An experimental model of an electrical injury to the peripheral nerve.

OBJECTIVE

Injury to the peripheral nerves is a common complication found in patients suffering from electrical burns. At present, there are many kinds of experimental models for electrical injury, but no report describes an animal-based experimental model for a relatively simple electrical injury to the peripheral nerves. We have designed and constructed a specific device to generate increasingly severe electrical shocks of a known voltage for the experiment. This device can simulate injuries of different degrees (minor, medium and severe) caused by shock to the right sciatic nerve of rats.

METHOD

Thirty Sprague-Dawley rats were randomly divided into Group I (3600 V, n=10), Group II (1000 V, n=10) and Group III (500 V, n=10). The voltage required for the electrical shock was generated by the above-mentioned device and was adjusted to deliver 3600, 1000 and 500 V, respectively. The specific voltage, as mentioned above, was delivered three times to the right sciatic nerve of the rats. The shock duration was set to last for 10 ms. The time interval between the shocks was 3 min. Three rats were randomly selected from each group to observe changes in the morphology, electric physiology of the nerve and their histology the first, second and fourth week after injury.

RESULTS

All rats survived the injuries. Leg function was partially impaired and swellings occurred on the injured extremity. However, by the second week after the injury the rats had recovered. Digit ulcers were observed by the fourth week after injury in Groups I and II. Neural electric physiology showed that the recovery rate of the neural conduction velocity (RNCV) disappeared in part or in whole immediately after the injury in experimental rats. RNCV recovered up to 65% in Group III and to 7% in Group II by the fourth week after injury, however, RNCV did not recover in Group I at all. Histology showed that blood vessel embolism occurred within the injured nerve. A large number of nerve fibres experienced Waller degeneration while the myelin sheath was vacuolated. The neural plate disintegrated largely by the first week after injury and the myelin sheath disintegrated into a loose structure by the second week after injury in Group I. Group II displayed a similar situation as Group I, wherein some nerve fibres experienced Waller degeneration and disintegration. Regenerative myelin appeared in some rats at about the fourth week after injury. The following changes were seen in Group III: The degree of neural injuries was different. The point of entry of the electric currents showed obvious Waller degeneration and disintegration of the myelin sheath, while some nerves showed a regenerated myelin sheath by the second week after injury. The morphology (such as quantity and diameter) of the injured myelin was basically normal by the fourth week after injury.

CONCLUSION

This device can produce controlled injuries to the sciatic nerve giving different degrees of severity (minor, medium and severe), by means of varying the electrical shock voltage and shock duration on the rats. It is a useful model for experimental studies of injuries to peripheral nerves.