Laryngeal Tremor Medication

Updated: Apr 06, 2021
  • Author: Thomas L Carroll, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Medication Summary

As previously stated, botulinum toxin A (BTA) is the mainstay of treatment for spasmodic dysphonia (SD) and has also been used to treat essential tremor of the voice (ETV), albeit with mixed results. [8, 18]

The benefits of propranolol, primidone, and methazolamide in the treatment of ETV are not known. Although propranolol and primidone have been used successfully against essential tremor, research has not yet indicated that they can effectively treat ETV. Methazolamide showed promising results in the treatment of laryngeal tremor when studied in a small, open trial, but these results were not supported in a subsequent placebo-controlled, blinded investigation of 9 patients by Busenbark et al. [15]


Beta-Blockers, Nonselective

Class Summary

These agents compete with beta-adrenergic agonists for available beta-receptor sites.

Propranolol (Inderal, InnoPran XL)

Propranolol is often the first choice for tremor control in essential tremor and can be used as adjunctive medical therapy.


Anticonvulsants, Other

Class Summary

These agents are used to manage severe muscle spasm.

Primidone (Mysoline)

The low-dose form of primidone is the traditional second choice for the treatment of essential tremor. It is also possibly effective as an adjunct in the treatment of prominent tremor.


Antiglaucoma, Carbonic Anhydrase Inhibitors

Class Summary

Methazolamide showed promising results in a small, open trial but not in a double-blind study. [15]

Methazolamide (Neptazane)

Methazolamide reduces aqueous humor formation by inhibiting the enzyme carbonic anhydrase, in this way decreasing intraocular pressure.


Neuromuscular Blockers, Botulinum Toxins

Class Summary

These agents block neuromuscular transmissions.

OnabotulinumtoxinA A (BOTOX)

OnabotulinumtoxinA A (BOTOX)

This is one of several toxins produced by Clostridium botulinum. It blocks neuromuscular transmission through a 3-step process.

Step 1

BOTOX® 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.

Step 2

BOTOX® 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.

Step 3

BOTOX® 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. The toxin does not affect the

synthesis or storage of acetylcholine or the conduction of electrical signals along the nerve fiber.

Typically, a 24- to 72-hour delay occurs between the administration of toxin and the onset of clinical effects, which terminate in 2-6 months. This purified neurotoxin complex is a vacuum-dried form of purified botulinum toxin A, which contains 5ng of neurotoxin complex protein per 100U. It treats excessive, abnormal contractions associated with blepharospasm.

BOTOX® must be reconstituted with 2mL of 0.9% sodium chloride diluent. With this solution, each 0.1 mL results in a 5-U dose. The patient should receive 5-10 injections per visit.

BOTOX® must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative, using the manufacturer's instructions, to provide an injection volume of 0.1mL. It must be used within 4 hours of storage in a refrigerator at 2-8°C. Preconstituted dry powder must be stored in a freezer at below 5°C.