Objective: To evaluate the efficacy of direct current electrical fields and peripheral external electrical stimulation to promote regeneration of the transected rat sciatic nerve.
Method: Four groups were studied: three experimental groups and one control group. Cathod distal (CD) group; nerves were treated with 1.0 μA direct current with the cathode oriented distally to the lesion, anode distal (AD) group; nerves were treated with the anode oriented distally to the lesion, external stimulation (ES) group; nerves were treated with 3 mA, 60 Hz, galvanic current, using a ring electrode at ankle joint 3 times per day. No current was delivered in control group. Electrophysiologic and functional assessments were conducted at 3 weeks postoperatively.
Results: All experimental groups showed significantly higher electrophysiologic and functional improvement than the control group. However, there is no significant differece in improvement among experimental groups.
Conclusion: Both direct current electrical field and peripheral external electrical stimulation can effectively promote peripheral nerve regeneration.
Objective: To evaluate the changes of motor unit number estimation (MUNE) and the amplitude of compound muscle action potential (CMAP) according to severity of nerve injury in rat.
Method: The sciatic nerve was compressed with two different severity (mild, severe) in 20 rats each. MUNE was performed in gastrocnemius of rat using the Poisson statistics. MUNE and amplitude of CMAP were compared according to severity of injury at two and four weeks after injury.
Results: The MUNE and amplitude of CMAP were significantly diminished at two and four weeks after nerve injury in severely injured rat. Both values were also diminished at two weeks after injury in mildly injured rat. The amplitude of CMAP was slightly increased at four weeks after mild injury despite of further decrement of MUNE.
Conclusion: The MUNE and amplitude of CMAP changed differently according to severity of nerve injury in rat, which might represent different denervation and reinnervation process.
The peripheral nerves can restore their impaired function after injuries from trauma or surgery. The known factors affecting the recovery of damaged peripheral nerves include the severity of damage, nerve growth factor(NGF) from the damaged area and the concentrations of fibrinogen and thrombin. One of polypeptides, transforming growth factors beta(TGF-β) has been known to be related to inflammation and healing process of various wound. The TGF-β has to three subtypes, TGF-β1, TGF-β2 and TGF-β3. This study was performed to explore the effects of TGF-β subtypes on the recovery phase of damaged nerve. Sciatic nerves of rat were compressed 200 dyne/mm2. The latencies were measured by stimulation of proximal and distal portion of compression injury site and expression of TGF-β isoforms was studied in proximal and distal nerve of compression site and spinal cord by using avidin-biotin complex immunoperoxidase technique.
The latencies were increased at one week after nerve injury and then recovered progressively following 4 weeks. The latencies were restored to almost normal values at 4 weeks after nerve injury. TGF-β1 and TGF-β3 were expressed weakly at the cytoplasm of Schwann cell in the distal portion after 12 hours of injury. The values of TGF-β1 and TGF-β3 were increased at 3rd day after injury and lasted till the 4th week which was the end point of nerve regeneration. The changes of proximal portion were different from those of distal portion. TGF-β1 and TGF-β3 of proximal portion showed stronger positive reaction than that of distal portion and the reaction was peaked at 3rd day after injury. TGF-β subtypes were rarely present at neuronal cells and astrocytes in spinal cord from 12th hour to 3rd day after injury. The TGF-β subtypes were weakly appeared at the 1st week after injury and successively increased to 4th week at which the latencies were restored to almost normal value. The patterns of revelation of TGF-β subtypes showed that TGF-β1 was predominant at neuronal cell and TGF-β2 was at glial cells.
We suggest that TGF-β subtypes might be related to the regeneration process of nerve injuery.