Spinal Stenosis Treatment & Management

  • Author: John K Hsiang, MD, PhD; Chief Editor: Stephen Kishner, MD, MHA  more...
Updated: Jun 13, 2016

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.[10] 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.

Patient characteristics associated with greater treatment effects of surgery include baseline Oswestry Disability Index ≤56, not smoking, neuroforaminal stenosis, predominant leg pain, not lifting at work, and the presence of a neurologic deficit. In general, with the exception of smokers, patients who meet strict inclusion criteria improve more with surgery than with other treatments. Patients with spinal stenosis should consider smoking cessation before surgery.[39]

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.[40, 41, 42]

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.[11]

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.[43]

Physical therapy with traction and strengthening exercises helps to relieve associated symptoms or muscular spasms and mechanical back pain. Unfortunately, most of these approaches provide only temporary relief. Decompression and inversion tables have also been used, with great initial success and varying amounts of lasting benefit.[44]

With all these different modalities, it is not uncommon for patients, and even practitioners, to debate whether surgical treatment or conservative management is most appropriate. A recent study of comparative effectiveness evidence for intervertebral disk herniation, spinal stenosis, and degenerative spondylolisthesis from the Spine Patient Outcomes Research Trial (SPORT) shows good value for surgery compared with nonoperative care over 4 years.[45]

A study by Pochon et al indicated that although women with disk herniation, degenerative spondylolisthesis, or spinal stenosis tend to have worse preoperative symptoms than men do, postoperative outcomes for these conditions do not significantly differ by sex. In the study, which included 1518 patients (812 men and 706 women), the investigators found that women scored worse preoperatively on the Core Outcome Measures Index (COMI) for all three disorders; 12 months postoperatively, however, COMI scores showed no significant variation between males and females, with the minimal clinically important change score having been reached by 71.3% of men and 72.9% of women.[46]

Evidence-based guidelines from the North American Spine Society (NASS) for the diagnosis and treatment of degenerative lumbar spinal stenosis (LSS) state that medical/interventional treatment may be considered for patients with moderate symptoms of LSS. These treatments include all nonoperative options, including physical therapy, medications, exercise, and spinal interventions such as epidural steroid injections (ESIs).[47, 48]


Nonsteroidal 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 TCAs are 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. All patients on long-term opiates may be expected to sign a medication agreement restricting them to 1 practitioner, 1 pharmacy, scheduled medication use, scheduled refills, and no medication sharing, selling, or other transfers. They are also typically expected to partake in random urine screening.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis.[49] 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.[50] 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.

Citing insufficient evidence, the North American Spinal Society (NASS), in a set of evidence-based guidelines on the diagnosis and treatment of degenerative LSS, states that a recommendation cannot be made for or against the pharmacologic treatment of LSS.[47, 48]


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 North American Spine Society (NASS), in its evidence-based guidelines for the diagnosis and treatment of degenerative LSS, suggests that, in patients with radiculopathy or neurogenic intermittent claudication from LSS, medium-term pain relief (ie, 3-36 months) can be achieved with a multiple-injection regimen of radiographically guided transforaminal ESIs or caudal injections. In this regimen, the patient is injected either on demand or when his or her pain exceeds a preset level.[47, 48]

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); such large volumes may dilute the effect of the corticosteroid. Alternatively, a catheter may be used through the caudal ESI needle for more directed medication placement requiring smaller volumes.

Interlaminar ESI entails needle passage through the interlaminar space, with subsequent injection directly into the posterior 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. Interlaminar ESIs should not be attempted at levels where posterior surgery has been performed, since a scarred or absent ligamentum flava typically results in a dural puncture. 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, may prove more efficacious in reducing pain. Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis. Unilateral transforaminal ESI will typically not result in bilateral flow.

Bilateral transforaminal ESI may be used to treat bilateral foraminal pathology or central stenosis-induced neurogenic claudication (NC) pain. It is also preferred when imaging studies demonstrate limited posterior epidural space or at levels with previous posterior surgery, when safe interlaminar ESI is precluded. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.

Anticoagulation and ESI

Relative contraindications to ESI include bleeding diathesis and anticoagulation (AC) therapy, because of the increased risk of epidural hematoma. However, the actual incidence of this complication is unknown; estimates in the literature suggest that it occurs in less than 1 in 150,000 outpatient epidural injections. It is worth noting that most studies evaluating the epidural hematoma risk are based on thoracic epidurals or procedures involving catheters on fully anticoagulated patients (ie, heparin, warfarin). Even these studies do not show a significantly increased incidence of hematoma formation in patients who undergo anticoagulation.[51] Several practice audits and case reports have demonstrated minimal risk of adverse events with neuroaxial procedures.[52, 53]

In some patients, it is riskier to stop their AC, since this can potentially lead to a life-threatening event, such as myocardial infarction. Current cardiac guidelines typically recommend AC therapy 12 months after stent placement.[54] Patients are anticoagulated for many reasons, including, but not limited to, a history of deep venous thrombosis (DVT), pulmonary embolus (PE) or cerebral vascular accident (CVA). Some have mechanical cardiac valves or cardiac stents or have atrial fibrillation, and the AC is preventing embolic and/or ischemic events.[55]

For those patients with recent stent placement or who have mechanical heart valves, their acute risk from stopping the ACs is extremely high. For other patients, such as those with atrial fibrillation, the short-term risk from AC cessation is much lower. The stroke literature suggests that holding AC leads to an increased risk of thrombotic events.[56] Therefore, International Spine Intervention Society (ISIS) guidelines recommend that the risk/benefit ratios be contemplated on an individualized basis in conjunction with the prescribing physician.[52]

When stopping AC therapy (eg, warfarin, heparin), it should be done a few days prior to injection, based on medication half-life and hematologic profile. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking warfarin, prothrombin time/international normalized ratio (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.[53]

Other contraindications

Absolute contraindications to ESIs include systemic infection 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.

