[Histopathological study of the recovery process in experimental facial nerve palsy induced by freezing].

The facial nerve has a specific anatomical feature in that it pursues a relatively long course through a bony canal, originating in the fundus of the internal auditory meatus, until emerging at the stylomastoid foramen. Facial nerve palsy, which is often observed clinically, exhibits a high recovery rate of facial movement. There is no consensus, however, as to the influence of the anatomical features of the facial nerve on the pathological evolution of the palsy. The purpose of this study is to investigate how histological alterations, following injury of the nerve, are influenced by the anatomical feature mentioned above. Mongolian gerbils, weighing 60 g-90 g, were used. Facial nerve palsy was induced by freezing the tympanic part of the facial nerve. Myringotomy was then performed using microscope. The middle ear space was frozen at -2 degrees C to -8 degrees C for 30 seconds through perforation with dimethylether liquid propane gas. Facial nerve palsy was confirmed by loss of the blink reflex and whisker movement. Specimens were removed from the tympanic part of the facial nerve, embedded in epon, and the sections were examined under light and electron microscopy. Out of 16 ears (13 animals) thus frozen, 15 (94%) exhibited complete facial palsy. Facial movement recovered within the 21-to 35-day period after freezing. At thirty-six hours after freezing, thin regenerating axons were seen in Schwann cell basal lamina scaffolds. Even on the seventh day after freezing, when connective tissue around the nerve trunk was thickest, regenerating axons continued to grow and did not degenerate.(ABSTRACT TRUNCATED AT 250 WORDS)