eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders

Lumbar Degenerative Disk Disease: Treatment & Medication

Author: Rajeev K Patel, MD, Assistant Professor, Department of Orthopedics, University of Rochester; Consulting Surgeon, Strong Health Spine Center, Strong Memorial Health System
Coauthor(s): Curtis W Slipman, MD, Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center
Contributor Information and Disclosures

Updated: Aug 3, 2009

Treatment

Rehabilitation Program

Physical Therapy

Physical rehabilitation with active patient participation is a key approach to treatment of patients with diskogenic pain. Physical therapy programs prescribed specifically to address the primary site of injury and secondary sites of dysfunction can provide a means of treatment, with or without adjunct medications, therapeutic procedures, or surgical intervention.

Relative rest, which restricts all occupational and avocational activities, for up to the first 2 days after an acute episode, may be indicated to help calm initial pain. Rest for longer periods has not been shown to be beneficial and can cause deconditioning, loss of bone density, decreased intradiskal nutrition, loss of muscle strength and flexibility, and increased segmental stiffness. Passive modalities are valuable during the initial 48 hours of relative rest to aid in pain relief, but protracted courses of passive treatments become counterproductive, as they place patient in a dependent role instead of an active one.

Education is one of the most important components of any back-care program and should include an explanation of the natural history of acute, subacute, and chronic disk injury. The physical rehabilitation program should also include training in proper body mechanics and lumber ergonomics during various functional, occupational, and avocational activities. Manual techniques may be applied to increase soft tissue pliability when secondary myofascial tightness is present. If the aforementioned measures are appropriate and completed, an active, dynamic rehabilitation program to stabilize the lumbar spine may be started on an outpatient basis. In addition, rehabilitation of other associated components of the functional kinetic chain may be appropriate, as these structures may also be affected.

Dynamic lumbar-spine stabilization programs are aimed at maintaining a neutral spine position throughout various daily activities. An extension bias commonly is used to help reduce intradiskal pressure. This position allows for balanced segmental force distribution between the disk and zygapophyseal joints, it provides functional stability with axial loading to help minimize the chance for acute dynamic overload upon the disks, it minimizes tension on ligaments and fascia planes, and it decreases symptoms. Repetition is key to increasing flexibility, building endurance, and developing the required muscle motor engrams that subconsciously activate a series of key multimuscular contractions to maintain the lumbar spine in a neutral position throughout static and dynamic activities.

For athletes, the aforementioned program can be progressively combined with sport-specific plyometrics to help the lumbar spine maintain neutral position during high-intensity, unpredictable, reaction-intensive sports. Rehabilitation of athletes should also train them to maintain a neutral spine position in sport-specific motions. These component motions should then be grouped into a new, safe spine-stable movement. Cardiovascular training is an important adjunct to comprehensive rehabilitation programs because it provides endurance necessary to prevent fatigue of the muscles that stabilize the spine.

Occupational Therapy

Occupational therapy can be an important adjunct in the rehabilitation process when generalized muscular deconditioning has created adverse effects on strength, endurance, and flexibility of the upper extremities and/or impairment in activities of daily living (ADLs).

An occupational therapist often provides this portion of the rehabilitation program. Essential elements consist of ensuring proper ergonomics at the work site, which may involve simply reconfiguring a desktop and/or workstation, or it may require complex solutions. Another aspect involves rehabilitation before the patient resumes full-time duties. After the offending source of pain is resolved, the patient typically has deconditioning and may require activity-specific reconditioning to prevent new or recurring injury.

Recreational Therapy

Recreation therapy may have a role in assisting the patient to resume avocational activities, possibly with adaptations in technique or with the use of adaptive equipment.

Medical Issues/Complications

Medical causes of LBP include the spondyloarthropathies (eg, enteric arthropathy, Reiter syndrome, ankylosing spondylitis, psoriatic arthritis), Marfan syndrome, fibromyalgia, myofascial pain syndrome, diskitis, and neoplastic disease.

Surgical Intervention

Available surgical approaches include anterior, posterior, or combined procedure; interbody fusion with allograft autologous bone or threaded titanium cage; and intertransverse process in situ fusion with or without instrumentation. The introduction of disk arthroplasty has been proposed as a possible surgical option in those patients who would like to maintain as much segmental motion as possible.

