Cervical Disc Disease Medication

Updated: Feb 14, 2022
  • Author: Michael B Furman, MD, MS; Chief Editor: Dean H Hommer, MD  more...
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Medication Summary

NSAIDs are first-line pharmacologic intervention for most cervical conditions. NSAIDs reduce pain at low doses and decrease inflammation at high doses. Patients require a therapeutic NSAID plasma level to achieve an anti-inflammatory effect. NSAIDs with once-a-day dosing improve compliance and increase the probability of achieving therapeutic levels. Controlling inflammation is paramount when treating cervical radiculopathy.

Aspirin rarely is recommended, because it binds irreversibly to cyclooxygenase (COX) and incites gastritis, requiring large doses to reach anti-inflammatory effect. Traditional NSAIDs provoke multiorgan toxicity, including peptic ulcer disease, renal insufficiency, and hepatic dysfunction. COX isomer type 2 (COX-2) NSAID inhibitors confer the same analgesic/anti-inflammatory benefits without multiorgan toxicity. All NSAIDs have a dose-related ceiling point for analgesia above which higher doses fail to provide additional pain relief. The same precautions should be observed with COX-2 NSAIDs, despite their reduced risk of organ toxicity.

Use muscle relaxants to potentiate the NSAID analgesic effect and not necessarily to control muscle spasm. Muscle relaxants primarily sedate by relaxing muscle with subsequent relaxation of the patient.

Oral corticosteroids treat inflammatory cervical radiculopathy. No documented case of avascular necrosis exists in the literature when the total prednisone dose or corticosteroid equivalent stayed under 550 mg. Some providers use a methylprednisolone dose pack (tapers from 24 to 0 mg over 7 days); however, concern exists regarding adequate dosing to treat radiculopathy. A prednisone dose schedule outlined below stays within the 550-mg limiting amount.

Tricyclic antidepressants (TCAs) decrease pain and reduce nonrestorative sleep. Side effects include dry mouth, constipation, and weight gain. Selective serotonin reuptake inhibitors (SSRIs), despite lacking side effects associated with TCAs, are inferior to TCAs in treating diabetic peripheral neuropathic pain, and their efficacy in relieving neck and back pain compared with that of other antidepressants remains unknown. Additional medications include membrane-stabilizing agents (eg, gabapentin, carbamazepine). Gabapentin has demonstrated efficacy in treating diabetic peripheral neuropathic pain. Pregabalin (Lyrica) has been used as an off-label treatment for radicular pain with some efficacy. Other analgesics (acetaminophen, tramadol) provide pain relief without inflammation control.

Opioids may be prescribed orally, transdermally, rectally, or sublingually on a scheduled basis. Patients on opioids should sign a medication agreement restricting them to a single physician and pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling medication. Patients with a previous history of alcoholism or other addiction who are prescribed opioids long term are at risk for dependence. Therefore, consider recommending cotreatment of these patients with a psychologist or other addiction specialist.

Lastly, many short-acting opioid preparations contain acetaminophen, which may be toxic in doses above 3 g per day. Consequently, patients should be counseled to avoid toxicity by avoiding other pharmaceuticals containing acetaminophen.



Class Summary

Used to treat inflammatory cervical radiculopathy. Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Sterapred)

Decreases inflammation by inhibiting polymorphonuclear leukocyte and fibroblast migration, stabilizing lysosomes, and decreasing capillary permeability.

Methylprednisolone dose pack (Solu-Medrol, Medrol, Depo-Medrol)

Decreases inflammation by inhibiting polymorphonuclear leukocyte and fibroblast migration, stabilizing lysosomes, and decreasing capillary permeability.



Class Summary

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

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.

Carbamazepine (Tegretol)

May reduce polysynaptic responses and block posttetanic potentiation. Inhibits nerve impulses by decreasing influx of sodium ions into cell membrane.


Structural derivative of GABA. Mechanism of action unknown. Binds with high affinity to alpha2 -delta site (a calcium channel subunit). In vitro, reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.



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.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

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

Tramadol (Ultram)

Inhibits ascending pain pathways, altering perception of and response to pain. Inhibits also reuptake of norepinephrine and serotonin.