eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders

Spinal Stenosis and Neurogenic Claudication: Treatment & Medication

Author: Michael B Furman, MD, MS, Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Orthopedic and Spine Specialists
Coauthor(s): Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute; Robert Pannullo, MD, Interventional Spinal Care Fellow, Department of Physical Medicine and Rehabilitation, KDV Orthopaedics and Rehabilitation Ltd; Jeremy Simon, MD, Attending Physician, Department of Physical Medicine, The Rothman Institute
Contributor Information and Disclosures

Updated: Jun 16, 2009

Treatment

Rehabilitation Program

Physical Therapy

Patients with lumbar spinal stenosis (LSS) often benefit from conservative treatment and participation in a physical therapy (PT) program. 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 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.20

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.

Medical Issues/Complications

In rare cases, central canal stenosis may provoke cauda equina syndrome with associated saddle anesthesia, bladder and/or bowel dysfunction and altered muscle reflexes. Additionally, patients with lateral recess stenosis – induced radiculopathy may manifest significant lower limb weakness or numbness. Lastly, intractable axial, radicular, or NC pain may result.

Surgical Intervention

Lumbar spinal stenosis (LSS) remains one of the most common conditions leading to lumbar spine surgery in adults aged 65 years and older. Increasing rates of LSS surgery among the Medicare population have been shown to be due possibly to imaging techniques that enable physicians to diagnose LSS more frequently. Other contributing factors may include improved surgical techniques that might allow patients previously managed conservatively to undergo surgery, as well as a philosophy that LSS surgery prevents future morbidity.

  • Widely agreed upon indications for LSS surgery do not exist. Typically, patients undergo elective surgery to improve walking tolerance and disabling leg and back pain. Preoperatively, such disability infrequently is measured in objective quantitative terms. Some suggest preoperative treadmill testing to facilitate objective selection of potential surgical candidates.25 Surgical emergencies (eg, cauda equina syndrome, rapid neurologic deterioration) rarely arise.
    • Surgical techniques include standard wide laminectomy and decompression, which first removes lamina and ligamentum flavum from the lateral borders of one lateral recess to the other and then decompresses entrapped nerve roots.26
    • Foraminal enlargement surgery is used to address refractory foraminal stenosis-induced radicular pain. Other surgical decompressions include the following:
      • Laminotomy
      • Medial facetectomy
      • Medial or lateral foraminotomy.
    • Midline interlaminar approaches are used to address concurrent central and foraminal stenosis.
    • The Wiltse approach with foraminotomy is used for isolated foraminal stenosis by providing the following:
      • Widening the longissimus-multifidus muscle interval
      • Removing the lateral pars interarticularis and facet joint
      • Exposing the nerve root with subsequent decompression
    • In addition to decompression and foraminal enlargement, some patients with segmental instability from facet joint removal and pain secondary to DDD may require fusion. (See images below and Images 8-9.)
      • Fusion stabilizes the intervertebral segment while maintaining lordosis and foraminal size.
      • Additional options include arthrodesis and instrumentation.


Lateral view of a lumbar myelogram performed in a...

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.

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Lateral view of a lumbar myelogram performed in a...

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 ...

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 intervertebral distance.

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Sagittal view of a 3-dimensional volume image of ...

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 intervertebral distance.

  • Surgical outcomes for patients with LSS vary.
    • Surgical outcome literature is difficult to assess due to observer bias, inadequate outcome data categorization, vaguely defined outcome measures, and study design.
    • Reports show widely varied outcomes (26-100% success and 31% dissatisfaction at 4.6 years), due to disparate research methodologies.
  • Conservative versus surgical treatment for LSS remains controversial due to wide variations in outcome study type and quality.
    • Johnsson and colleagues document improvement in 60% of surgically treated patients with 25% worsened, compared with improvement in 30% of conservatively treated patients and no change in 60%.27
    • Atlas and colleagues tracked 67 conservatively treated and 81 surgically treated patients over 12 months; surgically treated patients reported greater improvement in pain relief than those treated conservatively.28
    • 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 cite that 12 of 49 patients treated conservatively with incorporation of analgesics, physical therapy, and epidural steroid injection, reported sustained improvement.29 Conservative and surgical treatments have not been subjected to rigorous well-designed study.

