Benign paroxysmal positioning vertigo (BPPV) is generally thought to be caused by canalolithiasis in the posterior semicircular canal, an organ that is innervated by the inferior vestibular nerve. We hypothesized that absent vestibular evoked myogenic potentials (VEMPs) would indicate involvement of the inferior vestibular nerve and that posterior semicircular canal—type BPPV could not develop after vestibular neurolabyrinthitis (VNL) in patients with absent VEMPs.
To find out if VEMPs could be helpful in evaluating involvement of the inferior vestibular nerve in acute VNL.
We reviewed the VEMP findings in 47 patients (34 men and 13 women) with acute VNL, 10 of whom had then developed posterior semicircular canal—type BPPV.
While p13-n23, the first positive-negative peak of the VEMP, was ipsilaterally present on stimulation of the unaffected side in all patients, it was absent on the affected side in 16 patients (34%). The absence or presence of p13-n23 was independent of the results of caloric tests, pure tone audiometry, and auditory brain-stem responses. Typical posterior semicircular canal BPPV developed in 10 of the 47 patients after the acute attack of VNL, always on the same side as the neurolabyrinthitis. The p13-n23 potentials were preserved on stimulation of the affected ear in all 10 patients with BPPV.
These results suggest that if VEMPs are absent from an ear that has suffered acute VNL, then posterior semicircular canal BPPV is unlikely to develop as a consequence of the VNL. The reason for this appears to be that the absence of VEMPs is due to involvement of the inferior vestibular nerve or involvement of the structures that it innervates.Arch Otolaryngol Head Neck Surg. 1996;122:845-848