Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective ...Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective and safe therapy for strabismus and focal dystonia. However, muscular weakness is temporary and after 3-4 months, muscle strength usually recovers because function- al recovery is mediated by nerve sprouting and reconstruction of the neuromuscular junction. Acrylamide may produce neurotoxic substances that cause retrograde necrotizing neuropathy and inhibit nerve sprouting caused by botulinum toxin type A. This study investigated whether acrylamide inhibits nerve sprouting after intramuscular injection of botulinum toxin type A. A tibial nerve sprouting model was established through local injection of botulinum toxin type A into the right gastrocnemius muscle of Sprague-Dawley rats. Following intramuscular injection, rats were given intraperitoneal injection of 3% acrylamide every 3 days for 21 days. Nerve sprout- ing appeared 2 weeks after intramuscular injection of botulinum toxin type A and single-fiber electromyography revealed abnormal conduction at the neuromuscular junction I week after intra- muscular injection of botulinum toxin type A. Following intraperitoneal injection of acrylamide, the peak muscle fiber density decreased. Electromyography jitter value were restored to normal levels 6 weeks after injection. This indicates that the maximal decrease in fiber density and the time at which functional conduction of neuromuscular junction was restored were delayed. Addition- ally, the increase in tibial nerve fibers was reduced. Acrylamide inhibits nerve sprouting caused by botulinum toxin type A and may be used to prolong the clinical dosage of botulinum toxin type A.展开更多
Background： Single-fiber electromyography （SFEMG） has been suggested as a quantitative method for supporting chronic partial denervation in amyotrophic lateral sclerosis （ALS） by the revised El Escorial criteria....Background： Single-fiber electromyography （SFEMG） has been suggested as a quantitative method for supporting chronic partial denervation in amyotrophic lateral sclerosis （ALS） by the revised El Escorial criteria. Although concentric needle （CN） electrodes have been used to assess jitter in myasthenia gravis patients and healthy controls, there are few reports using CN electrodes to assess motor unit instability and denervation in neurogenic diseases. The aim of this study was to determine whether quantitative changes in jitter and spike number using CN electrodes could be used for ALS studies. Methods： Twenty-seven healthy controls and 23 ALS patients were studied using both CN and single-fiber needle （SFN） electrodes on the extensor digitorum communis muscle with an SFEMG program. The SFN-jitter and SFN-fiber density data were measured using SFN electrodes. The CN-jitter and spike number were measured using CN electrodes. Results： The mean CN-j itter was significantly increased in ALS patients （47.3 ±17.0 μs） than in healthy controls （27.4 ± 3.3 las） （P 〈 0.001 ）. Besides, the mean spike number was significantly increased in ALS patients （2.5 ± 0.5） than in healthy controls （1.7 ± 0.3） （P 〈 0.001）. The sensitivity and specificity in the diagnosis of ALS were 82.6% and 92.6% for CN-jitter （cut-offvalue： 32 gs）, and 91.3% and 96.3% for the spike number （cut-off value： 2.0）, respectively. There was no significant difference between the SFN-jitter and CN-jitter in ALS patients; meanwhile, there was no significant difference between the SFN-jitter and CN-jitter in healthy controls. Conclusion： CN-jitter and spike number could be used to quantitatively evaluate changes due to denervation-reinnervation in ALS.展开更多
基金supported by TCM General Research Project of Zhejiang Province,No.2014ZA071Health General Research Project of Zhejiang Province,No.2014KYA106
文摘Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective and safe therapy for strabismus and focal dystonia. However, muscular weakness is temporary and after 3-4 months, muscle strength usually recovers because function- al recovery is mediated by nerve sprouting and reconstruction of the neuromuscular junction. Acrylamide may produce neurotoxic substances that cause retrograde necrotizing neuropathy and inhibit nerve sprouting caused by botulinum toxin type A. This study investigated whether acrylamide inhibits nerve sprouting after intramuscular injection of botulinum toxin type A. A tibial nerve sprouting model was established through local injection of botulinum toxin type A into the right gastrocnemius muscle of Sprague-Dawley rats. Following intramuscular injection, rats were given intraperitoneal injection of 3% acrylamide every 3 days for 21 days. Nerve sprout- ing appeared 2 weeks after intramuscular injection of botulinum toxin type A and single-fiber electromyography revealed abnormal conduction at the neuromuscular junction I week after intra- muscular injection of botulinum toxin type A. Following intraperitoneal injection of acrylamide, the peak muscle fiber density decreased. Electromyography jitter value were restored to normal levels 6 weeks after injection. This indicates that the maximal decrease in fiber density and the time at which functional conduction of neuromuscular junction was restored were delayed. Addition- ally, the increase in tibial nerve fibers was reduced. Acrylamide inhibits nerve sprouting caused by botulinum toxin type A and may be used to prolong the clinical dosage of botulinum toxin type A.
文摘Background： Single-fiber electromyography （SFEMG） has been suggested as a quantitative method for supporting chronic partial denervation in amyotrophic lateral sclerosis （ALS） by the revised El Escorial criteria. Although concentric needle （CN） electrodes have been used to assess jitter in myasthenia gravis patients and healthy controls, there are few reports using CN electrodes to assess motor unit instability and denervation in neurogenic diseases. The aim of this study was to determine whether quantitative changes in jitter and spike number using CN electrodes could be used for ALS studies. Methods： Twenty-seven healthy controls and 23 ALS patients were studied using both CN and single-fiber needle （SFN） electrodes on the extensor digitorum communis muscle with an SFEMG program. The SFN-jitter and SFN-fiber density data were measured using SFN electrodes. The CN-jitter and spike number were measured using CN electrodes. Results： The mean CN-j itter was significantly increased in ALS patients （47.3 ±17.0 μs） than in healthy controls （27.4 ± 3.3 las） （P 〈 0.001 ）. Besides, the mean spike number was significantly increased in ALS patients （2.5 ± 0.5） than in healthy controls （1.7 ± 0.3） （P 〈 0.001）. The sensitivity and specificity in the diagnosis of ALS were 82.6% and 92.6% for CN-jitter （cut-offvalue： 32 gs）, and 91.3% and 96.3% for the spike number （cut-off value： 2.0）, respectively. There was no significant difference between the SFN-jitter and CN-jitter in ALS patients; meanwhile, there was no significant difference between the SFN-jitter and CN-jitter in healthy controls. Conclusion： CN-jitter and spike number could be used to quantitatively evaluate changes due to denervation-reinnervation in ALS.
