| Autor: |
Adler M; Neuroscience Department, Medical Toxicology Division, U.S. Army Medical Research Institute of Chemical Defense, 8350 Ricketts Point Rd., Aberdeen Proving Ground, MD 21010, USA., Pellett S; Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Drive, Madison, WI 53706, USA., Sharma SK; Division of Microbiology, Center for Food Safety and Applied Nutrition, Food and Drug Administration, College Park, MD 20740, USA., Lebeda FJ; Biotechnology, Protein Bioinformatics, Zanvyl Krieger School of Arts & Sciences, Johns Hopkins University, Advanced Academic Programs, 9601 Medical Center Drive, Rockville, MD 20850, USA., Dembek ZF; Department of Military and Emergency Medicine, Uniformed Services University of Health Sciences, 3154 Jones Bridge Rd., Bethesda, MD 20814, USA., Mahan MA; Department of Neurosurgery, Clinical Neurosciences, University of Utah, 175 N Medical Drive East, Salt Lake City, UT 84132, USA. |
| Abstrakt: |
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. |
