Results of singular neurectomy in the posterior ampullary recess.

OBJECTIVE: To determine the effect on hearing and balance symptoms following singular neurectomy (SN) for benign paroxysmal positional vertigo (BPPV) in the ampullary recess of the posterior semicircular canal. RESEARCH DESIGN: The charts of 242 patients with chronic disabling BPPV who were treated with SN over a 29-year period (1972-2001) were reviewed. The results on relief of BPPV and hearing function were recorded. A subset of 16 patients where the posterior ampullary recess was entered to expose the SN is described in detail with regard to an effect on hearing and balance. RESULTS: A total of 252 SN were performed in 242 patients. Ten patients underwent bilateral SN sequentially; the remaining 232 patients had unilateral SN. The ages of the patients ranged from 21 to 86 years, with a mean at 57 years. The female:male ratio was 174:68. Complete relief of BPPV was achieved in 244 patients (96.8%), incomplete relief in 3 (1%), and no relief in 5 (2%). Sensorineural hearing loss (SNHL) occurred in 9 patients (3.7%). A subset of 16 patients in whom the ampullary recess was opened during SN ranged in age from 21 to 79 years, with a mean at 56 years. The female:male ratio was 12:4, with right and left sides divided almost equally. Relief of BPPV was achieved in all 16 patients with no loss of hearing function. Five patients complained of a fistula response postoperatively (31%). The fistula response resolved by 6 months postoperatively in all 5 patients. CONCLUSIONS: SN is effective in relief of BPPV with little risk of SNHL (3.7%). The risk of SNHL is not increased when the posterior ampullary recess must be entered in order to transect the singular nerve. A positive fistula response may be present temporarily in almost one third of these patients.

The three faces of vestibular ganglionitis.

We present temporal bone and clinical evidence that common syndromes of recurrent vertigo are caused by a viral infection of the vestibular ganglion. In the present series, histopathologic and radiologic changes in the vestibular ganglion and meatal ganglion were consistent with a viral inflammation of ganglion cells in cases of Meniere's disease, benign paroxysmal positional vertigo, and vestibular neuronitis. Clinical observations of multiple neuropathies involving cranial nerves V, VII, and VIII on the same side in patients with recurrent vertigo are best explained by a cranial polyganglionitis caused by a neurotrophic virus, which is reactivated by a stressful event later in life. The reactivation of the latent virus may manifest as one of the above vertigo syndromes, depending on the part of the vestibular ganglion that is inflamed, the type and strain of the virus, and host resistance.