Ocular vestibular-evoked myogenic potentials (oVEMP) to skull taps in normal and dehiscent ears: mechanisms and markers of superior canal dehiscence.

The site of stimulus delivery modulates the waveforms of cervical- and ocular vestibular-evoked myogenic potentials (cVEMP and oVEMP) to skull taps in healthy controls. We examine the influence of stimulus location on the oVEMP waveforms of 18 patients (24 ears) with superior canal dehiscence (SCD) and compare these with the results of 16 healthy control subjects (32 ears). oVEMPs were recorded in response to taps delivered with a triggered tendon-hammer and a hand-held minishaker at three midline locations; the hairline (Fz), vertex (Cz) and occiput (Oz). In controls, Fz stimulation evoked a consistent oVEMP waveform with a negative peak (n1) at 9.5 ± 0.5 ms. In SCD, stimulation at Fz produced large oVEMP waveforms with delayed n1 peaks (tendon-hammer = 13.2 ± 1.0 ms and minitap = 11.5 ± 1.1 ms). Vertex taps produced diverse low-amplitude waveforms in controls with n1 peaks at 15.5 ± 1.2 and 13.2 ± 1.3 ms for tendon-hammer taps and minitaps, respectively; in SCD, they produced large amplitude oVEMP waveforms with n1 peaks at 12.9 ± 0.8 ms (tendon-hammer) and 12.1 ± 0.5 ms (minitap). Occiput stimulation evoked oVEMPs with similar n1 latencies in both groups (tendon-hammer = 11.3 ± 1.3 and 10.7 ± 0.8; minitap = 10.3 ± 0.9 and 11.1 ± 0.4 for control and SCD ears, respectively). Compared to reflex amplitudes, n1 peak latencies to Fz taps provided clearer separation between SCD and control ears. The distinctly different effects of Fz and vertex taps on the oVEMP waveforms may represent an additional non-osseous mechanism of stimulus transmission in SCD. For skull taps at Fz, a prolonged n1 latency is an indicator of SCD.