Consultations

  • Consultation with an internal medicine specialist or subspecialty may be indicated when low back pain (LBP) suggests an underlying systemic illness such as malignancy, infection, or metabolic bone disease. Also, if the diagnosis of vascular claudication is in question, referral to an internist is indicated.
  • Consultation with a rheumatologist may be considered when back pain suggests a rheumatologic condition such as ankylosing spondylitis, rheumatoid arthritis, osteoporosis, or fibromyalgia.
  • Consultation with a surgeon is warranted for deteriorating neurologic status (eg, cauda equina syndrome), segmental instability, and/or intractable radicular or NC pain.

Other Treatment

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. 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
    • 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
    • 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, like 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
    • Transforaminal ESI facilitates precise deposit of higher steroid concentrations closer to the involved spinal segment, and, consequently, might prove more efficacious in reducing pain.
    • Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis.
    • Bilateral transforaminal ESI also may be used to treat bilateral central stenosis-induced NC pain when imaging studies demonstrate limited posterior epidural space, thereby precluding safe interlaminar ESI. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.
  • Absolute contraindications to ESI include bleeding diathesis and anticoagulation therapy because of the increased risk of epidural hematoma. While the actual incidence of this complication is unknown, estimates in the literature suggest is occurs less than 1 in 150,000 outpatient epidural injections. Anticoagulation therapy (eg, warfarin, heparin) should be stopped a few days prior to injection. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking Coumadin, 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.
  • 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.30 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 epidural steroid injection (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.
  • Recent studies assessing efficacy of fluoroscopically guided, contrast-enhanced ESI, even for 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.

Medication

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.

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.

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.

Tramadol and acetaminophen confer analgesia but do not affect inflammation.

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.

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.31 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.

Anticonvulsants

Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain.32 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.


Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, exact mechanism of action is unknown. Structurally related to GABA but does not interact with GABA receptors.

Adult

900-1800 mg/d PO tid; may start 300 mg d 1, 300 mg bid d 2, and 300 mg tid d 3; may increase up to 1800 mg/d by adding 300 mg on following days

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Antacids may reduce bioavailability of gabapentin significantly (administer at least 2 h following antacids); may increase norethindrone levels significantly

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic disease, breastfeeding women, and elderly patients


Carbamazepine (Tegretol)

Inhibits nerve impulses by decreasing cell membrane sodium ion influx.

Adult

100 mg PO bid with meals; may increase 100 mg q12h until pain decreases; not to exceed 1.2 g/d; maintenance dose 200-400 mg bid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Fatal reaction with MAOIs; toxicity with clarithromycin, verapamil, lithium, propoxyphene, isoniazid, diltiazem, cimetidine, erythromycin, and troleandomycin; decreased effects with thyroid hormones, theophylline, oral contraceptives, warfarin, primidone, phenytoin, and phenobarbital; increased effects of lithium, desmopressin, lypressin, and vasopressin

Documented hypersensitivity, bone marrow depression, and concomitant MAOI use

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Not to be used for relief of minor aches or pains; caution with increased intraocular pressure; obtain CBC counts (may cause aplastic anemia) and serum-iron baseline prior to treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; caution with breastfeeding, psychosis, cardiac disease, and renal or hepatic disease

Analgesics

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


Acetaminophen (Tylenol, Feverall)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Adult

325-650 mg PO q4h prn; not to exceed 4 g/d

Pediatric

10-15 mg/kg PO q4h

Decrease effects of chloramphenicol; caffeine and diflunisal may increase effects of acetaminophen; colestipol, anticholinergics, oral contraceptives, rifampin, and cholestyramine decrease effects of acetaminophen; severe hypothermia may occur with phenothiazines; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose; caution in hepatic or renal disease


Tramadol (Ultram)

Mechanism not entirely known. Binds to opioid receptors; inhibits reuptake of serotonin, norepinephrine.

Adult

50-100 mg PO q4-6h prn; not to exceed 400 mg/d

Pediatric

Not established

Decreased tramadol levels with carbamazepine; increased CNS depression with opiates, hypnotics, sedatives, and alcohol; norepinephrine and serotonin reuptake inhibition (use together with MAOIs with caution)

Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 d; use of SSRIs, TCAs, opioids, and acute alcohol intoxication

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism; caution in elderly patients, pregnancy, and breastfeeding; seizures; development of tolerance or dependency with extended use

Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects and sedative effects. They have central effects on pain transmission. They block the active reupdate of norepinephrine and serotonin.


Amitriptyline (Elavil)

Analgesic for certain chronic and neuropathic pain. Blocks reuptake of norepinephrine and serotonin, which increases concentration in the CNS. Decreases pain by inhibiting spinal neurons involved in pain perception. Highly anticholinergic. 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 mo may be needed to obtain clinical effects.

