Spinal Stenosis

Spinal Stenosis

  • Author: John K Hsiang, MD, PhD; Chief Editor: Rene Cailliet, MD more…


Acute and chronic neck and lower back pain represents a major health care problem in the United States. An estimated 75% of all people will experience back pain at some time in their lives. Most patients who present with an acute episode of back pain recover without surgery, while 3-5% of patients presenting with back pain have a herniated disc, and 1-2% have compression of a nerve root. Older patients present with more chronic or recurrent symptoms of degenerative spinal disease. (See Epidemiology.)

Spinal stenosis is part of the aging process, and predicting who will be affected is not possible. No clear correlation is noted between the symptoms of stenosis and race, occupation, sex, or body type. The degenerative process can be managed, but it cannot be prevented by diet, exercise, or lifestyle.

Progressive narrowing of the spinal canal may occur alone or in combination with acute disc herniations. Congenital and acquired spinal stenoses place the patient at a greater risk for acute neurologic injury. Spinal stenosis is most common in the cervical and lumbar areas.[1, 2, 3] (See the images below.)




Oblique view of the cervical spine demonstrates 2 levels of foraminal stenosis (white arrows) resulting from facet hypertrophy (yellow arrow) and uncovertebral joint hypertrophy.







Axial cervical CT myelogram demonstrates marked hypertrophy of the right facet joints (black arrows), which results in tight restriction of the neuroforaminal recess and lateral neuroforamen.


Short recovery time T1-weighted spin-echo sagittal MRI scan demonstrates marked spinal stenosis of the C1/C2 vertebral level cervical canal resulting from formation of the panus (black arrow) surrounding the dens in a patient with rheumatoid arthritis. Long recovery time T2*-weighted fast spin-echo sagittal MRI scans better define the effect of the panus (yellow arrow) on the anterior cerebrospinal fluid space. Note the anterior displacement of the upper cervical cord and the lower brainstem.



Posterior view from a radionuclide bone scan. A focally increased uptake of nuclide (black arrow) is demonstrated within the mid-to-upper thoracic spine in a patient with Paget disease.



Lumbar spinal stenosis (LSS) implies spinal canal narrowing with possible subsequent neural compression. Although the disorder often results from acquired degenerative changes (spondylosis), spinal stenosis may also be congenital in nature (see Etiology). 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), intervertebral disk, and epidural fat. Congenital stenosis may predispose an individual with mild degenerative changes to become symptomatic earlier in life. (See the images below.)



T2-weighted sagittal MRI of the cervical spine demonstrating stenosis from ossification of the posterior longitudinal ligament, resulting in cord compression.




Severe cervical spondylosis can manifest as a combination of disk degeneration, osteophyte formation, vertebral subluxation, and attempted autofusion as depicted in this sagittal MRI. Also, note the focal kyphosis, which is typical in severe forms.


LSS is classified by anatomy or etiology. Anatomic subclassifications include central canal and lateral recess stenosis. The classification of lumbar stenosis is important because of the implications of the underlying etiology and because it affects the therapeutic strategy, specifically the surgical approach.

Stenosis of the central cervical and thoracic spine may result in myelopathy from cord compression.[4, 5] Canal stenosis in the lumbosacral region often results in radicular pain, neurogenic claudication, or both. (See Clinical Presentation.)

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. (See Treatment and Management.) Surgical decompression is indicated in persons who experience incapacitating pain, claudication, neurologic deficit, or myelopathy.[6, 7] Concomitant stabilization is reserved for individuals in whom segmental instability is suspected (ie, patients with spondylolisthesis showing abnormal movement on dynamic studies).



Central canal stenosis, commonly occurring at an intervertebral disk level, defines midline sagittal spinal canal diameter narrowing that may elicit neurogenic claudication (NC) or pain in the buttock, thigh, or leg. Such stenosis results from ligamentum flavum hypertrophy, inferior articulating process (IAP), facet hypertrophy of the cephalad vertebra, vertebral body osteophytosis, vertebral body compression fractures, and herniated nucleus pulposus (HNP). Abnormalities of the disk usually do not cause symptoms of central stenosis in a normal-sized canal. In developmentally small canals, however, a prominent bulge or small herniation can cause symptomatic central stenosis. Large disk herniations can compress the dural sac and compromise its nerves, particularly at the more cephalad lumbar levels where the dural sac contains more nerves. (See the images below.)



Lateral T2-weighted magnetic resonance imaging (MRI) scan demonstrating narrowing of the central spinal fluid signal (L4-L5), suggesting central canal stenosis.







Axial T2 magnetic resonance imaging (MRI) scan (L4-L5) in the same patient as in the above image, confirming central canal stenosis.




Trefoil appearance characteristic of central canal stenosis due to a combination of zygapophysial joint and ligamentum flavum hypertrophy.




Lumbar computed tomography (CT) myelogram scan dem

Lumbar computed tomography (CT) myelogram scan demonstrates a normal central canal diameter.



Lateral recess stenosis (ie, lateral gutter stenosis, subarticular stenosis, subpedicular stenosis, foraminal canal stenosis, intervertebral foramen stenosis) is defined as narrowing (less than 3-4 mm) between the facet superior articulating process (SAP) and the posterior vertebral margin. Such narrowing may impinge the nerve root and subsequently elicit radicular pain. This lateral region is compartmentalized into entrance zone, mid zone, exit zone, and far-out stenosis. Amundsen and colleagues found concomitant lateral recess stenosis in all cases of central canal stenosis.[8] (See the image below.)

Lateral and axial magnetic resonance imaging (MRI) scan demonstrating right L4 lateral recess stenosis secondary to combination of far lateral disk protrusion and zygapophysial joint hypertrophy.


