The effects of experimental neurolysis on ectopic firing in a rat chronic constriction nerve injury model.
OBJECTIVE
We studied the effects of experimental neurolysis on ectopic firing in a rat chronic constriction nerve injury (CCI) model.


METHODS
Sixteen Wistar rats were used as CCI models; 8 in a neurolysis group and 8 in a sham operation group. Eight additional Wistar rats were used in a normal control group. The CCI model was created by loosely ligating the sciatic nerve with 4-0 chromic gut sutures. Seven days after surgery the same portion of the sciatic nerve, now embedded in scar tissue, was exposed. For the neurolysis group all sutures and scar tissue around the nerve were removed, and for the sham operation group only exposure of the sciatic nerve embedded in scar tissue was performed. Fourteen days after the first surgery the spinal cords of all animals in the 3 groups were transeated at the most rostral level of the spinal cord and ectopic firing was recorded antidromically from the sural nerve. The spontaneous ectopic firing frequency and the firing pattern at rest and the ectopic firing frequency under a hypoxic condition were analyzed.


RESULTS
The ectopic firing frequency in the neurolysis group was significantly lower than that of the sham operation group but higher than that of the normal control group. Also the appearance rate of an on-off pattern was 0% in the neurolysis and normal control groups and 38% in the sham operation group. Finally the accumulated number of ectopic firings under a hypoxic condition was significantly smaller in the neurolysis and normal control groups than that of the sham operation group.


CONCLUSIONS
Experimental neurolysis significantly improved the abnormal ectopic firing frequency and on-off firing pattern in the injured nerve of the CCI model. These findings may explain the efficacy of neurolysis on sensory symptoms such as numbness or spontaneous pain in chronic compression neuropathy.
Nakamura
Satoru
S
Department of Orthopedic Surgery, Asahikawa Medical College, Midorigaoka-Higashi, Asahikawa, Hokkaido, Japan.
Atsuta
Yuji
Y
D000818:Animals; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D009408:Nerve Compression Syndromes / Q000503:physiopathology*; D009431:Neural Conduction / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012584:Sciatic Nerve / Q000503:physiopathology / Q000601:surgery; D013497:Sural Nerve / Q000503:physiopathology