The medical term for the action of Botox is selective muscle denervation. Normally, to make a muscle contract, a nerve sends a signal to the muscle. The point where the nerve and the muscle meet is called the neuromuscular junction. When the signal gets to the neuromuscular junction a chemical called acetylcholine is released from the nerve side of the junction and binds to the muscle side of the junction causing more chemical reactions that make the muscle contract.
Botox® is available in a freeze-dried powder that clumps at the bottom of the vial. During reconstitution, the rubber seal on the vial should be wiped with an alcohol swab before using a 5 ml, 30-guage needle syringe to inject the desired volume of normal preservative-free saline.
Dentists have much expertise in the oral and maxillo facial areas. We are also trained to be experts in the muscles of mastication and the muscles of facial
expression which routinely receive these treatments.
There is no definite scheme, but currently, a follow-the-pain approach is used, i.e. if the patient's got his neuralgia in V3 right, you inject in the corresponding dermatome. There are few data on trigeminal neuropathy, and no real clues whether other neuropathic conditions may benefit (e.g. migraine with facial projection). According to newer data on the action of Botox in chronic migraine, binding to nociceptive c-fibers with subsequent transport to the CNS or meningeal nociceptors is presumed zo the mechanism of action, not relating to neuromuscular blockage.
Most practitioners recommend to avoid performing procedures at the site of allodynia as it will likely make it worse. If a patient is feeling pain in the V1 or 2 or 3, it would not be advisable to start injecting anything in that area which is why the "standard of care" advocates to perform procedures away from the pain (i.e. Gausserian, SPG or Stellate Blocks)
Dear Vinisha,
I have attached an article which I find interesting related to your query.
Review Article:
Role of Botulinum Toxin Type-A (BTX-A) in
the Management of Trigeminal Neuralgia
In an article that we published in Neurology some years ago we approach the pain with injections in the "way of pain". We usualy ask the patient to show, or even draw in the face, where was the pain traject, and we injected a low dose of toxin each 2 cm, subcutaneously. The result can be found in the article, and was very impressive. I still using this approach with very good results.
There is more and more agreement that botulinum toxin type A by axonal transport enters the CNS, motor but also sensory nuclei (Matak, I., Lacković, Z. 2014 Botulinum toxin A, brain and pain. Prog Neurobiol. 119-20, 39-59. Review). Our experinece on experimental animals (infraorbital nerve constrictioninjury) is that botulinum toxin is effective in reducing pain if applied in the painful region of the head as well as directly in trigeminal ganglia. Thus place of maximal pain or "way of pain" as Marcus Coletta describes should be beneficial.
BoNT/A is reducing neurotransmitters release from motoneurons and muscle afferent fibers (especially afferents III and IV for pain). This particularity easily explain why an injection at the pain location could be the best to relief pain. However, muscle paralysis associated with BoNT/A injection also induce changes in muscle/nerve/blood supply properties
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