The pathophysiology of compression injuries of the peripheral facial nerve

The buccolabial branches of guniea pig facial nerves were crushed to produce axonotmesis, Wallerian degeneration, and demyelination. The lesions were followed from 1 to 8 weeks by transmission electron microscopy, electrophysiological tests, and cytochemical staining methods for Na+ channels. The first week demonstrated the classic degenerative neural changes. At 2 weeks the axoplasmic side of the demyelinated axolemma demonstrated diffuse staining for Na+ channels at a distance of 1 micrometer. At 4 weeks multiple condensed areas of dense staining were noted along the demyelinated axolemma. These staining areas resemble in character and length a normal node of Ranvier and denote new Na+ channels. The internodal distance is shorter than for the normal facial nerve. At 6 weeks a thin layer of myelin covered the nerve fibers. At 8 weeks half of the nerves were normal sized and the myelin sheath was normal in width. Following nerve crushing, electrical activity is present for 24-48 hours in the axonotmetic distal stump. Then the axon becomes unresponsive to electrical stimulation. There is gradual resumption of electrical activity between 5 and 14 days. Normal conduction resumes by 8 weeks. This study provides ultrastructural and cytochemical evidence for nerve fiber reorganization, axolemmal plasticity and sodium channel production and redistribution following Wallerian degeneration and demyelination in axonotmesis. Resumption of electrical neural excitability is achieved by an increase in the density of sodium channels and reduction in the internodal distance as a means for impedence matching. Reduction of the cross sectional diameter of the regenerating axon facilitates electrical conduction.