For patients with injectate allergies, such as to contrast agents or anesthetics, ESI may be performed with premedication protocols or without using the offending medication.

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.[57] 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.

A meta-analysis by Manchikanti et al suggested that epidural injection with lidocaine alone or in combination with a corticosteroid is significantly effective on pain and function in spinal stenosis (as well as lumbar radiculopathy), with the impact of lidocaine by itself being comparable to that of the combination. However, bupivacaine and sodium chloride solution were each found to be ineffective.[58]

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.


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.[47] 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.[59]

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

The North American Spine Society (NASS), in its aforementioned guidelines on the diagnosis and treatment of degenerative LSS, states that there is insufficient evidence to either support the use of physical therapy or exercise as a stand-alone treatment for LSS or to recommend against it. However, the guidelines' physical therapy/exercise work group suggests that despite an absence of reliable evidence regarding its efficacy, a limited course of active physical therapy should nonetheless be a treatment option in LSS.[47, 48]


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. More often than not, fusion is not necessary after decompressive lumbar laminectomy.

A study by Försth et al indicated that in patients with lumbar spinal stenosis (LSS), with or without spondylolisthesis, treatment with decompressive surgery by itself was no less effective than treatment with decompressive surgery plus fusion surgery. The study, which included 247 patients, found that the mean Oswestry Disability Index score did not significantly differ between the two groups at 2-year follow-up. Clinical outcomes also did not significantly differ between members of the two groups who were followed up at 5 years.[60]

In recent years, the availability of interspinous process devices, such as X-stop and Coflex, has provided a less-invasive surgical approach for LSS. The success of this type of surgery relies on careful patient selection.[61, 62, 63, 64]

Outcomes for LSS surgery 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 LSS with significant symptoms can benefit from lumbar decompressive surgery. However, whether patients with moderate LSS with less severe symptoms should also have surgery is unclear. A randomized, controlled study of 94 patients with moderate LSS who underwent either surgical or nonsurgical treatment suggested that decompressive surgery of moderate lumbar spinal stenosis can provide slight, but consistent, functional ability improvement, especially compared with nonoperative measures. The results were based on a 6-year follow-up.[65]

North American Spine Society (NASS) guidelines suggest the use of decompressive surgery as a means of improving outcomes not only in patients with severe symptoms of LSS but in those with moderate symptoms as well.[47, 48]

A study by Sobottke et al indicated that open decompression is effective in the treatment of LSS for patients in all age groups. Using data from 4768 patients, as drawn internationally from the Spine Tango registry, the investigators found after dividing the patients into three age groups (20-64 years, 65-74 years, 75 years and older) that age had no significant impact on the outcomes of decompression with regard to improvement in quality of life and relief from back and leg pain.[66]

A study by Hermansen et al found clinical outcomes for three different lumbar decompressive procedures to be comparable in patients with LSS. Patients underwent spinous process osteotomy (103 patients), bilateral laminotomy (966 patients), or unilateral laminotomy with crossover (462 patients), with mean improvements in the Oswestry Disability Index score at 12 months being 15.2, 16.9, and 16.7, respectively. Length of hospital stay was shortest for the bilateral laminotomy patients (2.1 days) and longest for patients who underwent spinous process osteotomy (6.9 days).[67]



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.[68] 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.

Contributor Information and Disclosures

John K Hsiang, MD, PhD Director of Spine Surgery, Swedish Neuroscience Institute, Swedish Medical Center

John K Hsiang, MD, PhD is a member of the following medical societies: American Association of Neurological Surgeons, North American Spine Society, Sigma Xi, Society of Critical Care Medicine

Disclosure: Nothing to disclose.


Michael B Furman, MD, MS Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Pain Medicine, Director, Spine and Sports Fellowship, Orthopaedic and Spine Specialists, Sinai Hospital of Baltimore

Michael B Furman, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, North American Spine Society, International Spine Intervention Society, American Association of Neuromuscular and Electrodiagnostic Medicine, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.


Patrick M Foye, MD Director of Coccyx Pain Center, Associate Professor and interim Chair of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital, Newark, New Jersey

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Robert Pannullo MD, Staff Physician at Ocean Medical Center, Central Jersey Surgical Center

Robert Pannullo is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa

Disclosure: Nothing to disclose.

Paul L Penar, MD, FACS Professor, Department of Surgery, Division of Neurosurgery, Director, Functional Neurosurgery and Radiosurgery Programs, University of Vermont College of Medicine

Paul L Penar, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, Congress of Neurological Surgeons, and World Society for Stereotactic and Functional Neurosurgery

Disclosure: Nothing to disclose.

Kirk M Puttlitz, MD Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute

Kirk M Puttlitz, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa

Disclosure: Nothing to disclose.

K Daniel Riew, MD Mildred B Simon Distinguished Professor of Orthopedic Surgery, Professor of Neurologic Surgery, Washington University School of Medicine; Chief, Cervical Spine Surgery, Department of Orthopedic Surgery, Barnes-Jewish Hospital

K Daniel Riew, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, AO Foundation, Cervical Spine Research Society, North American Spine Society, and Scoliosis Research Society

Disclosure: Medtronic Royalty Medtronic Vertex; Biomet Royalty Maxan anterior cervical plate; Osprey Royalty Interbody Graft; Osprey Stock Options None; SpineMedica None None; Synthes Consulting fee Other

Jeremy Simon, MD Attending Physician, Department of Physical Medicine, The Rothman Institute

Jeremy Simon, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Amir Vokshoor, MD Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic and Interventional Spinal Care, St John's Health Center

Amir Vokshoor, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Medical Association, and North American Spine Society

Disclosure: Nothing to disclose.

