Neoplastic Brachial Plexopathy Medication

No medications are specific for this diagnostic entity. Typical analgesic and adjunct analgesic agents may be worthwhile in managing neoplastic plexopathy.

Opioid analgesics (eg, long-acting oxycodone or fentanyl) are associated with fewer concerns about tolerance and dependency than many other opiates. A ceiling effect is also absent with these agents, while use of combination agents like hydrocodone/acetaminophen may be limited by maximum dose of acetaminophen allowable (4 g/d). Opiates may be effective at acceptable doses and often are tried first. For more mild symptoms, topical analgesics should be tried.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can be helpful and usually are tried in conjunction with other agents.

Adjunct agents such as tricyclic antidepressants (eg, nortriptyline, amitriptyline) or other antidepressants (eg, sertraline, venlafaxine), anticonvulsants (Lyrica, gabapentin, Tegretol), and, less commonly, antiarrhythmics (eg, mexiletine) may be used for control of neuropathic pain.

Class Summary

Should be used early in the disease. As in most painful conditions, begin with low potency medications at low doses and taper to desired response.

Hydrocodone and acetaminophen (Vicodin, Lortab, Norcet)

Drug combination indicated for moderate to severe pain.

Oxycodone (OxyContin)

Indicated for the relief of moderate to severe pain.

Fentanyl (Duragesic)

Potent opioid analgesic with much shorter half-life than morphine sulfate. DOC for conscious sedation analgesia.

Excellent choice for pain management and sedation with short duration (30-60 min) and easy to titrate. Easily and quickly reversed by naloxone.

Class Summary

Can be helpful since inflammation may be part of the pathophysiology of the pain of NBP, as previously mentioned.

Prednisone (Deltasone, Orasone, Meticorten)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Class Summary

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek lowest dose for each patient.

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions. Inexpensive older NSAIDs like ibuprofen or naproxen may be considered; however, COX-2 inhibitors with their lower GI toxicity are often first-line agents.

Ibuprofen (Motrin, Ibuprin)

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

Naproxen (Naprosyn, Naprelan, Anaprox)

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

Class Summary

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

Amitriptyline (Elavil)

Analgesic for certain chronic and neuropathic pain. Used as adjunct therapy.

Nortriptyline (Pamelor, Aventyl HCl)

Used as adjunct therapy. Has demonstrated effectiveness in the treatment of chronic pain. Used as adjunct agent.

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 CNS.

Pharmacodynamic effects such as the desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors also appear to play a role in its mechanisms of action.

Class Summary

Use of certain antiepileptic 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. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Carbamazepine (Tegretol)

May reduce polysynaptic responses and block post-tetanic potentiation. Used as adjunct therapy.

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. There are no firm rules, but, in elderly patients, less potentially anticholinergic medications like gabapentin may be a good first choice. Used as adjunct therapy.