Temporomandibular Disorders Medication

Updated: Feb 22, 2017
  • Author: Joseph Rios, MD; Chief Editor: Robert A Egan, MD  more...
  • Print
Medication

Medication Summary

Medications are helpful only for symptomatic relief and should be used only for short periods. NSAIDs, whenever used, should be administered on a short-term regular basis and not prn.

Next:

Nonsteroidal anti-inflammatory agents (NSAIDS)

Class Summary

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase 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.

Ibuprofen (Motrin, Ibuprin)

DOC for mild to moderately severe pain; inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Aleve, Naprelan, Naprosyn)

For relief of mild to moderately severe pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis.

Previous
Next:

Muscle relaxant

Class Summary

These agents relieve muscle spasms.

Methocarbamol (Robaxin)

Reduces nerve impulse transmission from spinal cord to skeletal muscle.

Cyclobenzaprine (Flexeril)

Skeletal muscle relaxant that acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons. Structurally related to tricyclic antidepressants; therefore, has some of same limitations.

Previous
Next:

Benzodiazepines

Class Summary

By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.

Diazepam (Valium, Diastat)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Individualize dosage and increase cautiously to avoid adverse effects.

Previous
Next:

Neuromuscular Blocker Agent, Toxin

Class Summary

Used experimentally.

Botulinum toxin type A (BOTOX)

One of several toxins produced by Clostridium botulinum. Blocks neuromuscular transmission through a 3-step process, as follows: (1) blockade of neuromuscular transmission; botulinum toxin type A (BTA) binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. (2) BTA is internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. (3) BTA blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter.

The affected terminals are inhibited from stimulating muscle contraction. Toxin does not affect synthesis or storage of acetylcholine or conduction of electrical signals along the nerve fiber. Typically, a 24-72 h delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 mo. This purified neurotoxin complex is a vacuum-dried form of purified BTA, which contains 5 ng of neurotoxin complex protein per 100 U.

Treats excessive, abnormal contractions associated with blepharospasm. BTA has to be reconstituted with 2 mL of 0.9% sodium chloride diluent. With this solution, each 0.1 mL results in 5 U dose. Patient should receive 5-10 injections per visit. Must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative using manufacturer's instructions to provide injection volume of 0.1 mL; must be used within 4 h of storage in refrigerator at 2-8°C. Preconstituted dry powder must be stored in freezer at < 5°C.

Reexamine patient 7-14 d after initial dose to assess for response. Increase doses 2-fold over previous one for patients experiencing incomplete paralysis of target muscle. Do not exceed 25 U when giving it as single injection or 200 U as cumulative dose in 30-d period. For the purpose of TMD treatment, studies are limited and the medication is not approved. The dosing approach to specific muscles, such as they are known, is given in the article by Schwartz and Freund.

Previous