The entrance zone lies medial to the pedicle and SAP and, consequently, arises from facet joint SAP hypertrophy. Other causes include developmentally short pedicle and facet joint morphology, as well as osteophytosis and HNP anterior to the nerve root. The lumbar nerve root compressed below SAP retains the same segmental number as the involved vertebral level (eg, L5 nerve root is impinged by L5 SAP).

The mid zone extends from the medial to the lateral pedicle edge. Mid-zone stenosis arises from osteophytosis under the pars interarticularis and bursal or fibrocartilaginous hypertrophy at a spondylolytic defect.

Exit-zone stenosis involves an area surrounding the foramen and arises from facet joint hypertrophy and subluxation, as well as superior disk margin osteophytosis. Such stenosis may impinge the exiting spinal nerve.

Far-out (extracanalicular) stenosis entails compression lateral to the exit zone. Such compression occurs with far lateral vertebral body endplate osteophytosis and when the sacral ala and L5 transverse process impinge on the L5 spinal nerve.


Cervical stenosis

The anteroposterior (AP) diameter of the normal adult male cervical canal has a mean value of 17-18 mm at vertebral levels C3-5. The lower cervical canal measures 12-14 mm. Cervical stenosis is associated with an AP diameter of less than 10 mm, while diameters of 10-13 mm are relatively stenotic in the upper cervical region. (See image below.)

Sagittal measurements taken of the anteroposterior diameter of the cervical spinal canal are highly variable in otherwise healthy persons. An adult male without spinal stenosis has a diameter of 16-17 mm in the upper and middle cervical levels. Magnetic resonance imaging (MRI) scans and reformatted computed tomography (CT) images are equally as effective in obtaining these measurements, while radiography is not accurate.


Movement of the cervical spine exacerbates congenital or acquired spinal stenosis. In hyperextension, the cervical cord increases in diameter. Within the canal, the anterior roots are pinched between the annulus margins and spondylitic bony bars. In the posterior canal, hypertrophic facet joints and thickened infolded ligamentum flavum compress the dorsal nerve roots. In hyperflexion, neural structures are tethered anteriorly against the bulging disc annulus and spondylitic bars. In the event of a vertebral collapse, the cervical spine loses its shape, which may result in anterior cord compression.

In the central cervical spinal region, hypertrophy of the ligamentum flavum, bony spondylitic hypertrophy, and bulging of the disc annulus contribute to development of central spinal stenosis. In each case, the relative significance of each structure contributing to the stenotic pattern is variable.

Congenital stenosis of the cervical spine may predispose an individual to myelopathy as a result of minor trauma or spondylosis.[4, 5, 9, 10, 11, 12, 13]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 evidenceofspondylosis.[4, 10, 12, 13, 14, 15, 16]

Lateral cervical stenosis results from encroachment on the lateral recess and the neuroforamina of the cervical region, primarily as a result of hypertrophy of the uncovertebral joints, lateral disc annulus bulging, and facet hypertrophy.

Thoracic spinal stenosis

The thoracic spinal canal varies from 12 to 14 mm in diameter in the adult. Thoracic spinal stenosis is often associated with focal disease of a long-standing nature. It 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. Primary central thoracic spinal stenosis is rare. In some cases, hypertrophy or ossification of the posterior longitudinal ligament results in central canal stenosis.[5] Lateral thoracic stenosis may result from hypertrophy of facet joints with occasional synovial cyst encroachment.

Lumbar spinal stenosis

The diameter of the normal lumbar spinal canal varies from 15 to 27 mm. Lumbar stenosis results from a spinal canal diameter of less than 12 mm in some patients; a diameter of 10 mm is definitely stenotic.

Keim and colleagues present the following lumbar spinal stenosis (LSS) anatomical classification scheme[17] :

  • Lateral, secondary to superior articulating process (SAP) hypertrophy
  • Medial, secondary to inferior articulating process (IAP) hypertrophy
  • Central, due to hypertrophic spurring, bony projection, or ligamentum flavum/laminar thickening
  • Fleur de lis (clover leaf), from laminar thickening with subsequent posterolateral bulging


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 spine responds to physiological stresses with bone growth at the superior and inferior margins of the vertebral body (osteophytes). Osteophytes can form anteriorly or posteriorly. Posterior osteophytes narrow the intraspinal diameter and also cause lateral recess stenosis. This results in spinal cord or nerve root impingement. Furthermore, arthritic degeneration causes formation of synovial cysts and hypertrophy of the facet joints, which further compromise the patency of the spinal canal and the neural foramina.

Spinal stenosis results from progressive narrowing of the central spinal canal and the lateral recesses. The essential content of the spinal canal includes the spinal cord, the cerebrospinal fluid (CSF) of the thecal sac, and the dural membranes that enclose the thecal sac. In the absence of prior surgery, tumor, or infection, the spinal canal may become narrowed by bulging or protrusion of the intervertebral disc annulus, herniation of the nucleus pulposus posteriorly, thickening of the posterior longitudinal ligament, hypertrophy of the facet joints, hypertrophy of the ligamentum flavum, epidural fat deposition, spondylosis of the intervertebral disc margins, uncovertebral joint hypertrophy in the neck, or a combination of 2 or more of the above factors.[18]

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.[5, 19]

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.[5]

Disk desiccation and degenerative disk disease (DDD) with resulting loss of disk height may induce segmental instability. Such instability incites vertebral body and facet joint hypertrophy. Cephalad vertebral body IAP hypertrophy promotes central spinal canal stenosis. Further canal volume loss results from HNP, ligamentum flavum hypertrophy, and disk space narrowing.

Alternatively, the caudal vertebral body superior articulating process (SAP) contributes to lateral recess and foraminal stenosis (see the image below). Indeed, facet hypertrophy between L4 and L5 vertebrae may impinge the L4 nerve root in the foramen and the L5 proximal nerve root sheath in the lateral recess. The 2 lower motion segments (L3-L4, L4-L5) are most commonly affected by degenerative stenosis. These segments are in a transition zone from the rigid sacrum to the mobile lumbar spine. In addition, the posterior joints in this area have less of a sagittal orientation, which affords more rotation and are therefore more vulnerable to rotatory strains.