  • To date, no prospective randomized blind study has demonstrated the superiority of any surgical approach or technique. One retrospective study was performed to compare posterolateral fusion with iliac-crest allografting and translaminar facet-screw augmentation, anterior interbody fusion with fibula allografting, posterolateral fusion with pedicle screw-rod fixation, and anterior interbody threaded cage fusion combined with facet-joint fusion and posterolateral fusion. The results suggested that the last procedure may provide superior outcomes.
  • Other investigators report outcome rates ranging from 39% to 82-93% for various procedures. With respect to disk arthroplasty, the literature is not clear on its definitive role, if any, in the treatment of symptomatic LDDD.
  • In a study of 59 patients suffering from low back pain and 1- or 2-level LDDD, Freudenberger et al compared the effectiveness of anterior lumbar interbody fusion with anterior tension band plating (ALIF-ATB) with that of posterior lumbar interbody fusion (PLIF) with pedicle screw instrumentation.40 The investigators found that both techniques had similar fusion rates, but that patients who underwent PLIF had greater estimated blood loss and required more surgical time than did patients who were treated with ALIF-ATB.

Consultations

Consultation of the primary care physician with a nonsurgical spine specialist is appropriate for patients with symptoms lasting longer than 6 weeks secondary to LDDD. Consultation with a spinal surgeon may be appropriate for patients with intractable severe function-limiting symptoms secondary to IDD, at 1 or 2 contiguous levels, for those with symptoms lasting longer than 6 months who have had no relief from nonsurgical approaches, and for persons with abnormal neurologic findings.

Other Treatment

New intradiskal techniques are being investigated to ascertain whether they can obviate fusion procedures. With intradiskal electrothermal therapy, a navigable intradiskal catheter is used to heat the posterior annular wall at the nuclear interface corresponding to the 4- to 8-o'clock zone.41,42 Temperatures produced in the outer annulus (46-48°C) are sufficient for thermal coagulation of nervous tissue. Temperatures in the nucleus and the annulus (65-75°C) are sufficient for collagen contraction or shrinkage.

Saal and colleagues observed 20% focal nuclear shrinkage (by volume) and 7% total nuclear shrinkage after treatment.43 Therefore, some authorities postulate that this intervention may cause thermocoagulation of annular nerve fibers. In addition, by means of collagen shrinkage, it may also result in tightening of the fibrous structure of annular tissue that then may enhance structural integrity of a degenerated or damaged disk and possibly stabilize annular fissures. Intradiskal electrothermal therapy showed great promise in initial studies and was touted as being effective at controlling diskogenic axial lumbar back pain. However, a later investigation, a double-blinded, controlled study conducted by Freeman and colleagues, established safety with limited efficacy.44

  • Saal and Saal reported their results in 36 patients who were followed up for 6-13 months.43 Improvement in function, lowering of pain scores, and improvement in sitting tolerance times were observed in 75%.
  • In a clinical trial of 20 patients, Derby reported a mean 2-point decrease on a 10-point visual analog scale (P <.05) at 6 months.45 In addition, 73% reported satisfaction with outcome and indicated that they would repeat the procedure for the same outcome. Although early results are promising with this exciting novel technique, no definitive judgments can be made because only preliminary outcomes with short-term follow-up have been reported to date.
  • The idea of intradiskal injections and procedures is becoming exciting with new trials of OB1 and other biological therapies being developed in the hopes of being able to regenerate diskal materials and reverse the degenerative cascade underway.
  • Since their discovery by Marshall Urist, MD at UCLA, bone morphogenetic proteins have been categorized as either growth or differentiation factors and consist of a family of proteins with important regulatory and developmental effects on bone growth and the development of musculoskeletal tissue. These proteins are clinically used by spine surgeons to facilitate bony fusion and obviate the need for autografting. Studies have shown that these proteins are capable of controlling the mRNA transcription of cells within human and animal disk models. At the 2002 North American Spine Society (NASS) annual meeting, studies were presented that showed great promise with regard to the development of treatments for degenerative disk disease using bone morphogenic proteins 2 and 7, with augmentation of diseased disks employed at an early stage to offset the degenerative cascade.46,47

    Miyamoto and colleagues showed restoration of disk viscoelastic properties in a rabbit model of degenerative disk disease after injection of osteogenic protein 1 (OP-1). It is hoped that disk regenerative therapy using intradiskal injections of biological pharmaceuticals will become an effective treatment for degenerative disk disease.48

Medication

Medications are an integral part of treatment of LDDD. A myriad of medications of various subtypes has been prescribed by a wide array of medical specialties to help patients with sequelae of LDDD. Several types of medications may be helpful in treatment of diskogenic pain (eg, analgesics [peripheral and centrally acting], muscle relaxants, sedatives, glucocorticoids, anticonvulsants, antidepressants, antihistamines, stimulants). Mainstays of oral treatment of LDDD, peripherally acting analgesics, are discussed here. The following information was collected from the Physician's Desk Reference.