J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR Professor of Physical Medicine and Rehabilitation, Associate Dean, Consultant in Sports Medicine, Assistant Vice President of Program Development, Division of Health Sciences, Lincoln Memorial University-DeBusk College of Osteopathic Medicine

J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Academy of Sports Medicine, and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

  1. Lee SY, Kim TH, Oh JK, Lee SJ, Park MS. Lumbar Stenosis: A Recent Update by Review of Literature. Asian Spine J. 2015 Oct. 9 (5):818-28. [Medline]. [Full Text].

  2. Greenberg MS. Spinal stenosis. Handbook of Neurosurgery. Lakeland, Fla: Greenburg Graphics, Inc; 1997. Vol 1: 207-217.

  3. White AA III, Panjabi MM. Clinical Biomechanics of the Spine. 2nd ed. Philadelphia, Pa: JB Lippincott; 1990. 342-378.

  4. Kalichman L, Cole R, Kim DH, Li L, Suri P, Guermazi A, et al. Spinal stenosis prevalence and association with symptoms: the Framingham Study. Spine J. 2009 Jul. 9(7):545-50. [Medline].

  5. Bernhardt M, Hynes RA, Blume HW, White AA 3rd. Cervical spondylotic myelopathy. J Bone Joint Surg Am. 1993 Jan. 75(1):119-28. [Medline].

  6. Heller JG. The syndromes of degenerative cervical disease. Orthop Clin North Am. 1992 Jul. 23(3):381-94. [Medline].

  7. Caputy AJ, Luessenhop AJ. Long-term evaluation of decompressive surgery for degenerative lumbar stenosis. J Neurosurg. 1992 Nov. 77(5):669-76. [Medline].

  8. Harkey HL, al-Mefty O, Marawi I, Peeler DF, Haines DE, Alexander LF. Experimental chronic compressive cervical myelopathy: effects of decompression. J Neurosurg. 1995 Aug. 83(2):336-41. [Medline].

  9. Amundsen T, Weber H, Lilleås F, Nordal HJ, Abdelnoor M, Magnaes B. Lumbar spinal stenosis. Clinical and radiologic features. Spine (Phila Pa 1976). 1995 May 15. 20(10):1178-86. [Medline].

  10. Alexander JT. Natural history and nonoperative management of cervical spondylosis. Menezes AH, Sonntag VKH, et al, eds. Principles of Spinal Surgery. New York, NY: McGraw-Hill; 1996. Vol 1: 547-557.

  11. Benner BG. Etiology, pathogenesis and natural history of discogenic neck pain, radiculopathy, and myelopathy. The Cervical Spine Research Society Editorial Committee. The Cervical Spine. 3rd ed. Philadelphia, Pa: Lippincott; 1998. 735-740.

  12. Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J Neurosurg. 1966 Jul. 25(1):57-66. [Medline].

  13. McCormack BM, Weinstein PR. Cervical spondylosis. An update. West J Med. 1996 Jul-Aug. 165(1-2):43-51. [Medline]. [Full Text].

  14. Teresi LM, Lufkin RB, Reicher MA, Moffit BJ, Vinuela FV, Wilson GM, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology. 1987 Jul. 164(1):83-8. [Medline].

  15. Young WF. Cervical spondylotic myelopathy: a common cause of spinal cord dysfunction in older persons. Am Fam Physician. 2000 Sep 1. 62(5):1064-70, 1073. [Medline].

  16. Kasai Y, Akeda K, Uchida A. Physical characteristics of patients with developmental cervical spinal canal stenosis. Eur Spine J. 2007 Jul. 16(7):901-3. [Medline]. [Full Text].

  17. Matz PG, Anderson PA, Holly LT, Groff MW, Heary RF, Kaiser MG, et al. The natural history of cervical spondylotic myelopathy. J Neurosurg Spine. 2009 Aug. 11(2):104-11. [Medline].

  18. Keim HA, Hajdu M, Gonzalez EG, Brand L, Balasubramanian E. Somatosensory evoked potentials as an aid in the diagnosis and intraoperative management of spinal stenosis. Spine (Phila Pa 1976). 1985 May. 10(4):338-44. [Medline].

  19. Daffner SD, Wang JC. The pathophysiology and nonsurgical treatment of lumbar spinal stenosis. Instr Course Lect. 2009. 58:657-68. [Medline].

  20. Panjabi MM, Krag MH, Chung TQ. Effects of disc injury on mechanical behavior of the human spine. Spine (Phila Pa 1976). 1984 Oct. 9(7):707-13. [Medline].

  21. Jenis LG, An HS. Spine update. Lumbar foraminal stenosis. Spine (Phila Pa 1976). 2000 Feb 1. 25(3):389-94. [Medline].

  22. Ooi Y, Mita F, Satoh Y. Myeloscopic study on lumbar spinal canal stenosis with special reference to intermittent claudication. Spine (Phila Pa 1976). 1990 Jun. 15(6):544-9. [Medline].

  23. Fritz JM, Delitto A, Welch WC, Erhard RE. Lumbar spinal stenosis: a review of current concepts in evaluation, management, and outcome measurements. Arch Phys Med Rehabil. 1998 Jun. 79(6):700-8. [Medline].

  24. Porter RW, Hibbert C, Evans C. The natural history of root entrapment syndrome. Spine (Phila Pa 1976). 1984 May-Jun. 9(4):418-21. [Medline].

  25. Johnsson KE, Rosén I, Udén A. The natural course of lumbar spinal stenosis. Clin Orthop Relat Res. 1992 Jun. 82-6. [Medline].

  26. Malmivaara A, Slätis P, Heliövaara M, et al. Surgical or nonoperative treatment for lumbar spinal stenosis? A randomized controlled trial. Spine (Phila Pa 1976). 2007 Jan 1. 32(1):1-8. [Medline].