Oblique 3-dimensional shaded surface display CT reconstruction of right foraminal stenosis resulting from unilateral facet hypertrophy (black arrow). The volume of the reconstruction has been cut obliquely across the neuroforaminal canal.

Jenis and An eloquently describe foraminal stenosis pathoanatomy, characterized by disk desiccation and DDD, which narrows disk height, permitting the caudad SAP to sublux anterosuperiorly.[20] Such subluxation decreases foraminal space. Continued subluxation with resulting biomechanical disruption provokes osteophytosis and ligamentum flavum hypertrophy, further compromising foraminal volume. Anteroposterior (transverse) stenosis ultimately results from narrow disk height and hypertrophy anterior to the facet; specifically, the SAP and posterior vertebral body transversely trap the nerve root. Furthermore, in vertical (craniocaudal) stenosis, posterolateral vertebral endplate osteophytes and a lateral HNP may impinge the spinal nerve against the superior pedicle.

Dynamic foraminal stenosis implies intermittent lumbar extension-provoked nerve root impingement from HNP, osteophytosis, and vertebral body slippage. Such dynamic stenosis with associated intermittent position-dependent symptoms may not manifest on imaging studies, thereby confounding diagnosis. Other factors promoting development of LSS include shortened gestational age and synovial facet joint cysts with resulting radicular compression. Adult degenerative scoliosis, secondary to DDD-induced instability with subsequent vertebral rotation and asymmetric disk space narrowing, promotes facet hypertrophy and subluxation in the curve concavity. Degenerative spondylolisthesis, when combined with facet hypertrophy, causes central canal and lateral recess stenosis.

Proposed mechanisms for development of neurogenic claudication (NC) include cauda equina microvascular ischemia, venous congestion, axonal injury, and intraneural fibrosis. Ooi and colleagues myeloscopically observed ambulation-provoked cauda equina blood vessel dilation with subsequent circulatory stagnation in patients with LSS who have NC.[21] They proposed that ambulation dilates the epidural venous plexus, which, amidst narrow spinal canal diameter, increases epidural and intrathecal pressure. Such elevation of pressure ultimately compresses the cauda equina, compromises its microcirculation, and causes pain.

Another pain generator may be the dorsal root ganglion (DRG), which contains pain-mediating neuropeptides, such as substance P, that possibly increase with mechanical compression. The DRG varies spatially within the lumbosacral spine, with L4 and L5 DRG in an intraforaminal position and S1 DRG located intraspinally. Such foraminal placement may predispose to stenotic compression with subsequent radicular symptomology.


Primary stenosis is uncommon, occurring in only 9% of cases. Congenital malformations include the following:

  • Incomplete vertebral arch closure (spinal dysraphism)
  • Segmentation failure
  • Achondroplasia
  • Osteopetrosis

Developmental flaws include the following:

  • Early vertebral arch ossification
  • Shortened pedicles
  • Thoracolumbar kyphosis
  • Apical vertebral wedging
  • Anterior vertebral beaking (Morquio syndrome)
  • Osseous exostosis

Secondary (acquired) stenosis arises from degenerative changes, iatrogenic causes, systemic processes, and trauma. Degenerative changes include central canal and lateral recess stenosis from posterior disk protrusion, zygapophyseal joint and ligamentum flavum hypertrophy, and spondylolisthesis. Iatrogenic changes result following surgical procedures such as laminectomy, fusion, and diskectomy. Systemic processes that may be involved in secondary stenosis include Paget disease, fluorosis, acromegaly, neoplasm, and ankylosing spondylitis. (See the image below.)

Anterior view of a lumbar myelogram demonstrates stenosis related to Paget disease. Myelography is limited because of the superimposition of multiple spinal structures that contribute to the overall pattern of stenosis.


The central canal and the neurorecess may be compromised by tumor infiltration, such as metastatic disease of the spine, or by infectious spondylitis. An abscess may directly compress the spinal cord if it is contained in the epidural space, while discitis and vertebral osteomyelitis may compress the canal following vertebral collapse. Paget disease results in spinal stenosis as a result of enlargement of the vertebral body, while idiopathic ossification of the posterior longitudinal ligament directly narrows the central spinal canal most often in the cervical or thoracic regions.

Skeletal conditions that predominantly lead to stenosis or deformity of the cervical spinal canal include rheumatoid arthritis, ankylosing spondylitis, and ossification of posterior longitudinal ligament (OPLL). Genetic factors play a major role in the geographic prevalence of these conditions.



Approximately 250,000-500,000 US residents have symptoms of spinal stenosis. This represents about 1 per 1000 persons older than 65 years and about 5 of every 1000 persons older than 50 years. About 70 million Americans are older than 50 years, and this number is estimated to grow by 18 million in the next decade alone, suggesting that the prevalence of spinal stenosis will increase. Lumbar spinal stenosis (LSS) remains the leading preoperative diagnosis for adults older than 65 years who undergo spine surgery. The incidence of lateral nerve entrapment is reportedly 8-11%. Some studies implicate lateral recess stenosis as the pain generator for 60% of patients with symptomatology of failed back surgery syndrome.

As many as 35% of persons who are asymptomatic and aged 20-39 years demonstrate disc bulging. CT scanning and MRI studies in patients who are asymptomatic and younger than 40 years demonstrate a 4-28% occurrence of spinal stenosis. Most persons older than 60 years have spinal stenosis to some degree. Because most patients with mild spinal stenosis are asymptomatic, the absolute frequency can only be estimated.[3]

Incidence of foraminal stenosis increases in lower lumbar levels because of increased dorsal root ganglion (DRG) diameter with resulting decreased foramen (ie, nerve root area ratio). Jenis and An cite commonly involved roots as L5 (75%), L4 (15%), L3 (5.3%), and L2 (4%).[20] The lower lumbar levels maintain greater obliquity of nerve root passage, as well as higher incidence of spondylosis and DDD, further predisposing patients to L4 and L5 nerve root impingement.

