Physical Medicine and Rehabilitation for Thoracic Outlet Syndrome Medication

Updated: May 15, 2017
  • Author: Benjamin M Sucher, DO, FAOCPMR, FAAPMR; Chief Editor: Dean H Hommer, MD  more...
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Medication

Medication Summary

Muscle relaxants (eg, Flexeril, Soma, Robaxin, Parafon forte) are options to help decrease muscle tightness and restriction, thereby facilitating conservative treatment with exercise and manipulation. Tizanidine (Zanaflex) is being used for muscle tension cephalgia and may hold promise for thoracic outlet syndrome (TOS).

Anti-inflammatory medication can decrease irritability and pain and enhance conservative treatment results. Long-acting preparations often are most effective and are tolerated better (eg, Relafen, Daypro, Celebrex). Voltaren or Arthrotec and Celebrex are relatively long-acting alternatives that are less irritating to the GI tract than Naproxen or Clinoril.

Some internists or rheumatologists may recommend vasodilators and calcium-channel blockers, if significant vascular and vasoconstrictive involvement exists. These agents are not primary drugs of choice for TOS but should be considered ancillary or secondary options to be considered and integrated into treatment as clinically indicated.

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Muscle relaxants

Class Summary

Used to relax and loosen the tight musculature involved in TOS, facilitate stretching and manipulation treatments, relieve pain, and assist with sleep.

Cyclobenzaprine (Flexeril)

Muscle relaxer of moderate duration, centrally acting, related to TCAs chemically. This drug often produces a "hangover" effect, which can be minimized by taking the nighttime dose 2-3 h before going to sleep.

Carisoprodol (Soma)

Short-acting medication that works at spinal cord level.

Methocarbamol (Robaxin)

Short-acting muscle relaxer that probably works through CNS mechanisms.

Chlorzoxazone (Flexaphen, Paraflex, Parafon Forte)

Short-acting muscle relaxer, working via central pathways (spinal cord and subcortical).

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Nonsteroidal anti-inflammatory drugs

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but 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.

Nabumetone (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclo-oxygenase enzyme, which in turn inhibits pain and inflammation.

Oxaprozin (Daypro)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.

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 of celecoxib for each patient.

Naproxen (Anaprox, Naprelan, Naprosyn)

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.

Sulindac (Clinoril)

Decreases activity of cyclo-oxygenase and in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Diclofenac (Voltaren, Cataflam)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase which in turn decreases formation of prostaglandin precursors.

Diclofenac and misoprostol (Arthrotec)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase which in turn decreases formation of prostaglandin precursors.

Misoprostol is prostaglandin analog that protects lining of GI tract by replacing depleted prostaglandin E1 in prostaglandin-inhibiting therapies.

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