  27. Geisser ME, Haig AJ, Tong HC, Yamakawa KS, Quint DJ, Hoff JT, et al. Spinal canal size and clinical symptoms among persons diagnosed with lumbar spinal stenosis. Clin J Pain. 2007 Nov-Dec. 23(9):780-5. [Medline].

  28. Thomas NW, Rea GL, Pikul BK, Mervis LJ, Irsik R, McGregor JM. Quantitative outcome and radiographic comparisons between laminectomy and laminotomy in the treatment of acquired lumbar stenosis. Neurosurgery. 1997 Sep. 41(3):567-74; discussion 574-5. [Medline].

  29. Watson JC, Broaddus WC, Smith MM, Kubal WS. Hyperactive pectoralis reflex as an indicator of upper cervical spinal cord compression. Report of 15 cases. J Neurosurg. 1997 Jan. 86(1):159-61. [Medline].

  30. Katz JN, Dalgas M, Stucki G, Katz NP, Bayley J, Fossel AH, et al. Degenerative lumbar spinal stenosis. Diagnostic value of the history and physical examination. Arthritis Rheum. 1995 Sep. 38(9):1236-41. [Medline].

  31. Goh KJ, Khalifa W, Anslow P, Cadoux-Hudson T, Donaghy M. The clinical syndrome associated with lumbar spinal stenosis. Eur Neurol. 2004. 52(4):242-9. [Medline].

  32. Getty CJ. Lumbar spinal stenosis: the clinical spectrum and the results of operation. J Bone Joint Surg Br. 1980 Nov. 62-B(4):481-5. [Medline].

  33. Schönström N, Lindahl S, Willén J, Hansson T. Dynamic changes in the dimensions of the lumbar spinal canal: an experimental study in vitro. J Orthop Res. 1989. 7(1):115-21. [Medline].

  34. Hall S, Bartleson JD, Onofrio BM, Baker HL Jr, Okazaki H, O'Duffy JD. Lumbar spinal stenosis. Clinical features, diagnostic procedures, and results of surgical treatment in 68 patients. Ann Intern Med. 1985 Aug. 103(2):271-5. [Medline].

  35. Dyck P. The stoop-test in lumbar entrapment radiculopathy. Spine (Phila Pa 1976). 1979 Jan-Feb. 4(1):89-92. [Medline].

  36. Burgstaller JM, Schuffler PJ, Buhmann JM, et al. Is There An Association Between Pain and Magnetic Resonance Imaging Parameters in Patients with Lumbar Spinal Stenosis?. Spine (Phila Pa 1976). 2016 Mar 2. [Medline].

  37. [Guideline] Chou R, Qaseem A, Snow V, Casey D, Cross JT Jr, Shekelle P, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007 Oct 2. 147(7):478-91. [Medline]. [Full Text].

  38. [Guideline] Chou R, Qaseem A, Owens DK, Shekelle P, Clinical Guidelines Committee of the American College of Physicians. Diagnostic imaging for low back pain: advice for high-value health care from the American College of Physicians. Ann Intern Med. 2011 Feb 1. 154(3):181-9. [Medline]. [Full Text].

  39. Pearson A, Lurie J, Tosteson T, Zhao W, Abdu W, Weinstein J. Who Should Have Surgery for Spinal Stenosis?. Spine (Phila Pa 1976). 2012 Jun 11. [Medline].

  40. Ikuta K, Tono O, Tanaka T, Arima J, Nakano S, Sasaki K, et al. Evaluation of postoperative spinal epidural hematoma after microendoscopic posterior decompression for lumbar spinal stenosis: a clinical and magnetic resonance imaging study. J Neurosurg Spine. 2006 Nov. 5(5):404-9. [Medline].

  41. Lee JW, Kim SH, Lee IS, Choi JA, Choi JY, Hong SH, et al. Therapeutic effect and outcome predictors of sciatica treated using transforaminal epidural steroid injection. AJR Am J Roentgenol. 2006 Dec. 187(6):1427-31. [Medline].

  42. Malmivaara A, Slätis P, Heliövaara M, et al. Surgical or nonoperative treatment for lumbar spinal stenosis? A randomized controlled trial. Spine (Phila Pa 1976). 2007 Jan 1. 32(1):1-8. [Medline].

  43. Simotas AC, Dorey FJ, Hansraj KK, Cammisa F Jr. Nonoperative treatment for lumbar spinal stenosis. Clinical and outcome results and a 3-year survivorship analysis. Spine (Phila Pa 1976). 2000 Jan 15. 25(2):197-203; discussions 203-4. [Medline].

  44. Swezey RL, Swezey AM, Warner K. Efficacy of home cervical traction therapy. Am J Phys Med Rehabil. 1999 Jan-Feb. 78(1):30-2. [Medline].

  45. Tosteson AN, Tosteson TD, Lurie JD, et al. Comparative effectiveness evidence from the spine patient outcomes research trial: surgical versus nonoperative care for spinal stenosis, degenerative spondylolisthesis, and intervertebral disc herniation. Spine (Phila Pa 1976). 2011 Nov 15. 36(24):2061-8. [Medline].

  46. Pochon L, Kleinstuck FS, Porchet F, Mannion AF. Influence of gender on patient-oriented outcomes in spine surgery. Eur Spine J. 2015 Jul 5. [Medline].

  47. [Guideline] Kreiner DS, Shaffer WO, Baisden JL, Gilbert TJ, Summers JT, Toton JF, et al. An evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spinal stenosis (update). Spine J. 2013 Jul. 13(7):734-43. [Medline].

  48. NASS Evidence-Based Clinical Guidelines Committee. Diagnosis and Treatment of Degenerative Lumbar Spinal Stenosis (2011 Revised). 2011. Available at https://www.spine.org/Documents/ResearchClinicalCare/Guidelines/LumbarStenosis.pdf.

  49. Yaksi A, Ozgönenel L, Ozgönenel B. The efficiency of gabapentin therapy in patients with lumbar spinal stenosis. Spine (Phila Pa 1976). 2007 Apr 20. 32(9):939-42. [Medline].