Cervical stenosis resulting from ossification of the posterior longitudinal ligament is more common among Asians, and LSS occurs most frequently in males. Patients with LSS due to degenerative causes generally are aged at least 50 years; however, LSS may be present at earlier ages in cases of congenital malformations.


Spinal stenosis can result in significant morbidity. Severe disability and death may result from the association of cervical stenosis with even minor trauma resulting in the central cord syndrome. Both upper (cervical) and lower (lumbar) spinal stenosis may result in motor weakness and chronic pain. Severe lumbar stenosis is associated with cauda equina syndrome.

In the patient with spinal canal stenosis, flexion or marked hyperextension may result in further compromise of the spinal canal in the absence of a fracture. Anterior compression of the cord may result in a central spinal cord syndrome, and dorsal compression may result in a partial dorsal column syndrome.

Central spinal stenosis of the cervical or thoracic regions may result in neurosensory changes at the level of the spinal stenosis or may further compress the spinal cord, resulting in myelopathy. The effects of central spinal canal stenosis may result in lower extremity weakness and gait disturbance.

Lateral spinal stenosis generally results in symptoms that are directly related to compression of the nerve roots at the level of the stenosis. Both pain and muscular weakness may result from hypertrophy of the facet joints, spondylosis deformity, bulging of the disc annulus, or herniation of the nucleus pulposus. Although large central disc herniations occur, most extruded disc fragments migrate laterally, and some disc fragments move to a position that is superior or inferior to the interspace.

Many patients with lumbar spinal stenosis (LSS) show symptomatic and functional improvement or remain unchanged over time.[22] In one study 90% of 169 untreated patients with suspected lateral recess stenosis improved symptomatically after 2 years.[23] A 4-year study of 32 patients treated conservatively for moderate stenosis reported unchanged symptoms in 70% of patients, improvement in 15%, and worsening in 15%. Walking capacity improved in 37% of patients, remained unchanged in 33%, and worsened in 30%.[24]

The natural history of LSS 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 leads 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.[9, 25]

Patient Education

Patients with lumbar spinal stenosis should be educated to avoid aggravating factors, such as excessive lumbar extension and downhill ambulation. Additionally, patients should be instructed on correct posture and should also receive instructions concerning a home exercise program (eg, flexion-biased lumbar stabilization, flexibility training, gluteal strengthening, aerobic conditioning).

For excellent patient education resources, visit eMedicine’s Back, Ribs, Neck, and Head Center and Muscle Disorders Center. Also, see eMedicine’s patient education articles, Back Pain, Lumbar Laminectomy, and Chronic Pain.


Clinical Presentation


The primary clinical manifestation of spinal stenosis is chronic pain. In patients with severe stenosis, weakness and regional anesthesia may result. Among the most serious complications of severe spinal stenosis is central cord syndrome. Central cord syndrome is the most common incomplete cord lesion. The presentation commonly is associated with an extension injury in a patient with an osteoarthritic spine. In hyperextension injury, the cord is injured within the central gray matter, which results in proportionally greater loss of motor function of upper extremities than loss of motor function of lower extremities, with variable sensory sparing.

Patients with spinal stenosis become symptomatic when pain, motor weakness, paresthesia, or another neurologic compromise causes distress. Spinal stenosis of the thoracic spine is more likely to directly affect the spinal cord because of the relatively narrow thoracic spinal canal.

Spinal stenosis of the cervical and thoracic regions may contribute to neurologic injury, such as development of a central spinal cord syndrome following spinal trauma. Spinal stenosis of the lumbar spine is associated most commonly with midline back pain and radiculopathy. In cases of severe lumbar stenosis, innervation of the urinary bladder and the rectum may be affected, but lumbar stenosis most often results in back pain with lower extremity weakness and numbness along the distribution of nerve roots of the lumbar plexus.

Spinal canal size is not always predictive of clinical symptoms, and some evidence suggests that body mass may play a role in limitations of function in this population.[26]

Severe radiologic stenosis in otherwise asymptomatic individuals suggests inflammation, not just mechanical nerve root compression. Specific inflammation generators may include herniated nucleus pulposus (HNP), ligamentum flavum, and facet joint capsule.

Metastatic and infectious processes that affect the spine may present with both regional pain and signs of central spinal canal narrowing. The regional pain may result from pathologic fractures or nerve root compression by the tumor or abscess. Long tract findings may result from bone fragments, a hemorrhage, an abscess, or a tumor compressing the spinal cord.

Cervical stenosis

Stenosis of the cervical spine causes the clinical syndrome of cervical spondylotic myelopathy (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.[4, 10, 11, 27, 28]

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.

Lumbar stenosis

Katz and colleagues report that the historical findings most strongly associated with lumbar spinal stenosis (LSS) include advanced age, severe lower extremity pain, and absence of pain when the patient is in a flexed position.[29] Fritz and colleagues contend that the most important elements involve the postural nature of the patient’s pain, stating that absence of pain or improvement of symptoms when seated assists in ruling in LSS.[22] Conversely, LSS cannot be ruled out when sitting is the most comfortable position for the patient and standing/walking is the least comfortable.

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.

LSS classically presents as bilateral neurogenic claudication (NC). Unilateral radicular symptoms may result from severe foraminal or lateral recess stenosis. Patients, typically aged more than 50 years, report insidious-onset NC manifesting as intermittent, crampy, diffuse radiating thigh or leg pain with associated paresthesias. Indeed, leg pain affects 90% of patients with LSS.

