The aim of the study was to investigate the possibility of using great auricular nerve - facial nerve (GAN-FN) coaptation in the correction of experimentally induced facial paralysis according to clinical, histological and histomorphometrical analysis in dogs. Five mongrel dogs of different age (range 2 to 6 years) and sex (2 male and 3 female) were the study material. Facial paralysis was induced by neurectomy at the side of the facial nerve trunk passing through the stylomastoid foramen. The great auricular nerve (GAN) was freed, neurectomized behind the furcations and transposed to the distal part of the neurectomized facial nerve trunk. Both nerve stumps were coapted by epiperineural sutures. All 5 dogs were kept under clinical control for 6 months. At the end of the observation period, each dog was anesthetized and the operated area exposed. Specimens were taken from the coapted area and about 1 cm proximal and distal of the coapted area. The remaining facial nerve stumps were repaired by nerve grafting and the animals were used for another study. The specimens were evaluated histologically and histomorphometrically with respect to axon counts, myelin area and nerve fiber diameter. Clinical signs of facial paralysis had improved, except in one dog, which had wound dehiscence. There were no significant differences between the proximal and distal parts of the coapted area with respect to axonal counts, nerve fiber diameter and myelin area. In conclusion, in facial paralysis, GAN-FN coaptation can be a good alternative treatment for intracranial facial nerve lesions that can not be treated and injuries located at a point after the nerve exits the stylomastoid foramen.

The aim of the study was to investigate the possibility of using great auricular nerve - facial nerve (GAN-FN) coaptation in the correction of experimentally induced facial paralysis according to clinical, histological and histomorphometrical analysis in dogs. Five mongrel dogs of different age (range 2 to 6 years) and sex (2 male and 3 female) were the study material. Facial paralysis was induced by neurectomy at the side of the facial nerve trunk passing through the stylomastoid foramen. The great auricular nerve (GAN) was freed, neurectomized behind the furcations and transposed to the distal part of the neurectomized facial nerve trunk. Both nerve stumps were coapted by epiperineural sutures. All 5 dogs were kept under clinical control for 6 months. At the end of the observation period, each dog was anesthetized and the operated area exposed. Specimens were taken from the coapted area and about 1 cm proximal and distal of the coapted area. The remaining facial nerve stumps were repaired by nerve grafting and the animals were used for another study. The specimens were evaluated histologically and histomorphometrically with respect to axon counts, myelin area and nerve fiber diameter. Clinical signs of facial paralysis had improved, except in one dog, which had wound dehiscence. There were no significant differences between the proximal and distal parts of the coapted area with respect to axonal counts, nerve fiber diameter and myelin area. In conclusion, in facial paralysis, GAN-FN coaptation can be a good alternative treatment for intracranial facial nerve lesions that can not be treated and injuries located at a point after the nerve exits the stylomastoid foramen.