Abstract

Botulinum neurotoxins (BoNTs) produce local chemo-denervation by cleaving soluble N-ethylmaleimide-sensitive factor activating protein receptor (SNARE) proteins. Botulinum neurotoxins are therapeutically indicated in several neurological disorders and have been in use for three decades. The long-term efficacy, safety, and side effects of BoNTs have been well documented in the literature. However, the development of muscle atrophy following chronic exposure to BoNTs has not received sufficient attention. Muscle atrophy is not only cosmetically distressing, but also has an impact on future injections. An extensive literature search was conducted on atrophy and mechanisms of atrophy. Five hundred and four relevant articles in the English language were reviewed. This review revealed the surprising lack of documentation of atrophy within the literature. In addition, as demonstrated in this review, the mechanisms and the clinical factors that may lead to atrophy have also been poorly studied. However, even with this limited information it is possible to indicate factors that could modify the clinical approach to botulinum toxin injections. This review highlights the need for further study of atrophy following BoNT injections.

Highlights

  • Botulinum neurotoxins (BoNTs) have been injected for medical and cosmetic indications since1977 [1]

  • A recent review by Durand and colleagues [23] addressed the issue of BoNT-induced muscle atrophy in human subjects, but they were unable to formulate any conclusions about the mechanisms of

  • A comprehensive overview of factors including toxin characteristics, neuromuscular junction (NMJ), and muscle properties, which contribute to muscle atrophy is presented, and suggestions for how these factors can be used by clinicians to modify their BoNT injections are provided

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Summary

Introduction

Botulinum neurotoxins (BoNTs) have been injected for medical and cosmetic indications since. As a result of local chemo-denervation, BoNTs impair neuromuscular transmission thereby reducing muscle contractility. This phenomenon translates into BoNTs being an effective treatment for a variety of movement disorders and other neurological and non-neurological conditions. The literature on BoNT-induced muscle atrophy as an adverse reaction of chronic, repeated injections is sparse, as this side effect was not documented. A recent review by Durand and colleagues [23] addressed the issue of BoNT-induced muscle atrophy in human subjects, but they were unable to formulate any conclusions about the mechanisms of. A comprehensive overview of factors including toxin characteristics, neuromuscular junction (NMJ), and muscle properties, which contribute to muscle atrophy is presented, and suggestions for how these factors can be used by clinicians to modify their BoNT injections are provided

Method
Influence of Toxin Serotype on Muscle Atrophy
Factors Influencing Muscle Re-Innervation after BoNT Induced Paralysis
Satellite Cells and Their Role in Toxin-Induced Atrophy
Mitochondrial Dysfunction Following Botulinum Toxin Injection
Muscle Spindles and Their Role in BoNT-Induced Atrophy
Impact of Muscle Blood Perfusion on Toxin-Induced Atrophy
10. Why Fat Deposition Occurs after BoNT Injection
11. Conclusions
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