In a retrospective review of 75 patients with radiographically confirmed LSS, reports of weakness, numbness or tingling, radicular pain, and NC were in almost equal proportions. The most common symptom was numbness or tingling of the legs.[30]

NC pain is exacerbated by standing erect and downhill ambulation and is alleviated with lying supine more than prone, sitting, squatting, and lumbar flexion. Getty and colleagues documented 80% pain diminution with sitting and 75% with forward bending.[31] Lumbar spinal canal and lateral recess cross-sectional area increases with spinal flexion and decreases with extension. Furthermore, cross-sectional area is reduced 9% with extension in the normal spine and 67% with severe stenosis. The Penning rule of progressive narrowing implies that the more narrowed the canal by stenosis, the more it narrows with spinal extension. Schonstrom and colleagues have shown that spinal compressive loading from weight bearing reduces spinal canal dimensions.[32]

NC, unlike vascular claudication, is not exacerbated with biking, uphill ambulation, and lumbar flexion and is not alleviated with standing. Patients with LSS compensate for symptoms by flexing forward, slowing their gait, leaning onto objects (eg, over a shopping cart) and limiting distance of ambulation. Unfortunately, such compensatory measures, particularly in elderly osteoporotic females, promote disease progression and vertebral fracture. Pain radiates downward in NC and, in contrast, upward in vascular claudication. Hall and colleagues note the presence of radiculopathy in 6% and NC in 94% of patients with LSS.[33]

Distinguishing between neurogenic and vascular claudication is important because the treatments, as well as the implications, are quite different. Vascular claudication is a manifestation of peripheral vascular disease and arteriosclerosis. Other vessels, including the coronary, vertebral, and carotid, are also often affected. Further complicating diagnosis and treatment in some patients, neurogenic and vascular claudication may occur together. This is because both conditions frequently occur in the elderly population.

Physical Examination

Patients with cervical stenosis usually present with cervical radiculopathy, with or without myelopathy. Typically, the condition involves the lower cervical spine. Patients frequently complain of radiating arm pain with numbness and paresthesia in the involved dermatomes. Occasionally, associated weakness occurs in the muscles supplied by that nerve root. If the stenosis is severe enough, or if it is positioned centrally in the spine, patients may present with signs and symptoms of myelopathy (spinal cord dysfunction). Typically, these patients complain of finger numbness, clumsiness, and difficulty walking due to spasticity and loss of position sense. In more severe cases, the patients can have bowel and bladder control dysfunction. Upon examination, these patients have “long-tract signs” such as hyperreflexia and clonus.

Katz and colleagues report physical examination findings most strongly associated with lumbar spinal stenosis (LSS) include wide-based gait, abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular abnormalities[29] ; however, Fritz and colleagues state physical examination findings do not seem helpful in determining the presence or absence of LSS.[22]

Patients with LSS usually present with a constellation of symptoms that include lower back pain, radiating leg pain (unilateral or bilateral), and possible bladder and bowel difficulties. The classic presentation is radiating leg pain associated with walking that is relieved by rest (neurogenic claudication). When patients bend forward, the pain diminishes. Rarely, patients with LSS present with cauda equina syndrome (bilateral leg weakness, urinary retention due to atonic bladder).

Physical examination findings are frequently normal in patients with LSS. Nevertheless, review of the literature suggests diminished lumbar extension appears most consistently, varies less, and constitutes the most significant finding in LSS. Other positive findings include loss of lumbar lordosis and forward-flexed gait. Charcot joints may be present in long-standing disease. Radiculopathy may be noted with motor, sensory, and/or reflex abnormalities. Asymmetric muscle stretch reflexes and focal myotomal weakness with atrophy occur more with lateral recess than central canal stenosis. Some report objective neurologic deficits in approximately 50% of LSS cases. Provocative maneuvers include pain reproduction with ambulation and prone lumbar hyperextension. Pain alleviation occurs with stationary biking and lumbar flexion.

Patients may also have a positive result from the stoop test, which was described by Dyck in 1979.[34] This is performed by having the patient walk with an exaggerated lumbar lordosis until NC symptoms appear or are worsened. The patient is then told to lean forward. Reduction of NC symptoms is a positive result and is suggestive of NC.

Negative findings in the physical examination include skin color, turgor, and temperature; normal distal lower extremity pulses; and an absence of arterial bruits.

Importantly, remember the 5 P s of vascular claudication, as follows:

  • Pulselessness
  • Paralysis
  • Paresthesia
  • Pallor
  • Pain

The absence of these problems, excluding pain and paresthesias, which are common to neurogenic and vascular claudication, should give the clinician confidence in the diagnosis of NC. If vascular claudication is suspected, referral to an internist for a workup is indicated. This includes a serum cholesterol level, arterial Doppler studies, ankle-brachial index values, and, in some cases, arteriography.

Dural tension signs should be unremarkable. Lumbar segment mobilization often fails to reproduce pain, and palpation locates no trigger points.


Diagnostic Considerations

Problems to be considered in these patients include the following:

  • Rheumatologic – Ankylosing spondylitis/spondyloarthropathy, diffuse idiopathic skeletal hyperostosis (DISH)
  • Infectious – Epidural, subdural, intradural abscess; diskitis; Pott disease
  • Metabolic – Osteomalacia, parathyroid disease, vitamin B-12 or folic acid deficiency
  • Traumatic – Lumbar strain
  • Developmental/congenital – Scoliosis
  • Vascular – Peripheral vascular disease (with vascular claudication), abdominal aortic dissection
  • Psychogenic – Conversion disorder, malingering
  • Other – Metastatic breast cancer, prostate cancer, Paget disease


Approach Considerations

The goal of spinal imaging is to localize the site and level of disease. It also is used to help differentiate conditions for which patients require surgery and conditions for which patients can recover with conservative treatment. Imaging studies used in lumbar spinal stenosis include standard radiography, MRI, CT scanning, nuclear imaging, and angiography (rarely). Related studies that may be warranted are needle electromyography, nerve conduction studies, and somatosensory evoked potentials.