Adult

30-100 mg PO qhs

Pediatric

Children: 0.1 mg/kg PO qhs; increase, as tolerated, over 2-3 wk to 0.5-2 mg/d qhs
Adolescents: 25-50 mg/d PO initially; increase gradually to 100 mg/d in divided doses

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Documented hypersensitivity; use of MAOIs within 14 d of initiating therapy; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances and history of hyperthyroidism, renal impairment, or hepatic impairment; avoid use in elderly persons

More on Spinal Stenosis and Neurogenic Claudication

Overview: Spinal Stenosis and Neurogenic Claudication
Differential Diagnoses & Workup: Spinal Stenosis and Neurogenic Claudication
Treatment & Medication: Spinal Stenosis and Neurogenic Claudication
Follow-up: Spinal Stenosis and Neurogenic Claudication
Multimedia: Spinal Stenosis and Neurogenic Claudication
References
Further Reading
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Further Reading

Related eMedicine topics:
Cauda Equina
Cauda Equina and Conus Medullaris Syndromes
Cauda Equina Syndrome [Emergency Medicine]
Cauda Equina Syndrome [Orthopedic Surgery]
Degenerative Disk Disease
Degenerative Lumbar Disc Disease in the Mature Athlete
Lumbar Degenerative Disk Disease
Spinal Stenosis [Neurosurgery]
Spinal Stenosis [Orthopedic Surgery]
Spinal Stenosis [Radiology]

Clinical guidelines:
Diagnosis and treatment of degenerative lumbar spinal stenosis. North American Spine Society - Medical Specialty Society.  2002 (revised 2007 Jan).  262 pages.  NGC:005896 

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 9: fusion in patients with stenosis and spondylolisthesis. American Association of Neurological Surgeons - Medical Specialty Society
Congress of Neurological Surgeons - Professional Association.  2005 Jun.  7 pages.  NGC:005370

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 10: fusion following decompression in patients with stenosis without spondylolisthesis. American Association of Neurological Surgeons - Medical Specialty Society
Congress of Neurological Surgeons - Professional Association.  2005 Jun.  6 pages.  NGC:005371

Clinical trials:
A Pivotal Study of a Facet Replacement System to Treat Spinal Stenosis

Dynamic Stabilization for Lumbar Spinal Stenosis With Stabilimax NZ® Dynamic Spine Stabilization System

IDE Clinical Trial Comparing Coflex vs. Fusion to Treat Lumbar Spinal Stenosis (coflex)

Investigating Superion™ In Spinal Stenosis [ISISS]

Lumbar Stenosis Outcomes Research (LUSTOR)

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Keywords

spinal stenosis, neurogenic claudication, stenosis, stenosis lumbar, lumbar spinal stenosis, laminectomy, spine surgery, disk surgery, disc surgery, foraminal stenosis, stenosis surgery, spinal stenosis surgery, spinal stenosis treatment, central stenosis, central canal stenosis, claudication, intervertebral foramen stenosis, lateral gutter stenosis, lateral recess stenosis, subarticular stenosis, subpedicular stenosis, neural compression, spinal canal narrowing, ligamentum flavum hypertrophy, facet hypertrophy of cephalad vertebra, vertebral body osteophytosis, herniated nucleus pulposus, HNP, foraminal canal stenosis, incomplete vertebral arch closure, spinal dysraphism, segmentation failure, achondroplasia, osteopetrosis

early vertebral arch ossification, osseous exostosis, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking, Morquio syndrome, posterior disc protrusion, zygapophyseal joint hypertrophy, spondylolisthesis, diskectomy, discectomy, Paget disease, fluorosis, acromegaly, ankylosing spondylitis, disc desiccation, degenerative disk disease, degenerative disc disease, failed back surgery syndrome, bilateral neurogenic claudication, cauda equina microvascular ischemia, intraneural fibrosis, radiculopathy

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Contributor Information and Disclosures

Author

Michael B Furman, MD, MS, Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Orthopedic 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, Pennsylvania Medical Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: pfizer Honoraria Speaking and teaching

Coauthor(s)

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.

Robert Pannullo, MD, Interventional Spinal Care Fellow, Department of Physical Medicine and Rehabilitation, KDV Orthopaedics and Rehabilitation Ltd
Robert Pannullo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa
Disclosure: Nothing to disclose.

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.

Medical Editor

J Michael Wieting, DO, MEd, Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Sports Medicine, Associate Director of Physician Assistant Training 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 Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, 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, FAAPMR, FAAEM 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.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
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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