  50. Matsudaira K, Seichi A, Kunogi J, Yamazaki T, Kobayashi A, Anamizu Y, et al. The efficacy of prostaglandin E1 derivative in patients with lumbar spinal stenosis. Spine (Phila Pa 1976). 2009 Jan 15. 34(2):115-20. [Medline].

  51. Mehta Y, Arora D, Vats M. Epidural analgesia in high risk cardiac surgical patients. HSR Proc Intensive Care Cardiovasc Anesth. 2012. 4(1):11-4. [Medline]. [Full Text].

  52. [Guideline] Bogduk N. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. 2nd ed. San Francisco, CA: International Spine Intervention Society; 2013.

  53. Manchikanti L, Falco FJ, Benyamin RM, et al. Assessment of bleeding risk of interventional techniques: a best evidence synthesis of practice patterns and perioperative management of anticoagulant and antithrombotic therapy. Pain Physician. 2013 Apr. 16(2 Suppl):SE261-318. [Medline].

  54. Helft G. Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation. Arch Cardiovasc Dis. 2013 May. 106(5):271-3. [Medline].

  55. Sachdeva A, Bavisetty S, Beckham G, et al. Discontinuation of long-term clopidogrel therapy is associated with death and myocardial infarction after saphenous vein graft percutaneous coronary intervention. J Am Coll Cardiol. 2012 Dec 11. 60(23):2357-63. [Medline].

  56. Weimar C, Cotton D, Sha N, et al. Discontinuation of antiplatelet study medication and risk of recurrent stroke and cardiovascular events: results from the PRoFESS study. Cerebrovasc Dis. 2013. 35(6):538-43. [Medline].

  57. Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia. Anesth Analg. 1994 Dec. 79(6):1165-77. [Medline].

  58. Manchikanti L, Knezevic NN, Boswell MV, Kaye AD, Hirsch JA. Epidural Injections for Lumbar Radiculopathy and Spinal Stenosis: A Comparative Systematic Review and Meta-Analysis. Pain Physician. 2016 Mar. 19 (3):E365-410. [Medline].

  59. Wallbom AS, Geisser ME, Haig AJ, Koch J, Guido C. Alterations of F wave parameters after exercise in symptomatic lumbar spinal stenosis. Am J Phys Med Rehabil. 2008 Apr. 87(4):270-4. [Medline].

  60. Forsth P, Olafsson G, Carlsson T, et al. A Randomized, Controlled Trial of Fusion Surgery for Lumbar Spinal Stenosis. N Engl J Med. 2016 Apr 14. 374 (15):1413-23. [Medline].

  61. Davis RJ, Errico TJ, Bae H, et al. Decompression and Coflex interlaminar stabilization compared with decompression and instrumented spinal fusion for spinal stenosis and low-grade degenerative spondylolisthesis: two-year results from the prospective, randomized, multicenter, Food and Drug Administration Investigational Device Exemption trial. Spine (Phila Pa 1976). 2013 Aug 15. 38(18):1529-39. [Medline].

  62. Davis R, Auerbach JD, Bae H, et al. Can low-grade spondylolisthesis be effectively treated by either coflex interlaminar stabilization or laminectomy and posterior spinal fusion? Two-year clinical and radiographic results from the randomized, prospective, multicenter US investigational device exemption trial: clinical article. J Neurosurg Spine. 2013 Aug. 19(2):174-84. [Medline].

  63. Kim HY, Choi BW. Change of radiological parameters after interspinous implantation (X-stop®) in degenerative spinal stenosis. Eur J Orthop Surg Traumatol. 2013 Apr. 23(3):281-5. [Medline].

  64. Stromqvist BH, Berg S, Gerdhem P, et al. X-stop versus decompressive surgery for lumbar neurogenic intermittent claudication: randomized controlled trial with 2-year follow-up. Spine (Phila Pa 1976). 2013 Aug 1. 38(17):1436-42. [Medline].

  65. Slätis P, Malmivaara A, Heliövaara M, Sainio P, Herno A, Kankare J, et al. Long-term results of surgery for lumbar spinal stenosis: a randomised controlled trial. Eur Spine J. 2011 Jul. 20(7):1174-81. [Medline].

  66. Sobottke R, Herren C, Siewe J, Mannion AF, Roder C, Aghayev E. Predictors of improvement in quality of life and pain relief in lumbar spinal stenosis relative to patient age: a study based on the Spine Tango registry. Eur Spine J. 2015 Jul 3. [Medline].

  67. Hermansen E, Romild UK, Austevoll IM, et al. Does surgical technique influence clinical outcome after lumbar spinal stenosis decompression? A comparative effectiveness study from the Norwegian Registry for Spine Surgery. Eur Spine J. 2016 Jun 4. [Medline].

  68. Ciol MA, Deyo RA, Howell E, Kreif S. An assessment of surgery for spinal stenosis: time trends, geographic variations, complications, and reoperations. J Am Geriatr Soc. 1996 Mar. 44(3):285-90. [Medline].

  69. Atlas SJ, Keller RB, Robson D, Deyo RA, Singer DE. Surgical and nonsurgical management of lumbar spinal stenosis: four-year outcomes from the maine lumbar spine study. Spine (Phila Pa 1976). 2000 Mar 1. 25(5):556-62. [Medline].

  70. Barz T, Melloh M, Staub L, Roeder C, Lange J, Smiszek FG, et al. The diagnostic value of a treadmill test in predicting lumbar spinal stenosis. Eur Spine J. 2008 May. 17(5):686-90. [Medline]. [Full Text].

  71. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am. 1990 Mar. 72(3):403-8. [Medline].