Standard radiographs remain the recommended initial imaging study of choice. MRI remains the imaging modality of choice for lumbar spinal stenosis. CT scan provides excellent central canal, lateral recess, and neuroforaminal visualization. With regard to nuclear imaging, medical diseases related to the bones of the vertebral bodies present with markedly increased nuclide uptake. Angiography is rarely indicated except in patients with arteriovenous malformations, dural fistulas, and vascular spinal tumors.

Needle electromyography can help diagnose lumbosacral radiculopathy. Nerve conduction studies can help differentiate lumbar spinal stenosis from other confounding neuropathic conditions (eg, lumbosacral plexopathy, generalized peripheral neuropathy). Somatosensory evoked potentials are useful intraoperatively during decompressive surgery to assist the physician in diagnosis of lumbar spinal stenosis if clinical and imaging findings are equivocal.In 2007, the American College of Physicians (ACP) and the American Pain Society issued new guidelines for the diagnosis and treatment of low back pain that strongly oppose the early use of x-ray imaging, as randomized trials showed no benefit, and recommend avoiding other diagnostic imaging unless serious conditions such as cancer are suspected.[35]

These guidelines were reinforced by the ACP’s 2011 guidelines for the diagnostic imaging of low back pain, which emphasize even more strongly that routine diagnostic imaging of patients with low back pain does not improve the patient’s condition and may, in fact, cause harm. Early imaging is recommended only for patients who also have serious risk factors for cancer, spinal infection, cauda equina syndrome, or neurological disorders. Follow-up imaging is recommended only for patients who have undergone treatment and have minor risk factors for cancer, inflammatory back disease, vertebral compression fracture, radiculopathy, or symptomatic spinal stenosis.[36]


Approach Considerations

Management of spinal stenosis is aimed toward symptomatic relief and prevention of neurologic sequelae. Conservative measures, such as pharmacologic therapy and physical therapy, provide temporary relief but remain an important adjunct in the overall treatment algorithm preceding surgical decompression. Nonsurgical measures are aimed at symptomatic relief; analgesics, anti-inflammatory agents (including judicious use of steroids), and antispasmodics can provide relief during acute exacerbations.[9] Conservative and surgical treatments have not been subjected to rigorous well-designed study.

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.

Unlike acute lumbar disc herniation, spinal stenosis is not typically treated using interventional radiologic techniques. Pain management, including facet injections, may provide temporary relief in patients; however, biopsy of metastatic spinal disease is performed easily using CT guidance. Spinal stenosis associated with compression fractures has been successfully treated using percutaneous vertebroplasty.[37, 38, 39]

Cervical stenosis progresses to myelopathy in as many as one third of affected individuals. 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.[10]

Treatment outcome predictors do not exist; specifically, severe spinal degenerative changes do not necessarily correlate with an unfavorable prognosis or mandate surgery.

Simotas and colleagues noted that 12 of 49 patients treated conservatively with incorporation of analgesics, physical therapy, and epidural steroid injection reported sustained improvement.[40]

Although epidural steroids have been used for stenosis, 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 used with great initial success and varying amounts of lasting benefit.[41]

Pharmacologic Therapy

First-line pharmacotherapy for lumbar spinal stenosis (LSS) includes NSAIDs, which provide analgesia at low doses and quell inflammation at high doses. An appropriate therapeutic NSAID plasma level is required to achieve anti-inflammatory benefit.

Aspirin, which binds irreversibly to cyclo-oxygenase and requires larger doses to control inflammation, may cause gastritis; consequently, it is not recommended. Additionally, it may induce multiorgan toxicity, including renal insufficiency, peptic ulcer disease, and hepatic dysfunction. Cyclo-oxygenase isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control. Tramadol and acetaminophen confer analgesia but do not affect inflammation.

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation results from muscle relaxation, promoting further patient relaxation. Such sedative side effects encourage evening dosing for patients who need to get sufficient sleep but may limit safe performance of some functional activities.

Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their use in elderly persons. These include somnolence, dry mouth, dry eyes, and constipation. More concerning are the possible arrhythmias that may occur when used in combination with other medications.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, cotreatment with a psychologist or other addiction specialist is recommended for patients with a history of substance abuse. Patients may be asked to sign a medication contract restricting them to 1 practitioner, 1 pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling of medication.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis.[42] These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Matsudaira et al tested the effectiveness of limaprost, an oral prostaglandin E1 derivative, against that of etodolac, an NSAID, in improving the health-related quality of life in patients with symptomatic LSS.[43] In a randomized, controlled trial, 66 patients suffering from central stenosis with acquired, degenerative LSS, along with neurogenic intermittent claudication and bilateral leg numbness related to the cauda equina, were administered a daily dose of limaprost (15 μg) or etodolac (400 mg) for 8 weeks. The results indicated that limaprost was more effective than etodolac in improving patients’ physical functioning, vitality, and mental health and in reducing pain and leg numbness.

In 2008, the North American Spine Society (NASS) issued evidence-based guidelines for the diagnosis and treatment of degenerative lumbar spinal stenosis. Little evidence was found to support any long-term benefits from pharmacological treatment.[44]

Physical Therapy

Patients with lumbar spinal stenosis (LSS) often benefit from conservative treatment and participation in a physical therapy (PT) program. However, the NASS guideline states that there is insufficient evidence to support the effectiveness of physical therapy.[44] Lumbar extension exercises should be avoided in this population, as spinal extension and increased lumbar lordosis are known to worsen LSS. Flexion exercises for the lumbar spine should be emphasized, as they reduce lumbar lordosis and decrease stress on the spine. Spinal flexion exercises increase the spinal canal dimension, thus reducing neurogenic claudication (NC). Williams’ flexion-biased exercises target increased lumbar lordosis, paraspinal and hamstring inflexibility, and abdominal muscle weakness. These exercises incorporate knee-to-chest maneuvers, pelvic tilts, wall-standing lumbar flexion, and avoidance of lumbar extension.

