Hamilton, Ontario, Canada From the School of Biomedical Engineering, the Department of Psychiatry and Behavioural Neurosciences, and the Department of Surgery, Division of Plastic Surgery, McMaster University.
Plast Reconstr Surg. 2014 Nov;134(5):736e-745e. doi: 10.1097/PRS.0000000000000599.
Long-term muscle denervation leads to severe and irreversible atrophy coupled with loss of force and motor function. These factors contribute to poor functional recovery following delayed reinnervation. The authors' previous work demonstrated that temporarily suturing a sensory nerve to the distal motor stump (called sensory protection) significantly reduces muscle atrophy and improves function following reinnervation. The authors have also shown that 1 month of electrical stimulation of denervated muscle significantly improves function and reduces atrophy. In this study, the authors tested whether a combination of sensory protection and electrical stimulation would enhance functional recovery more than either treatment alone.
Rat gastrocnemius muscles were denervated by cutting the tibial nerve. The peroneal nerve was then sutured to the distal tibial stump following 3 months of treatment (i.e., electrical stimulation, sensory protection, or both). Three months after peroneal repair, functional and histologic measurements were taken.
All treatment groups had significantly higher muscle weight (p<0.05) and twitch force (p<0.001) compared with the untreated group (denervated), but fiber type composition did not differ between groups. Importantly, muscle weight and force were significantly greater in the combined treatment group (p<0.05) compared with stimulation or sensory protection alone. The combined treatment also produced motor unit counts significantly greater than sensory protection alone (p<0.05).
The combination treatment synergistically reduces atrophy and improves reinnervation and functional measures following delayed nerve repair, suggesting that these approaches work through different mechanisms. The authors' research supports the clinical use of both modalities together following peripheral nerve injury.
长期的肌肉失神经支配会导致严重且不可逆转的萎缩，同时伴有力量和运动功能丧失。这些因素导致延迟再神经支配后的功能恢复不良。作者之前的工作表明，暂时将感觉神经缝合到运动神经的远端残端（称为感觉保护）可显著减少再神经支配后的肌肉萎缩并改善功能。作者还表明，对失神经支配的肌肉进行 1 个月的电刺激可显著改善功能并减少萎缩。在这项研究中，作者测试了感觉保护和电刺激的联合应用是否比单独治疗更能增强功能恢复。
通过切断胫神经使大鼠腓肠肌失神经支配。然后，在治疗 3 个月后（即电刺激、感觉保护或两者结合），将腓神经缝合到胫骨残端的远端。在腓神经修复后 3 个月，进行功能和组织学测量。
与未治疗组（失神经支配）相比，所有治疗组的肌肉重量（p<0.05）和肌收缩力（p<0.001）均显著升高，但各组之间的纤维类型组成无差异。重要的是，与单独刺激或感觉保护相比，联合治疗组的肌肉重量和力量显著更大（p<0.05）。联合治疗还产生了比单独感觉保护更大的运动单位计数（p<0.05）。
联合治疗通过不同的机制协同减少失神经支配后的萎缩，并改善再神经支配和功能测量。作者的研究支持在周围神经损伤后同时使用这两种治疗方法的临床应用。
