Posttraumatic nerve repair continues to be a major challenge of restorative medicine. Although enormous progress has been made in surgical techniques over the past three decades, functional recovery after a severe lesion of a major nerve trunk is often incomplete and sometimes unsatisfactory. It is thus particularly important to investigate clinical protocols to enhance nerve regeneration after surgical nerve repair. The present article reviews literature on one possible rehabilitation approach for enhancing nerve recovery, namely phototherapy. The number of experimental studies that have reported on the promoting action of phototherapy on peripheral nerve regeneration, together with the few known side effects related to the use of this type of physical therapy, make it possible to suggest that the time for broader clinical trials has come.

Previous studies have shown that low-power laser biostimulation (lasertherapy) promotes posttraumatic nerve regeneration. The objective of the present study was to investigate the effects of postoperative lasertherapy on nerve regeneration after end-to-side neurorrhaphy, an innovative technique for peripheral nerve repair. After complete transection, the left median nerve was repaired by end-to-side neurorrhaphy on the ulnar "donor" nerve. The animals were then divided into four groups: one placebo group, and three laser-treated groups that received lasertherapy three times a week for 3 weeks starting from postoperative day 1. Three different types of laser emission were used: continuous (808 nm), pulsed (905 nm), and a combination of the two. Functional testing was carried out every 2 weeks after surgery by means of the grasping test. At the time of withdrawal 16 weeks postoperatively, muscle mass recovery was assessed by weighing the muscles innervated by the median nerve. Finally, the repaired nerves were withdrawn, embedded in resin and analyzed by light and electron microscopy. Results showed that laser biostimulation induces: (1) a statistically significant faster recovery of the lesioned function; (2) a statistically significant faster recovery of muscle mass; (3) a statistically significant faster myelination of the regenerated nerve fibers. From comparison of the three different types of laser emissions, it turned out that the best functional outcome was obtained by means of pulsed-continuous-combined laser biostimulation. Taken together, the results of the present study confirm previous experimental data on the effectiveness of lasertherapy for the promotion of peripheral nerve regeneration and suggest that early postoperative lasertherapy should be considered as a very promising physiotherapeutic tool for rehabilitation after end-to-side neurorrhaphy.

Data suggest that 660 nm LLLT with low (10 J/cm²) or moderate (60 J/cm²) energy densities is able to accelerate neuromuscular recovery after nerve crush injury in rats.

Neuromuscular recovery after peripheral nerve lesion depends on the regeneration of severed axons that re-establish their functional connection with the denervated muscle. The aim of this study was to determine the effects of electrical stimulation (ES) on the neuromuscular recovery after nerve crush injury in rats. Electrical stimulation was carried out on the tibialis anterior (TA) muscle after sciatic nerve crush injury in a rat model. Six ES sessions were administered every other day starting from day 3 postinjury until the end of the experiment (day 14). The sciatic functional index was calculated. Muscle excitability, neural cell adhesion molecule (N-CAM) expression, and muscle fiber cross-sectional area (CSA) were accessed from TA muscle. Regenerated sciatic nerves were analyzed by light and confocal microscopy. Both treated (crush+ES) and untreated (crush) groups had their muscle weight and CSA decreased compared with the normal group (P < 0.05). Electrical stimulation accentuated muscle fiber atrophy more in the crush+ES than in the crush group (P < 0.05). N-CAM expression increased in both crush and crush+ES groups compared with the normal group (P < 0.05). Regenerated nerves revealed no difference between the crush and crush+ES groups. Nevertheless, functional recovery at day 14 post-injury was significantly lower in crush+ES group compared with the crush group. In addition, the crush+ES group had chronaxie values significantly higher on days 7 and 13 compared with the crush group, which indicates a decrease in muscle excitability in the crush+ES animals. The results of this study do not support a benefit of the tested protocol of ES during the period of motor nerve recovery following injury.

Denervation causes muscle atrophy and incapacity in humans. Although electrical stimulation (ES) and stretching (St) are commonly used in rehabilitation, it is still unclear whether they stimulate or impair muscle recovery and reinnervation. The purpose of this study was to evaluate the effects of ES and St, alone and combined (ES + St), on the expression of genes that regulate muscle mass (MyoD, Runx1, atrogin-1, MuRF1 and myostatin), on muscle fibre cross-sectional area and excitability, and on the expression of the neural cell adhesion molecule (N-CAM) in denervated rat muscle. ES, St and ES + St reduced the accumulation of MyoD, atrogin-1 and MuRF1 and maintained Runx1 and myostatin expressions at normal levels in denervated muscles. None of the physical interventions prevented muscle fibre atrophy or N-CAM expression in denervated muscles. In conclusion, although ES, St and ES + St changed gene expression, they were insufficient to avoid muscle fibre atrophy due to denervation.

Denervation induces muscle fiber atrophy and changes in the gene expression rates of skeletal muscle. Electrical stimulation (ES) is a procedure generally used to treat denervated muscles in humans. This study evaluated the effect of ES based on chronaxie and rheobase on the expression of the myoD and atrogin-1 genes in denervated tibialis anterior (TA) muscle of Wistar rats. Five groups were examined: (1) denervated (D); (2) DϩES; (3) sham denervation; (4) normal (N); and (5) NϩES. Twenty muscle contractions were stimulated every 48 h using surface electrodes. After 28 days, ES significantly decreased the expression of myoD and atrogin-1 in DϩES compared to the D group. However, ES did not prevent muscle-fiber atrophy after denervation. Thus, ES based on chronaxie values and applied to denervated muscles using surface electrodes, as normally used in human rehabilitation, was able to reduce the myoD and atrogin-1 gene expressions, which are related to muscular growth and atrophy, respectively. The results of this study provide new information for the treatment of denervated skeletal muscle using surface ES.

The current study showed that LLLT increased MMPs activity, mainly MMP-9, and TNF-α protein level during the acute phase of nerve injury, modulating inflammation. Based on these results, it is recommended that LLLT should be started as soon as possible after peripheral nerve injury.

Stretching denervated muscle does not prevent atrophy, but it increases fibrosis via temporal modulation of TGF-β1/myostatin and MMP-9 cascades.