  72. Bridwell KH, Sedgewick TA, O'Brien MF, Lenke LG, Baldus C. The role of fusion and instrumentation in the treatment of degenerative spondylolisthesis with spinal stenosis. J Spinal Disord. 1993 Dec. 6(6):461-72. [Medline].

  73. Burnett MG, Stein SC, Bartels RH. Cost-effectiveness of current treatment strategies for lumbar spinal stenosis: nonsurgical care, laminectomy, and X-STOP. J Neurosurg Spine. 2010 Jul. 13(1):39-46. [Medline].

  74. Cavusoglu H, Kaya RA, Türkmenoglu ON, Tuncer C, Colak I, Aydin Y. Midterm outcome after unilateral approach for bilateral decompression of lumbar spinal stenosis: 5-year prospective study. Eur Spine J. 2007 Dec. 16(12):2133-42. [Medline]. [Full Text].

  75. Chou R, Baisden J, Carragee EJ, Resnick DK, Shaffer WO, Loeser JD. Surgery for low back pain: a review of the evidence for an American Pain Society Clinical Practice Guideline. Spine (Phila Pa 1976). 2009 May 1. 34(10):1094-109. [Medline].

  76. Conneely M, Park J, Demos TC. Radiologic case study. Cervical spine trauma: unstable fractures, C2-C7 injuries, and imaging guidelines. Orthopedics. 2008 Aug. 31(8):818. [Medline].

  77. de Graaf I, Prak A, Bierma-Zeinstra S, Thomas S, Peul W, Koes B. Diagnosis of lumbar spinal stenosis: a systematic review of the accuracy of diagnostic tests. Spine (Phila Pa 1976). 2006 May 1. 31(10):1168-76. [Medline].

  78. Detwiler PW, Marciano FF, Porter RW, Sonntag VK. Lumbar stenosis: indications for fusion with and without instrumentation. Neurosurg Focus. 1997 Aug 15. 3(2):e4; discussion 1 p following e4. [Medline].

  79. Deyo RA, Mirza SK, Martin BI, Kreuter W, Goodman DC, Jarvik JG. Trends, major medical complications, and charges associated with surgery for lumbar spinal stenosis in older adults. JAMA. 2010 Apr 7. 303(13):1259-65. [Medline]. [Full Text].

  80. diPierro CG, Helm GA, Shaffrey CI, et al. Treatment of lumbar spinal stenosis by extensive unilateral decompression and contralateral autologous bone fusion: operative technique and results. J Neurosurg. 1996 Feb. 84(2):166-73. [Medline].

  81. Dumitru D, Dreyfuss P. Dermatomal/segmental somatosensory evoked potential evaluation of L5/S1 unilateral/unilevel radiculopathies. Muscle Nerve. 1996 Apr. 19(4):442-9. [Medline].

  82. Engelhorn T, Rennert J, Richter G, Struffert T, Ganslandt O, Doerfler A. Myelography using flat panel volumetric computed tomography: a comparative study in patients with lumbar spinal stenosis. Spine (Phila Pa 1976). 2007 Aug 15. 32(18):E523-7. [Medline].

  83. Epstein NE. Beta tricalcium phosphate: observation of use in 100 posterolateral lumbar instrumented fusions. Spine J. 2009 Aug. 9(8):630-8. [Medline].

  84. Feffer HL, Wiesel SW, Cuckler JM, Rothman RH. Degenerative spondylolisthesis. To fuse or not to fuse. Spine (Phila Pa 1976). 1985 Apr. 10(3):287-9. [Medline].

  85. Fessler RG, Steck JC, Giovanini MA. Anterior cervical corpectomy for cervical spondylotic myelopathy. Neurosurgery. 1998 Aug. 43(2):257-65; discussion 265-7. [Medline].

  86. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg Am. 1991 Jul. 73(6):802-8. [Medline].

  87. Ikuta K, Tono O, Tanaka T, Arima J, Nakano S, Sasaki K, et al. Surgical complications of microendoscopic procedures for lumbar spinal stenosis. Minim Invasive Neurosurg. 2007 Jun. 50(3):145-9. [Medline].

  88. Johnsson KE, Rosén I, Udén A. Neurophysiologic investigation of patients with spinal stenosis. Spine (Phila Pa 1976). 1987 Jun. 12(5):483-7. [Medline].

  89. Johnsson KE, Udén A, Rosén I. The effect of decompression on the natural course of spinal stenosis. A comparison of surgically treated and untreated patients. Spine (Phila Pa 1976). 1991 Jun. 16(6):615-9. [Medline].

  90. Johnsson KE, Willner S, Johnsson K. Postoperative instability after decompression for lumbar spinal stenosis. Spine (Phila Pa 1976). 1986 Mar. 11(2):107-10. [Medline].

  91. Kapural L, Mekhail N, Bena J, McLain R, Tetzlaff J, Kapural M, et al. Value of the magnetic resonance imaging in patients with painful lumbar spinal stenosis (LSS) undergoing lumbar epidural steroid injections. Clin J Pain. 2007 Sep. 23(7):571-5. [Medline].

  92. Kohno K, Kumon Y, Oka Y, Matsui S, Ohue S, Sakaki S. Evaluation of prognostic factors following expansive laminoplasty for cervical spinal stenotic myelopathy. Surg Neurol. 1997 Sep. 48(3):237-45. [Medline].

  93. Kraft GH. A physiological approach to the evaluation of lumbosacral spinal stenosis. Phys Med Rehabil Clin N Am. 1998 May. 9(2):381-9, viii. [Medline].

  94. Kumar VG, Rea GL, Mervis LJ, McGregor JM. Cervical spondylotic myelopathy: functional and radiographic long-term outcome after laminectomy and posterior fusion. Neurosurgery. 1999 Apr. 44(4):771-7; discussion 777-8. [Medline].

  95. Lohman CM, Tallroth K, Kettunen JA, Lindgren KA. Comparison of radiologic signs and clinical symptoms of spinal stenosis. Spine (Phila Pa 1976). 2006 Jul 15. 31(16):1834-40. [Medline].