Two-stage treadmill testing has demonstrated longer walking times on an inclined treadmill, presumably due to promotion of spinal flexion. Conversely, level treadmill testing is thought to promote more spinal extension-induced NC and elicit earlier symptom onset and longer recovery time. Ancillary exercises to target weak gluteals, as well as shortened hip flexors and hamstrings, are indicated. Physical examination should be performed to assess for concurrent degenerative hip disease, which may mimic LSS. Traction harness-supported treadmill and aquatic ambulation to reduce compressive spine loading has been shown to improve lumbar range of motion (ROM), straight leg raising, gluteal and quadriceps femoris muscle force production, and maximal (up to 15 min) walking time.[45]

Others advocate stationary cycling and abdominal muscle strengthening. Passive modalities such as heat, cold, transcutaneous electrical nerve stimulation (TENS), and ultrasound may provide transient analgesia and increased soft tissue flexibility in LSS patients.

The addition of a rolling walker is often necessary in many cases. The rolling walker provides some stability and promotes a flexed posture, which allows the afflicted patient to ambulate greater distances.

Surgical Intervention

Surgery for spinal stenosis is indicated for significant myelopathy, radiculopathy, and/or neurogenic claudication. Which decompressive approach is chosen depends on the spinal region, the spinal alignment, and the anatomic nature of the compressive elements. Whether concomitant stabilization is needed remains controversial. Most often than not, fusion is not necessary after decompressive lumbar laminectomy. Outcomes for lumbar spinal stenosis vary and are difficult to assess because of vaguely defined outcome measures, study designs, observer bias, and inadequate outcome data categorization.

It is clear that patients with severe lumbar spinal stenosis with significant symptoms can benefit from lumbar decompressive surgery. However, whether patients with moderate lumbar spinal stenosis with less severe symptoms should also have surgery is unclear. A randomized controlled study of 94 patients with moderate lumbar spinal stenosis underwent either surgical treatment or nonsurgical treatment. The results of the study are based on a 6-year follow-up. The conclusion of this study suggests that decompressive surgery of moderate lumbar spinal stenosis provided slight but consistent functional ability improvement, especially compared to nonoperative measures.[46]

According to the 2008 NASS guideline, decompressive surgery alone helps 80% of patients with severe symptoms. In patients with moderate symptoms, surgery is more effective than other interventions.[44]

Epidural Steroid Injection

Epidural steroid injection (ESI) provides aggressive-conservative treatment for patients with lumbar spinal stenosis (LSS) who demonstrate limited response to oral medication, physical therapy, and other noninvasive measures. The 2008 NASS guideline states that nonfluoroscopically guided interlaminar epidural steroid injections can provide short-term relief. However, using contrast-enhanced fluoroscopy to guide epidural steroid injections improves the accuracy of medication delivery. A multiple injection regimen of radiographically-guided transforaminal or caudal ESI can produce long-term relief in patients with neurogenic claudication or radiculopathy.[44]

Corticosteroids may inhibit edema formation from microvascular injury sustained by mechanically compressed nerve roots. Furthermore, corticosteroids inhibit inflammation by impairing leukocyte function, stabilizing lysosomal membranes, and reducing phospholipase A2 activity. Lastly, corticosteroids may block nociceptive transmission in C fibers. When using oral steroids (in rapid tapering fashion), remember that possible side effects may include fluid retention, skin flushing, and shakiness. Local anesthetic may be combined with corticosteroids to provide immediate pain relief and diagnostic feedback on the proximity of the injectate to the putative pain generator.

Caudal ESI entails needle placement through the sacral hiatus into the sacral epidural space. Advantages include ease of performance and low risk of dural puncture. Disadvantages include large injectate volumes (6-10 mL) necessary to ensure adequate medication spread to more cephalad pathology (ie, above L4-L5). Furthermore, such large volumes potentially may dilute the effect of the corticosteroid.

Interlaminar ESI entails needle passage through the interlaminar space, with subsequent injection directly into the epidural space. Consequently, delivery of medication occurs closer to the affected spinal segmental level than in caudal ESI. Disadvantages include greater potential for dural puncture and, as with caudal ESI, limited spread of medication to the target site if a midline raphe or epidural scarring exists. Furthermore, interlaminar injection delivers medication to the posterior epidural space with possible limited ventral diffusion to nerve root impingement sites.

Transforaminal ESI facilitates precise deposit of higher steroid concentrations closer to the involved spinal segment and, consequently, might prove more efficacious in reducing pain. Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis. Bilateral transforaminal ESI also may be used to treat bilateral central stenosis-induced NC pain when imaging studies demonstrate limited posterior epidural space, thereby precluding safe interlaminar ESI. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.


Absolute contraindications to ESI include bleeding diathesis and anticoagulation therapy because of the increased risk of epidural hematoma. While the actual incidence of this complication is unknown, estimates in the literature suggest is occurs less than 1 in 150,000 outpatient epidural injections. Anticoagulation therapy (eg, warfarin, heparin) should be stopped a few days prior to injection. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking warfarin, PT/INR should be drawn the day of the procedure. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be discontinued before the procedure in accordance with their half-life and hematologic profile.

Other absolute contraindications include systemic infection, injectate allergy, and pregnancy (because of the teratogenicity of fluoroscopy). Relative contraindications include diabetes mellitus (DM) and congestive heart failure, given the hyperglycemic and fluid retention properties of corticosteroids, respectively. Other relative contraindications include adrenal dysfunction and hypothalamic-pituitary axis suppression.

