Adler Michael, Pellett Sabine, Sharma Shashi K, Lebeda Frank J, Dembek Zygmunt F, Mahan Mark A
Neuroscience Department, Medical Toxicology Division, U.S. Army Medical Research Institute of Chemical Defense, 8350 Ricketts Point Rd., Aberdeen Proving Ground, MD 21010, USA.
Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Drive, Madison, WI 53706, USA.
Microorganisms. 2022 Apr 24;10(5):886. doi: 10.3390/microorganisms10050886.
Traumatic peripheral nerve injuries tend to be more common in younger, working age populations and can lead to long-lasting disability. Peripheral nerves have an impressive capacity to regenerate; however, successful recovery after injury depends on a number of factors including the mechanism and severity of the trauma, the distance from injury to the reinnervation target, connective tissue sheath integrity, and delay between injury and treatment. Even though modern surgical procedures have greatly improved the success rate, many peripheral nerve injuries still culminate in persistent neuropathic pain and incomplete functional recovery. Recent studies in animals suggest that botulinum neurotoxin A (BoNT/A) can accelerate nerve regeneration and improve functional recovery after injury to peripheral nerves. Possible mechanisms of BoNT/A action include activation or proliferation of support cells (Schwann cells, mast cells, and macrophages), increased angiogenesis, and improvement of blood flow to regenerating nerves.
创伤性周围神经损伤在年轻的工作年龄人群中往往更为常见,并可导致长期残疾。周围神经具有令人印象深刻的再生能力;然而,损伤后的成功恢复取决于多种因素,包括创伤的机制和严重程度、损伤部位与再支配靶点之间的距离、结缔组织鞘的完整性以及损伤与治疗之间的延迟。尽管现代外科手术已大大提高了成功率,但许多周围神经损伤仍最终导致持续性神经病理性疼痛和不完全的功能恢复。最近在动物身上的研究表明,肉毒杆菌神经毒素A(BoNT/A)可以加速神经再生,并改善周围神经损伤后的功能恢复。BoNT/A作用的可能机制包括支持细胞(雪旺细胞、肥大细胞和巨噬细胞)的激活或增殖、血管生成增加以及流向再生神经的血流量改善。