  96. Lurie JD, Tosteson AN, Tosteson TD, Carragee E, Carrino JA, Kaiser J, et al. Reliability of readings of magnetic resonance imaging features of lumbar spinal stenosis. Spine (Phila Pa 1976). 2008 Jun 15. 33(14):1605-10. [Medline]. [Full Text].

  97. Macdonald RL, Fehlings MG, Tator CH, et al. Multilevel anterior cervical corpectomy and fibular allograft fusion for cervical myelopathy. J Neurosurg. 1997 Jun. 86(6):990-7. [Medline].

  98. Markwalder TM. Surgical management of neurogenic claudication in 100 patients with lumbar spinal stenosis due to degenerative spondylolisthesis. Acta Neurochir (Wien). 1993. 120(3-4):136-42. [Medline].

  99. McAfee P, Khoo LT, Pimenta L, Capuccino A, Sengoz A, Coric D, et al. Treatment of lumbar spinal stenosis with a total posterior arthroplasty prosthesis: implant description, surgical technique, and a prospective report on 29 patients. Neurosurg Focus. 2007 Jan 15. 22(1):E13. [Medline].

  100. Mullin BB, Rea GL, Irsik R, Catton M, Miner ME. The effect of postlaminectomy spinal instability on the outcome of lumbar spinal stenosis patients. J Spinal Disord. 1996 Apr. 9(2):107-16. [Medline].

  101. Naderi S, Benzel EC, Baldwin NG. Cervical spondylotic myelopathy: surgical decision making. Neurosurg Focus. 1996 Dec 15. 1(6):e1. [Medline].

  102. Nasca RJ. Rationale for spinal fusion in lumbar spinal stenosis. Spine (Phila Pa 1976). 1989 Apr. 14(4):451-4. [Medline].

  103. Nasca RJ. Surgical management of lumbar spinal stenosis. Spine (Phila Pa 1976). 1987 Oct. 12(8):809-16. [Medline].

  104. Oertel MF, Ryang YM, Korinth MC, Gilsbach JM, Rohde V. Long-term results of microsurgical treatment of lumbar spinal stenosis by unilateral laminotomy for bilateral decompression. Neurosurgery. 2006 Dec. 59(6):1264-9; discussion 1269-70. [Medline].

  105. Panjabi MM. Biomechanical evaluation of spinal fixation devices: I. A conceptual framework. Spine (Phila Pa 1976). 1988 Oct. 13(10):1129-34. [Medline].

  106. Papadopoulos SM, Hoff JT. Anatomical treatment of cervical spondylosis. Clin Neurosurg. 1994. 41:270-85. [Medline].

  107. Robinson LR. Electromyography, magnetic resonance imaging, and radiculopathy: it's time to focus on specificity. Muscle Nerve. 1999 Feb. 22(2):149-50. [Medline].

  108. Saint-Louis LA. Lumbar spinal stenosis assessment with computed tomography, magnetic resonance imaging, and myelography. Clin Orthop Relat Res. 2001 Mar. 122-36. [Medline].

  109. Sakamaki T, Sairyo K, Sakai T, Tamura T, Okada Y, Mikami H. Measurements of ligamentum flavum thickening at lumbar spine using MRI. Arch Orthop Trauma Surg. 2009 Oct. 129(10):1415-9. [Medline].

  110. Shim JH, Park CK, Lee JH, Choi JW, Lee DC, Kim DH, et al. A comparison of angled sagittal MRI and conventional MRI in the diagnosis of herniated disc and stenosis in the cervical foramen. Eur Spine J. 2009 Aug. 18(8):1109-16. [Medline]. [Full Text].

  111. Silvers HR, Lewis PJ, Asch HL. Decompressive lumbar laminectomy for spinal stenosis. J Neurosurg. 1993 May. 78(5):695-701. [Medline].

  112. Sonntag VK, Marciano FF. Is fusion indicated for lumbar spinal disorders?. Spine (Phila Pa 1976). 1995 Dec 15. 20(24 Suppl):138S-142S. [Medline].

  113. Sortland O, Magnaes B, Hauge T. Functional myelography with metrizamide in the diagnosis of lumbar spinal stenosis. Acta Radiol Suppl. 1977. 355:42-54. [Medline].

  114. Trouillier H, Birkenmaier C, Kluzik J, Kauschke T, Refior HJ. Operative treatment for degenerative lumbar spinal canal stenosis. Acta Orthop Belg. 2004 Aug. 70(4):337-43. [Medline].

  115. Vaccaro AR, Garfin SR. Internal fixation (pedicle screw fixation) for fusions of the lumbar spine. Spine (Phila Pa 1976). 1995 Dec 15. 20(24 Suppl):157S-165S. [Medline].

  116. Voulgaris S, Karagiorgiadis D, Alexiou GA, et al. Continuous intraoperative electromyographic and transcranial motor evoked potential recordings in spinal stenosis surgery. J Clin Neurosci. 2010 Feb. 17(2):274-6. [Medline].

  117. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical compared with nonoperative treatment for lumbar degenerative spondylolisthesis. four-year results in the Spine Patient Outcomes Research Trial (SPORT) randomized and observational cohorts. J Bone Joint Surg Am. 2009 Jun. 91(6):1295-304. [Medline]. [Full Text].

  118. Wilbourn AJ, Aminoff MJ. AAEM minimonograph 32: the electrodiagnostic examination in patients with radiculopathies. American Association of Electrodiagnostic Medicine. Muscle Nerve. Dec 1998. 21(12):1612-31.

