Abstract
Sound-induced vestibular-evoked myogenic potentials (VEMPs) can be used to investigate saccular function, measured from the tonically contracted sternocleidomastoid muscles (SCM) in response to loud sound stimuli. The aim of the present study was to assess VEMPs in patients with vestibular migraine and to determine whether saccular function is affected by the disease. Furthermore, tests such as tilts of subjective visual vertical (SVV) and caloric testing were conducted to test whether deficits in the various tests are associated with each other. The amplitude and latency of VEMPs were measured from the SCM in 63 patients with vestibular migraine (median age 47 years; range 24–70 years) and compared with those of 63 sex- and age-matched healthy controls (median age 46 years; range 17–73 years). Of the 63 patients with vestibular migraine, 43 (68%) had reduced EMG-corrected VEMP amplitudes compared to the controls. Thus, the mean of the p13–n23 amplitudes of the vestibular migraine patients were 1.22 (SE ±0.09) for the right and 1.21 (SE ±0.09) for the left side, whereas the averaged amplitudes of the 63 healthy controls showed a mean of 1.79 (SE ±0.09) on the right and of 1.76 (SE ±0.09) on the left. No difference was seen in the latencies and there was no correlation between VEMP amplitudes, tilts of SVV and caloric testing. Our data on patients with vestibular migraine indicate that the VEMP amplitudes are significantly and bilaterally reduced compared to those of controls. This electrophysiological finding suggests that both peripheral vestibular structures, such as the saccule, but also central vestibular structures are affected. Thus, beside the brainstem, structures in the inner ear also seem to contribute to vertigo in vestibular migraine.
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Acknowledgments
This study was supported by the Stiftung Rheinland-Pfalz für Innovation. We are grateful to thank Ms Benson for critically reading the manuscript.
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Baier, B., Stieber, N. & Dieterich, M. Vestibular-evoked myogenic potentials in vestibular migraine. J Neurol 256, 1447–1454 (2009). https://doi.org/10.1007/s00415-009-5132-4
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DOI: https://doi.org/10.1007/s00415-009-5132-4