Spinal Stenosis Treatment & Management

  • Author: John K Hsiang, MD, PhD; Chief Editor: Rene Cailliet, MD   more...
 
Updated: Dec 13, 2011
 

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]

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 disc 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.[42]

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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.[43] 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.[44] 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.[45]

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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.[45] 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.[46]

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.

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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.[47]

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.[45]

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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.[45]

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.

Contraindications

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.[48] 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.

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Complications

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.[49] Possible explanations may include the following:

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

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Contributor Information and Disclosures
Author

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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

Disclosure: Pfizer Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching

Lennard A Nadalo, MD  Clinical Professor, Department of Radiology, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Consulting Staff, Envision Imaging of Allen and Radiological Consultants Association

Lennard A Nadalo, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Radiological Society of North America, and Texas Radiological 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.

C Douglas Phillips, MD  Director of Head and Neck Imaging, Division of Neuroradiology, New York Presbyterian Hospital, Weill Cornell Medical College

C Douglas Phillips, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Head and Neck Radiology, American Society of Neuroradiology, Association of University Radiologists, and Radiological Society of North America

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

William O Shaffer, MD  Professor, Vice-Chairman and Residency Program Director, Department of Orthopedic Surgery, University of Kentucky at Lexington

William O Shaffer, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, International Society for the Study of the Lumbar Spine, Kentucky Medical Association, Kentucky Orthopaedic Society, North American Spine Society, Southern Medical Association, and Southern Orthopaedic Association

Disclosure: DePuySpine 1997-2007 (not presently) Royalty Consulting; DePuySpine 2002-2007 (closed) Grant/research funds SacroPelvic Instrumentation Biomechanical Study; DePuyBiologics 2005-2008 (closed) Grant/research funds Healos study just closed; DePuySpine 2009 Consulting fee Design of Offset Modification of Expedium

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.

James G Smirniotopoulos, MD  Professor of Radiology, Neurology, and Biomedical Informatics, Program Director, Diagnostic Imaging Program, Center for Neuroscience and Regenerative Medicine (CNRM), Uniformed Services University of the Health Sciences

James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America

Disclosure: Nothing to disclose.

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.

Specialty Editor Board

J Michael Wieting, DO, MEd  Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Program Development, Director of Sports Medicine, Associate Director of Physician Assistant Program, Department of Osteopathic Principles and Practice, Lincoln Memorial University-DeBusk College of Osteopathic Medicine

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

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

Patrick M Foye, MD  Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

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.

Allen R Wyler, MD  Former Medical Director, Northstar Neuroscience, Inc

Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Rene Cailliet, MD  Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center

Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association

Disclosure: Nothing to disclose.

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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.
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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