RESUMO
HYPOTHESIS: Anatomic differences may render the superior division of the vestibular nerve more susceptible to injury during vestibular neuritis. BACKGROUND: Neural degeneration has been identified in temporal bone studies of vestibular neuritis. Previous anatomic and physiologic studies of vestibular neuritis have demonstrated that the superior division of the vestibular nerve is preferentially affected, with sparing of the inferior division. A preliminary temporal bone study has implicated neural entrapment as a possible cause for this preferential injury. METHODS: Two independent unbiased observers performed histologic analysis of 184 temporal bones from our temporal bone library. Measurements of the medial, midpoint, and lateral portions of the superior vestibular, inferior vestibular, and the singular nerves and their bony channels lateral to the internal auditory canal were made. These measurements included the length and width of each bony channel and an estimated percent of each channel occupied by bony spicules at each location. RESULTS: The lengths of the bony channels of the singular nerve (0.598 mm) and the inferior vestibular nerve (0.277 mm) were significantly shorter than the average length of the superior vestibular channel (1.944 mm; p < 0.0001). The total percent of the channel occupied by bone at the midpoint was significantly greater for the superior vestibular (28%) compared with either the singular (0%) or the inferior vestibular channel (18%) (p < 0.0001). CONCLUSION: The lateral bony channel of the superior vestibular nerve is seven times longer than the inferior vestibular and more than three times longer than the singular channel. There are a larger percentage of bony spicules occupying the superior vestibular compared with the inferior vestibular or singular channels. In addition, the superior nerve passes through a longer area of severe narrowing compared with the inferior or singular nerves. This anatomic arrangement of a longer bony channel with more interspersed bony spicules could make the superior vestibular nerve more susceptible to entrapment and ischemia.
