Suprascapular Neuropathy Medication

Updated: Oct 11, 2018
  • Author: Thomas H Trojian, MD; Chief Editor: Sherwin SW Ho, MD  more...
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Medication

Medication Summary

To the author's knowledge, enteral pharmaceutical intervention to relieve symptoms associated with infraspinatus syndrome has not been studied or reported in the literature. For individuals with pain, a trial of nonsteroidal anti-inflammatory drugs early in the course of treatment seems reasonable. Alternatively, a trial of the gamma aminobutyric acid (GABA) analogue gabapentin may provide some analgesia.

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Antiepileptics

Class Summary

The use of certain antiepileptics (AEDs), such as the GABA analogue Neurontin (gabapentin), is helpful in some cases of neuropathic pain. Although unstudied, a trial of an AED agent might provide some analgesia in symptomatic athletes with suprascapular neuropathy.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown.

Structurally related to GABA but does not interact with GABA receptors.

Titration to effect can take place over several days (eg, 300 mg on day 1, 300 mg bid on day 2, 300 mg tid on day 3).

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Analgesic, Cox-2 Inhibitor

Class Summary

Cyclooxygenase (COX)-2 inhibitors have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action may be inhibition of COX activity and prostaglandin synthesis. Others may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

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, the COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek the lowest dose for each patient.

Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; downregulates 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; and 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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