ESI-associated limitations

Serious complications, although rare, include infection (eg, epidural or subdural abscess) and epidural hematoma. Epidural hematoma has been associated with traumatic needle insertions, but this is neither sensitive nor specific for predicting development. Vandermeulen and colleagues reported 61 case reports in the literature between 1904 and 1994 after central nervous blocks.[47] Dural puncture (in 5% of lumbar interlaminar ESIs and 0.6% of caudal injections) with possible subsequent subarachnoid anesthetic/corticosteroid deposition may provoke neurotoxicity, sympathetic blockade with hypotension, and/or spinal headache; however, contrast-enhanced fluoroscopic guidance minimizes the possibility of dural puncture and intravascular injection.

Therapeutic ESI techniques are performed ideally using fluoroscopic guidance and radiologic contrast dye enhancement to ensure delivery of injectate to the target site. Studies document misplacement of 40% of caudal and 30% of interlaminar injections performed without fluoroscopy, even by experienced injectionists.

Transient corticosteroid dose-related side effects include facial flushing, low-grade fever, insomnia, anxiety, agitation, hyperglycemia, and fluid retention. Steroids may suppress the hypothalamic-pituitary axis for 3 months following the injection. Lastly, vasovagal reaction, nerve root injury, injectate allergy, and temporary pain exacerbation can occur as well.

Results of ESI for spinal stenosis

Recent studies assessing efficacy of fluoroscopically guided, contrast-enhanced ESI, even for herniated nucleus pulposus (HNP)-induced radicular pain, appear promising, suggesting that a significant inflammatory component amenable to corticosteroid treatment may accompany HNP-nerve root pathology.

Studies of ESI for LSS treatment demonstrate mixed results due to varying injection and guidance techniques, patient populations, follow-up periods and protocols, ancillary treatments (eg, physical therapy, oral medication), and outcome measures. This lack of consistency limits the ability to assess ESI efficacy for LSS.

Some studies, nevertheless, suggest that, unlike HNP-provoked radicular pain, NC may be more mechanical or ischemic than inflammatory in nature. Consequently, corticosteroid anti-inflammatory properties may fail to provide designed long-term symptom relief. Studies report that 50% of patients with LSS or HNP-provoked radicular pain received temporary relief and that such results were close to those associated with the placebo effect.

Because of concomitant lateral recess stenosis from facet hypertrophy or lateral HNP, patients may fail transforaminal ESI therapy for HNP-induced radicular pain. ESI may do little to relieve chronic lateral recess stenosis-related radicular pain. Additionally, studies show patients with a preinjection duration of symptoms greater than 24 weeks may respond to ESI as favorably as those with symptoms of less than 24 weeks’ duration. This finding, may suggest that chronic nerve compression could induce irreversible neurophysiologic change that ultimately renders the nerve root refractory to ESI.

Future studies require controlled design, contrast-enhanced fluoroscopic guidance, and objective validated outcome measures before definitive conclusions can be drawn regarding efficacy of ESI treatment of LSS.


Complications that may develop in patients with lumbar spinal stenosis (LSS) include the following:

  • Cauda equina syndrome (in rare cases)
  • Lower extremity weakness and numbness
  • Intractable axial, radicular, or NC pain
  • Disability and loss of productivity

Complications that may develop in patients after surgery include the following:

  • Sustained axial and radicular pain
  • Progressive spinal deformity
  • Cerebrospinal fluid leak
  • Epidural hematoma
  • Pulmonary embolism (PE)

Some authors report spondylolisthesis as a complication of lumbar decompression without arthrodesis, especially after total facetectomy. Preoperative risk factors for postoperative development or progression of L4 or L5 spondylolisthesis include the following:

  • Absence of degenerative osteophytosis
  • Small and sagittally oriented facets
  • Well-maintained disk height

Ciol and colleagues report a substantial reoperation rate following LSS surgery in the Medicare population, for reasons that remain unclear.[48] Possible explanations may include the following:

  • Failure of implanted devices
  • Changed patient expectations
  • Aggressive surgical philosophy

Long-term Monitoring

Inpatient care is necessary for patients with lumbar spinal stenosis (LSS) who elect to undergo surgery. The length of stay in the hospital is dependent on the type of procedure performed, but, on average, the patient is released 2-5 days following surgery. Following the operation, it is important that these patients resume basic mobility, activities of daily living (ADL), and ambulation as soon as possible and become educated on proper body mechanics and back safety techniques before discharge. A short course of active physical therapy may be recommended after surgery to strengthen the lower back and abdominal muscles to speed recovery time. Ideally, an appropriate exercise program can be initiated before surgery and continued thereafter.

Many patients with lumbar spinal stenosis choose to receive conservative treatment for back and leg pain. An active physical therapy program often is beneficial for these patients to improve flexibility and strength to maintain or improve their current activity levels. Other forms of treatment (eg, ESI) may be administered on an outpatient basis and used in conjunction with other medications and physical therapy. Please see Physical Therapy for further discussion of these treatments.



Medication Summary

First-line pharmacotherapy for lumbar spinal stenosis (LSS) includes nonsteroidal anti-inflammatory drugs (NSAIDs), which provide analgesia at low doses and quell inflammation at high doses. An appropriate therapeutic NSAID plasma level is required to achieve anti-inflammatory benefit. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control.

Aspirin, which binds irreversibly to cyclo-oxygenase and requires larger doses to control inflammation, may cause gastritis; consequently, it is not recommended. Additionally, it may induce multiorgan toxicity, including renal insufficiency, peptic ulcer disease, and hepatic dysfunction. Cyclo-oxygenase (COX) isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. Tramadol and acetaminophen confer analgesia but do not affect inflammation.

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation results from muscle relaxation, promoting further patient relaxation. Such sedative side effects encourage evening dosing for patients who need to get sufficient sleep but may limit safe performance of some functional activities.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis. These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their use in elderly persons. These include somnolence, dry mouth, dry eyes, and constipation. More concerning are the possible arrhythmias that may occur when used in combination with other medications.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, co-treatment with a psychologist or other addiction specialist is recommended for patients with a history of substance abuse. Patients may be asked to sign a medication contract restricting them to 1 practitioner, 1 pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling of medication.



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