Analgesics act either peripherally or centrally. Peripherally acting analgesics include nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. NSAIDs are the drugs of choice (DOCs) in initial pharmacologic treatment of acute episodes of diskogenic pain or with acute exacerbation of chronic diskogenic pain. NSAIDs have mild-to-moderate analgesic, antipyretic, and anti-inflammatory properties. NSAIDs have multiple mechanisms of action, including inhibition of cyclo-oxygenase, competition with prostaglandin at receptor sites, and inhibition of WBC migration and of lysosomal enzymes from WBCs.

Analgesic effect appears earlier and at lower doses than anti-inflammatory effects. Increasing dosage usually increases analgesic effect, with a ceiling effect after which increasing dosages do not increase therapeutic efficacy but do increase toxicity. Use of these medications on a long-term basis is not advised. For reasons not well understood, some patients respond to some NSAIDs and not to others despite their apparently similar mechanisms of action.

This response does not correlate with the class of NSAIDs. Therefore, 7- to 14-day trials of up to 3 different NSAIDs should be performed before one deems NSAIDs ineffective for an individual patient. NSAIDs can be divided into categories based on the cyclo-oxygenase (COX-2) specificity and short, intermediate, or long half-lives. COX-2 specific NSAIDs are primarily beneficial because they do not inhibit the COX-1 isoenzyme. This property dramatically decreases risk of GI and renal adverse effects. NSAIDs with a short half-life (4-6 h) include aspirin, ibuprofen, ketoprofen, and flurbiprofen. Of these medications, aspirin and ibuprofen are the DOCs. NSAIDS with an intermediate half-life (8-12 h) include naproxen, etodolac, diclofenac, sulindac, and diflunisal. Of these, naproxen

Ketoralac requires special consideration because it is the NSAID best known for its analgesic effect at the opioid level. However, it should be used for a maximum of 5 days (in any form). Acetaminophen is effective for mild to moderate pain. It has analgesic and antipyretic properties but no anti-inflammatory action.

Nonsteroidal anti-inflammatory drugs

These drugs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. They may have other mechanisms as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.


Aspirin (Anacin, Bayer Aspirin, Ascriptin)

Best-known NSAID; widely available; cardioprotective, cerebroprotective, and anticoagulation properties. Treats mild to moderate pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Adult

650 mg PO q6h; not to exceed 3 g/d

Pediatric

90-130 mg/kg/d PO divided q6h with target plasma salicylate level of 150-300 mcg/mL

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Documented hypersensitivity, liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, and asthma; due to association of aspirin with Reye syndrome, do not use in children ( <16 y) with flu

Pregnancy

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

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia or a history of blood coagulation defects; avoid in patients taking anticoagulants


Ibuprofen (Ibuprin, Motrin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult

400 mg PO q4-6h; not to exceed 2400 mg/d

Pediatric

<6 months: Not established
6 months to 12 years: 10 mg/kg PO q6-8h; not to exceed 40 mg/kg
>12 years: Administer as in adults

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity, peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Pregnancy

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

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

Precautions

Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy


Naproxen (Naprelan, Naprosyn, Aleve)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, decreasing prostaglandin synthesis.

Adult

250, 375, or 500 mg PO bid; not to exceed 1500 mg/d

Pediatric

<2 years: Not established
>2 years: 5 mg/kg PO bid

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity, peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency

Pregnancy

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

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

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug


Nabumetone (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclooxygenase enzyme, which inhibits pain and inflammation.

Adult

1000 mg/d PO; not to exceed 1000 mg PO bid

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; active peptic ulceration, hepatic impairment

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

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

Precautions

Category D in third trimester of pregnancy; elderly may require lower doses; caution in hepatic and renal impairment


Meloxicam (Mobic)

Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Adult

7.5 mg PO qd; may increase to 15 mg PO qd

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; active GI bleeding

Pregnancy

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

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs)


Ketorolac (Toradol)

Inhibits prostaglandin synthesis by decreasing activity enzyme, cyclo-oxygenase, decreasing formation of prostaglandin precursors.

Adult

<65 years: 60 mg IM initially followed by 15-30 mg q6h prn; not to exceed 5 d of treatment
>65 years: 30 mg IM initially followed by 15 mg q6h prn; not to exceed 5 d of treatment

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; do not administer into CNS

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

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

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts (rare) usually return to normal during ongoing therapy; discontinue therapy if persistent leukopenia, granulocytopenia, or thrombocytopenia occur


Celecoxib (Celebrex)

Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek lowest dose for each patient.
Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).
Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.

Adult

200 mg/d PO qd; alternatively, 100 mg PO bid

Pediatric

Not established

CYP450 2C9 substrate; coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations

Pregnancy

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

Precautions

May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or lab results suggest liver dysfunction

Analgesics

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


Acetaminophen (Tylenol, Aspirin Free Anacin, Feverall)

Ensures patient comfort, promotes pulmonary toilet, and has sedating properties.

