Botulinum toxin A for patients with orofacial dystonia: prospective, observational, single-centre study

Ruiz-de-León-Hernández, Gonzalo; Díaz-Sánchez, Rosa-María; Torrés-Lagares, Daniel; Hernández-Pacheco, Esther; González-Martín, M.; Serrera-Figallo, María-Ángeles

doi:10.1016/j.ijom.2017.11.006

Cited by 5 publications

(2 citation statements)

References 16 publications

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“…BoNT injection is routinely administered using a fine-gauge needle (27-30G). As an adjunct, some physicians prefer to use EMG guidance to administer BoNT injections, thereby ensuring accurate muscle targeting, causing hyperactivity or hyperfunction [136,168,169]. As a precautionary measure, the patient was advised to avoid any strenuous activity or massage for up to two weeks after the injection.…”

Section: Preparation and Application Techniquesmentioning

confidence: 99%

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Mechanism and clinical use of botulinum neurotoxin in head and facial region

et al. 2023

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Food-borne botulism, derived from the Latin term "botulus," which means "sausage," was first described in the 18 th century. The term was used to define a fatal condition characterized by muscular paralysis resulting in respiratory arrest upon the consumption of raw sausages [1]. Botulinum neurotoxins (BoNTs), which cause botulism, are zinc-dependent metalloproteases produced by an anaerobic, spore-forming, Gram-positive bacterium, Clostridium botulinum, and are classified into seven serotypes (BoNT/A-G) based on their antigenic properties. Apart from the seven distinct BoNTs, an additional serotype has been reported; however, further validation is required for confirmation [2,3].Naturally produced BoNTs are non-covalently associated with one or several non-toxic neurotoxin-associated proteins (NAPs) and form high molecular weight (up to ~900kDa) progenitor toxin complexes (PTCs) at an acidic pH. The PTCs dissociate into BoNTs and NAPs at neutral or alkaline pH. NAPs play a vital role in protecting fragile BoNTs from the harsh environment of the gastrointestinal tract and in facilitating the passage of BoNTs through the intestinal epithelial barrier. BoNT is released from PTCs after absorption from the intestinal epithelial barrier. Free BoNTs are transported to neuromuscular junctions (NMJs) via general circulation, subsequently inhibiting acetylcholine exocytosis and resulting in flaccid paralysis [4]. BoNTs are potent toxins and are currently being extensively researched, not only for their lethality but also for their potential use in therapeutic interventions owing to their safety, efficacy, and long duration of action. BoNT/A and BoNT/B are widely used in clinical practice [5].In the early 19 th century, the first toxin of BoNT (BoNT/A) was identified. Immediately after its discovery, it was widely used for developing biological weapons, given its effects on the nervous system, and it was studied extensively during the Second World War. The therapeutic use of BoNT in the medical field began in the late 19 th century [6,7]. Human use of BoNT was first attempted to treat strabismus (crossed eyes) in 1977 by Scott [6]. Since then, many medical practitioners have used BoNT to treat eyelid twitching and muscle spasms [8]. BoNT/A has also been used to treat neurological J Prosthodont Res. 2023; **(**):

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Section: Preparation and Application Techniquesmentioning

confidence: 99%

“…The dosage varies depending on the severity of dystonia and the muscle affected. The average dose injected per site is 2.5-5 U, total average dose of injection used is 25 U [136].…”

Section: Orofacial Dystoniamentioning

confidence: 99%