Spinal Stenosis Medication

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

Medication Summary

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

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

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

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

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

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

Next

Nonsteroidal Anti-inflammatory Drugs

Class Summary

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

View full drug information

Ibuprofen (Motrin, Advil)

 

Ibuprofen is the drug of choice for patients with mild to moderate pain. Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

View full drug information

Naproxen (Naprosyn, Aleve, Anaprox, Anaprox DS, Naprelan)

 

Naproxen is used for the relief of mild to moderate pain. Naproxen inhibits inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis.

View full drug information

Diclofenac (Voltaren, Voltaren-XR, Cataflam)

 

Diclofenac is believed to inhibit the enzyme COX, which is essential in the biosynthesis of prostaglandins. Diclofenac has anti-inflammatory, analgesic, and antipyretic properties.

View full drug information

Etodolac

 

Etodolac is a short-acting indole NSAID with an intermediate half-life and is approved for analgesic use. Etodolac inhibits prostaglandin synthesis by decreasing activity of the enzyme, COX, which results in decreased formation of prostaglandin precursors. This, in turn, results in reduced inflammation. Has lower risk of producing GI complications and, as result, is especially well tolerated in elderly patients. Used for relief of mild to moderate pain.

View full drug information

Celecoxib (Celebrex)

 

Celecoxib is a nonsteroidal anti-inflammatory that selectively inhibits COX-2. COX-2 inhibitors have a lower incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, when compared with nonselective NSAIDs.

Previous
Next

Analgesics

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

View full drug information

Acetaminophen (Tylenol, FeverAll)

 

Acetaminophen may be used for pain control in patients who have documented hypersensitivity to aspirin or NSAIDs, who have upper GI disease, or who are taking oral anticoagulants.

View full drug information

Tramadol (Ultram)

 

Tramadol mechanism not entirely known. It binds to opioid receptors and inhibits reuptake of serotonin and norepinephrine.

View full drug information

Hydrocodone bitartrate and acetaminophen (Vicodin, Lortab)

 

Opioid analgesic that is indicated for moderate to severe pain. Binds to opioid receptors in the CNS and inhibits synthesis of prostaglandins. Oral opioids may be prescribed on a scheduled short-term basis.

Previous
Next

Muscle Relaxants

Class Summary

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation from muscle relaxation promotes 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.

View full drug information

Cyclobenzaprine (Flexeril)

 

Acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons. Acts to provide relief of muscle spasms associated with painful musculoskeletal conditions.

View full drug information

Methocarbamol (Robaxin)

 

Methocarbamol reduces nerve impulse transmission from spinal cord to skeletal muscle, providing pain relief for musculoskeletal conditions.

View full drug information

Carisoprodol

 

Carisoprodol is a short-acting medication that may have depressant effects at spinal cord level. Skeletal muscle relaxants have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle strains and, used intermittently, for diffuse and certain regional chronic pain syndrome.

Previous
Next

Anticonvulsants

Class Summary

Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain.[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.

View full drug information

Gabapentin (Neurotonin)

 

Gabapentin has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown. It is structurally related to GABA but does not interact with GABA receptors.

View full drug information

Carbamazepine (Tegretol)

 

Carbamazepine inhibits nerve impulses by decreasing cell membrane sodium ion influx.

Previous
Next

Antidepressant, Tricyclic

Class Summary

The tricyclic antidepressants are a complex group of drugs that have central and peripheral anticholinergic effects and sedative effects. They have central effects on pain transmission, and they block the active reuptake of norepinephrine and serotonin.

View full drug information

Amitriptyline (Elavil)

 

Amitriptyline has an analgesic effect for certain chronic and neuropathic pain. It blocks reuptake of norepinephrine and serotonin, which increases concentration in the CNS. Amitriptyline also decreases pain by inhibiting spinal neurons involved in pain perception. It is highly anticholinergic and is often discontinued because of somnolence and dry mouth. Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 month may be needed to obtain clinical effects.

View full drug information

Nortriptyline (Pamelor)

 

Nortriptyline has demonstrated effectiveness in the treatment of chronic pain. By inhibiting the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, this drug increases the synaptic concentration of these neurotransmitters in the central nervous system.

View full drug information

Clomipramine (Anafranil)

 

Clomipramine is useful for neuropathic pain because of its central effects on pain transmission. It inhibits the membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons.

