Onabotulinumtoxin A is one of the seven antigenically distinct serotypes of botulinum neurotoxins (BoNT, A to G) making up the clostridial family. BoNT-A is available commercially in the United States (Botox®, Allergan, Irvine, CA, USA). BoNT-A is FDA approved for chronic migraine, cervical dystonia, axillary hyperhidrosis, adult upper limb spasticity, strabismus, and blepharospasm associated with dystonia.
The toxin affects the nervous system predominantly by inhibiting the release of neurotransmitters from nerve terminals. This occurs through a three-stage process that begins with binding to the target nerve terminal membrane and internalization, translocation, and finally, cleavage of a target protein that is involved in neurotransmitter release.
A number of studies have examined the effect of BoNT-A in TN. The majority of studies used 20–50 U injected into the trigger zones, although lower (5–9 U)[170,171] and higher doses (75 U) have been successfully used. Overall, more than 60% of patients reported an improvement of ≥50% in both pain frequency and intensity. The major events reported were transient facial paresis/asymmetry, edema, ptosis, dysesthesia, and chewing difficulties, but all were rare. A recent meta-analysis found a superior effect for BoNT-A versus placebo in terms of proportion of responders (risk ratio [RR] = 2.87). The effect is achieved less rapidly than by using pharmacotherapy and usually appears after 1–2 weeks. This would suggest to us that combined approaches may be indicated including early pharmacotherapeutic intervention for rapid control continued until the BoNT-A effect occurs. More research is needed, particularly to replicate existing studies so as to confirm efficacy and elucidate the minimum effective dose and the number and sites of injection points. Data so far suggest that BoNT-A may bea significant addition to the ways in which we manage TN.
Headache. 2021;61(6):817-837. © 2021 Blackwell Publishing