Temporomandibular Joint Syndrome Medication
- Author: Vivian Tsai, MD, MPH, FACEP; Chief Editor: Herbert S Diamond, MD more...
Nonsteroidal anti-inflammatory drugs (NSAIDs) and benzodiazepines are the mainstays of pharmacologic treatment for temporomandibular joint (TMJ) syndrome in the emergency deparment. Patients eventually may require tricyclics, opioids, muscle relaxants, or steroid (intra-articular) therapy for protracted pain syndromes.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Most commonly used for relief of mild to moderate pain. Although effects of NSAIDs in treatment of pain tend to be patient specific, ibuprofen usually is the DOC for initial therapy. Other options include naproxen, flurbiprofen, mefenamic acid, ketoprofen, indomethacin, and piroxicam.
Usually DOC for treatment of mild to moderate pain if no contraindications exist; inhibits inflammatory reactions and pain, probably by decreasing activity of enzyme cyclooxygenase, which results in inhibition of prostaglandin synthesis.
Used for relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of enzyme cyclooxygenase, which results in decrease of prostaglandin synthesis.
Analgesic, antipyretic, and anti-inflammatory effects; may inhibit cyclooxygenase enzyme, causing inhibition of prostaglandin biosynthesis that in turn may result in analgesic and anti-inflammatory activities.
Used for relief of mild to moderate pain and inflammation; administer small dosages initially to patients with small bodies, older persons, and those with renal or liver disease; doses >75 mg do not increase therapeutic effects; administer high doses with caution and closely observe patient for response.
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
Decreases activity of cyclooxygenase, which, in turn, inhibits prostaglandin synthesis; effects decrease formation of inflammatory mediators.
Used for muscle relaxant properties but relatively contraindicated in pediatric patients because of sedating properties; appear to potentiate effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters by binding to specific receptor sites.
Depresses all levels of CNS, including limbic and reticular formation, possibly by increasing activity of GABA, a major inhibitory neurotransmitter.
Individualize dosage and increase cautiously to avoid adverse effects.
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