Update on the Pathology and Management of Benign Paroxysmal Positional Vertigo

Abstract

Objective: To describe the otopathology in benign paroxysmal positional vertigo (BPV) and report our experience with singular neurectomy (SN) over a 24-year period. Materials: (I) The temporal bones (TB) of 3 patients who demonstrated BPV before death were acquired and prepared for examination by light microscopy. (II) A clinical series of patients who underwent SN for chronic disabling BPV has been updated to December 1998. Results: (I) In each of the 3 TB representing the downmost ear in the Hallpike maneuver, two pathologic changes were observed: (1) scattered degenerative neurons were found in the facial nerve meatal ganglion (MG); (2) focal axonal degeneration of vestibular axons (2 TB) or degenerated ganglion cells (1 TB) were observed in the inferior vestibular division. (II) From 1974 to 1998, SN was performed unilaterally in 177 patients and bilaterally (sequential) in 10 patients (n = 197). The age, sex and etiologic factors in the series were consistent with the literature. In 189 patients (96%), BPV was completely relieved by SN, while 3 patients (1.5%) experienced partial relief and 5 patients (2.5%) failed to benefit from SN. Sensorineural hearing loss followed SN in 5 patients (2.5%). Conclusions: The focal degeneration in the inferior vestibular nerve or ganglion may result from reactivation of a latent neurotropic virus in inferior vestibular ganglion cells as a result of various stressors (upper respiratory infection, trauma, surgery, general anesthesia, pregnancy). The portal of entry of the virus is likely from the nose and oral cavity to the MG of the facial nerve where latency is assumed and spread to the vestibular ganglion develops. The series of 197 SN over a 24-year period demonstrates that SN is a safe, effective surgical maneuver to selectively ablate function of the posterior semicircular canal crista.