Lumbar Degenerative Disk Disease Medication

Updated: Aug 31, 2018
  • Author: Rajeev K Patel, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Medication

Medication Summary

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.

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Nonsteroidal anti-inflammatory drugs

Class Summary

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.

Ibuprofen (Ibuprin, Motrin)

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

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.

Nabumetone (Relafen)

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

Meloxicam (Mobic)

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

Ketorolac (Toradol)

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

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.

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Analgesics

Class Summary

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. The FDA has cleared duloxetine to treat chronic musculoskeletal pain.

Acetaminophen (Tylenol, Aspirin Free Anacin, Feverall)

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

Duloxetine (Cymbalta)

Potent inhibitor of neuronal serotonin and norepinephrine reuptake. Indicated for chronic musculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.

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Skeletal muscle relaxants

Class Summary

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.

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.

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