Adult

1000 mg PO q4-6h prn; not to exceed 4000 mg/d

Pediatric

<6 years: Not established
6-12 years: 325 mg PO q4-6h; not to exceed 1625 mg/d
>12 years: Administer as in adults

Rifampin can reduce analgesic effects; 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 alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; present in many OTC products, and combined use may result in cumulative doses exceeding recommended maximum

Skeletal muscle relaxants

These drugs are effective in reducing morbidity. Their mechanism of action not clearly understood.


Orphenadrine (Norflex)

Although the exact mode of action not well understood, has clinical effectiveness in muscular injury. Effectiveness may be related to analgesic properties. May have atropinelike effects and analgesic properties.

Adult

100 mg PO bid
60 mg IV/IM q12h

Pediatric

Not established

Documented hypersensitivity; GI obstruction, glaucoma, myasthenia gravis, or cardiospasm

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 cardiac arrhythmias and congestive heart failure


Cyclobenzaprine (Flexeril)

Acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons. Structurally related to tricyclic antidepressants.
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 syndromes. Long-term improvement over placebo has not been established. Often produces a "hangover" effect, which can be minimized by taking the nighttime dose 2-3 h before going to sleep.

Adult

10 mg PO tid with a range of 20-40 mg/d in divided doses; not to exceed 60 mg/d

Pediatric

Not recommended

Coadministration with MAO inhibitors and tricyclic antidepressants may increase toxicity; cyclobenzaprine may have additive effect when used concurrently with anticholinergics; effects of alcohol, CNS depressants, and barbiturates may be enhanced with cyclobenzaprine

Documented hypersensitivity; have taken MAO inhibitors within the last 14 d

Pregnancy

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

Precautions

Caution in angle closure glaucoma and urinary hesitance; may cause drowsiness, dizziness, and xerostomia

More on Lumbar Degenerative Disk Disease

Overview: Lumbar Degenerative Disk Disease
Differential Diagnoses & Workup: Lumbar Degenerative Disk Disease
Treatment & Medication: Lumbar Degenerative Disk Disease
Follow-up: Lumbar Degenerative Disk Disease
References
Further Reading
[ CLOSE WINDOW ]

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Further Reading

Related eMedicine topics:
Back Pain, Mechanical
Cervical Discogenic Pain Syndrome
Degenerative Lumbar Disc Disease in the Mature Athlete
Herniated Nucleus Pulposus
Lumbar Disk Problems in the Athlete
Lumbar (Intervertebral) Disk Disorders
Lumbosacral Discogenic Pain Syndrome
Mechanical Low Back Pain
Pathophysiology of Chronic Back Pain
Therapeutic Injections for Pain Management

Clinical guidelines:
ACR Appropriateness Criteria® low back pain

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 2: assessment of functional outcome

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 6: magnetic resonance imaging and discography for patient selection for lumbar fusion

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 8: lumbar fusion for disc herniation and radiculopathy

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 11: interbody techniques for lumbar fusion

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 12: pedicle screw fixation as an adjunct to posterolateral fusion for low-back pain

Low back disorders

Clinical trials:
Freedom Lumbar Disc in the Treatment of Lumbar Degenerative Disc Disease (FLD)

Pilot Study to Assess Safety/Preliminary Effectiveness of Prefix in Subjects With Degenerative Disc Disease (DDD) Undergoing Spine Fusion Surgery

Prospective Clinical Evaluation of the New Aegis Plate for Anterior Interbody Fusions

Safety and Efficacy Study of NeoFuse in Subjects Requiring Posterolateral Lumbar Fusion

Study of the Safety and Effectiveness of DIAM™ Spinal Stabilization System vs. Conservative Care

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Keywords

lumbar degenerative disk disease, lumbar degenerative disc disease, low back pain, LBP, bulging disc, lumbar spine, disc disease, degenerative disc, cervical disc, herniated disk, herniated disc, lumbar spondylosis, cervical surgery, cervical disc surgery, lumbar disc, spinal lumbar, annular tear, internal disc disruption syndrome, LDDD, internal disk disruption syndrome, lumbar strain, nucleus pulposus, annular delamination, annular lamellae, discogenic pain, diskogenic pain, disc degeneration, disk degeneration, lumbar arthrodesis, lumbar discectomy, lumbar laminectomy, spondylolisthesis, epidural steroid injection, ESI

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Contributor Information and Disclosures

Author

Rajeev K Patel, MD, Assistant Professor, Department of Orthopedics, University of Rochester; Consulting Surgeon, Strong Health Spine Center, Strong Memorial Health System
Rajeev K Patel, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Curtis W Slipman, MD, Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center
Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society
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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