists. The surgeon should consider concomitant fusion and/or stabilization in these individuals.19, 28, 33, 38, 40, 41, 43, 44, 45, 46, 47, 48 The need for any stabilization in stable spinal stenosis is clearly controversial. Some investigators have reported their results with the use of ipsilateral nerve root decompression and fusion; others have reported their preference of contralateral autologous bone fusion to preserve segmental stability.41, 49 The method employed classically is the posterolateral intertransverse fusion bilaterally through a midline approach with an autologous hip graft, local autograft (bone harvested during decompression), or allograft (ie, cadaveric). The most effective space to perform a fusion remains the interbody space because of the high loads afforded by the anterior column of the spine. The use of internal fixation is also controversial. Although better fusion results may be obtained, the outcome may not improve significantly with the addition of fixation. Pedicle screw fixation has become the most widely accepted device for spinal stabilization, but it is associated with morbidity and increased operative time. Some surgeons use translaminar facet screws instead of transpedicular screws to decrease operative time and, thus, potential morbidity. Minimally invasive techniques aiming to decrease surgical trauma and accomplish decompression of the neural elements and/or spinal stabilization will continue to gain popularity due to the potential for faster recovery and less postoperative discomfort. CONCLUSIONManagement of spinal stenosis is aimed toward symptomatic relief and prevention of neurologic sequelae. Conservative measures provide temporary relief but remain an important adjunct in the overall treatment algorithm preceding surgical decompression. Surgery is indicated when the signs and symptoms correlate with the radiologic evidence of spinal stenosis. Generally, surgery is recommended when significant radiculopathy, myelopathy (cervicothoracic), neurogenic claudication (lumbar), or incapacitating pain is present. The choice of surgical procedure and the decision to fuse the spine should be individualized to optimize the outcome. MULTIMEDIA
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