Previous
Next

Corticosteroids

Class Summary

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. 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. Corticosteroids may also block nociceptive transmission in C fibers.

View full drug information

Dexamethasone

 

Dexamethasone decreases inflammation by suppressing the production of inflammatory mediators and neutrophil migration. The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas.

View full drug information

Cortisone (Cortone)

 

Cortisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability as well as providing pain relief.

View full drug information

Methylprednisolone

 

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Previous
 
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.

References

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

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

  3. 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. Jul 2009;9(7):545-50. [Medline].

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

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

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

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

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

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

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

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

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

  13. 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. Jul 1987;164(1):83-8. [Medline].

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

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

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

  17. 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). May 1985;10(4):338-44. [Medline].

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

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

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

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

  22. 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. Jun 1998;79(6):700-8. [Medline].

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

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

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

  26. 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. Nov-Dec 2007;23(9):780-5. [Medline].

  27. 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. Sep 1997;41(3):567-74; discussion 574-5. [Medline].

  28. 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. Jan 1997;86(1):159-61. [Medline].

  29. 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. Sep 1995;38(9):1236-41. [Medline].

  30. 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].

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

  32. 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].

  33. 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. Aug 1985;103(2):271-5. [Medline].

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

  35. [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. Oct 2 2007;147(7):478-91. [Medline]. [Full Text].

  36. [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. Feb 1 2011;154(3):181-9. [Medline]. [Full Text].

  37. 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. Nov 2006;5(5):404-9. [Medline].

  38. 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. Dec 2006;187(6):1427-31. [Medline].

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

  40. 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). Jan 15 2000;25(2):197-203; discussions 203-4. [Medline].

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

  42. 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). Nov 15 2011;36(24):2061-8. [Medline].

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

  44. [Best Evidence] 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). Jan 15 2009;34(2):115-20. [Medline].

  45. [Guideline] Watters WC 3rd, Baisden J, Gilbert TJ, Kreiner S, Resnick DK, Bono CM, et al. Degenerative lumbar spinal stenosis: an evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spinal stenosis. Spine J. Mar-Apr 2008;8(2):305-10. [Medline]. [Full Text].

  46. 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. Apr 2008;87(4):270-4. [Medline].

  47. 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. Jul 2011;20(7):1174-81. [Medline].

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

  49. 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. Mar 1996;44(3):285-90. [Medline].

  50. 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). Mar 1 2000;25(5):556-62. [Medline].

  51. 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. May 2008;17(5):686-90. [Medline]. [Full Text].

  52. 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. Mar 1990;72(3):403-8. [Medline].

  53. 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. Dec 1993;6(6):461-72. [Medline].

  54. 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. Jul 2010;13(1):39-46. [Medline].

  55. 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. Dec 2007;16(12):2133-42. [Medline]. [Full Text].

  56. 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). May 1 2009;34(10):1094-109. [Medline].

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

  58. [Best Evidence] 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). May 1 2006;31(10):1168-76. [Medline].

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

  60. 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. Apr 7 2010;303(13):1259-65. [Medline]. [Full Text].

  61. 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. Feb 1996;84(2):166-73. [Medline].

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

  63. 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). Aug 15 2007;32(18):E523-7. [Medline].

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

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

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

  67. 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. Jul 1991;73(6):802-8. [Medline].

  68. 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. Jun 2007;50(3):145-9. [Medline].

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

  70. 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). Jun 1991;16(6):615-9. [Medline].

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

  72. 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. Sep 2007;23(7):571-5. [Medline].

  73. 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. Sep 1997;48(3):237-45. [Medline].

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

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

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

  77. 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). Jun 15 2008;33(14):1605-10. [Medline]. [Full Text].

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

  79. 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].

  80. 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. Jan 15 2007;22(1):E13. [Medline].

  81. 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. Apr 1996;9(2):107-16. [Medline].

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

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

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

  85. 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. Dec 2006;59(6):1264-9; discussion 1269-70. [Medline].

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

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

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

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

  90. 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. Oct 2009;129(10):1415-9. [Medline].

  91. 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. Aug 2009;18(8):1109-16. [Medline]. [Full Text].

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

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

  94. 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].

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

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

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

  98. 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. Jun 2009;91(6):1295-304. [Medline]. [Full Text].

  99. 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.

 
Previous
Next
 
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).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.