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 pannus (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 pannus (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.
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.
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 demonstrates a normal central canal diameter.
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.
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.
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.
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.
Lateral view of a lumbar myelogram performed in a patient who has been fused across the L4-L5 and the L5-S1 vertebral interspaces using transpedicular screws. Treatment of lumbar spinal stenosis may include decompression laminectomies, followed by the placement of transpedicular screws (yellow arrows) with a posterior stabilization bar.
Sagittal view of a 3-dimensional volume image of the lumbar spine in a patient with a posterior fusion using transpedicular screws in L4 and L5. Note that an interposition graft has been placed between L4 and L5 to maintain satisfactory
Lateral swimmer's radiographic view demonstrates compression of the anterior contrast-filled cervical thecal sac. The defect helps localize the stenosis; however, the pattern does not reflect lateral disc herniation or spondylosis directly.
Axial T2-weighted gradient echo MRI scan. Note the high-grade spinal stenosis resulting in severe upper cervical cord compression (arrows). This patient presented with a central spinal cord syndrome that improved following surgical decompression.
Sagittal T2-weighted MRI image demonstrates severe stenosis. Spinal stenosis is demonstrated at several levels (white and yellow arrows) resulting from a combination of disc annulus bulging (white arrow) and epidural soft-tissue thickening (yellow arrow).
Superior-to-inferior view of 3-dimensional volume reconstruction of central canal spinal stenosis resulting from chronic disc herniation. The patient presented with lower extremity weakness and loss of bladder control.
: Sagittal T2 weighted fast spin-echo (FSE) MRI scan of a meningioma of the lower thoracic spine obtained without contrast enhancement. The effect of the mass is better seen because of the contrast between the mass and the cerebrospinal fluid (CSF). The anterior spinal canal is occupied by a mass that displaces and compresses the conus medullaris (C) at the T12 level. The mass (white arrow) is of intermediate increased signal brightness, compared to the normal spinal cord.
Sagittal T1-weighted spin-echo (SE) MRI scan of a meningioma of the lower thoracic spine obtained following IV gadolinium contrast enhancement. The mass is better seen because of the contrast enhancement within the meningioma (M). The anterior spinal canal is occupied by a mass that displaces and compresses (white arrows) the conus medullaris (C) at the T12 level. The mass (white arrow) is of intermediate increased signal brightness, compared to the normal spinal cord.
Normal findings in the thoracic spine as demonstrated by CT myelography. Note the detail of the spinal cord and the ventral and dorsal nerves surrounded by contrast.
nal-cut view of 3-dimensional reconstruction CT scan of the thoracic spine in tuberculosis spondylitis. Note the central spinal cavity (black arrow). The vertebral endplate has compressed downward (double blue arrows). The advantage of 3-dimensional reconstructions is the ability to better evaluate preoperatively the type of surgery needed to stabilize spinal compression fractures.
Paraspinal abscess aspiration biopsy. The stains were positive for mycobacteria (black arrows; acid-fast stain, magnification X100).
With the patient in a prone position and using CT localization, a bone biopsy and aspiration were performed from the area of greatest destruction within the vertebral endplate (arrow).
Aspergillosis organisms were recovered from a lumbar disc space abscess. The patient had received a renal transplant 12 months prior to the infection (hematoxylin and eosin, magnification X40).
Long recovery time T2*-weighted fat-suppressed sagittal MRI scan of the thoracic spine demonstrates subtle enlargement of a thoracic vertebral body (double white arrows) and a slightly increased degree of signal brightness within the vertebral body (yellow arrow).
Paget disease of the thoracic spine. Thoracic spinal CT scan demonstrates enlarged vertebral body endplates (black arrows). The axial image on the left demonstrates the characteristic thickening of the bony matrix of the vertebral body.
Axial lumbar CT scan demonstrates marked right-sided spinal canal stenosis (black arrow) resulting from advanced right-sided facet hypertrophy. Note the vacuum disc sign within the intervertebral disc (double yellow arrow). The vacuum disc sign is further indication of degenerative changes and spinal instability.
Pantopaque tracer in the epidural spaces. Pantopaque can remain in the epidural and facial spaces for years following a myelogram. Chronic inflammatory arachnoiditis has been associated with a combination of trauma (bleeding) with administration of Pantopaque.
Localization of thoracic lesion prior to surgical correction. A needle/wire localization technique is used to ensure the correct surgical level. Such preoperative localizations save time in the operating suite while reducing the need for intraoperative radiology.
Sagittal 3-dimensional CT reconstruction of the lumbar spine in a patient with multiple myeloma. The central portions of the vertebral bodies (yellow arrows) have been replaced by the nonossified tumor.
Biopsy (yellow arrow) of a multiple myeloma mass (black arrow) that has replaced the lumbar spinal canal (blue arrow) completely.
Multiple myeloma. Photomicrograph of an aspiration biopsy specimen.
Three-dimensional surface CT image of the lumbar spine following transpedicular screw placement across the L4-L5 interspace. Note how the tips of the screws project beyond the anterior margins of the L5 vertebral body.
Axial CT image taken through L5 in a patient in whom transpedicular screws have been placed. Note that the screws (black arrows) are too far lateral and anterior. The iliac veins lie just anterior to tips of the screws (white arrows). Both the angle of screw placement and the length of the screws must be tailored to the individual patient.
Spinal stenosis. Sagittal multiplanar reconstruction (MPR) image from a CT scan of the lumbar spine following posterior decompression and fusion of the L4-L5 interspace. The interposition graft (white arrow) is posterior to the desired position. The patient remained asymptomatic. Follow-up imaging should focus upon the stability of the posterior fusion, the position of the pedicle screws, and the position of the interposition graft.
Sagittal reformatted image from a CT of the cervical spine following anterior spinal decompression and fusion. Surgical treatment of spinal canal stenosis often involves anterior vertebrectomy and bone graft interposition. The goal in such cases is to restore cervical spinal alignment (white line) while securing anterior stability. In this patient, the bone graft (double black arrows) has migrated forward (double yellow arrows).
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