Abstract OBJECTIVE: To analyze and model the effects of acoustic stimulus duration on cervical vestibular evoked myogenic potentials (cVEMPs). DESIGN: Subjects with normal hearing and no vestibular or cervical disorders were tested using 1 kHz tone bursts (TBs) of different durations to evoke cVEMPs from the ipsilateral sternocleidomastoid muscle. VEMP modeling was performed in Labview. RESULTS: The increase in TB duration initially resulted in a non-linear increase in cVEMP amplitude, followed by more complex cVEMP modifications that were mainly related to the appearance of a new wave (nX) that interfered with n23. With long TBs there were two distinct negative peaks with an identical threshold, suggesting a common vestibular nature. A two-level inhibition model qualitatively accounted for the two distinct negative peaks. However, good fitting of the cVEMP waveform required a multi-level model that included an excitatory phase after the inhibitory period. CONCLUSIONS: The two negative components (n23 and nX) observed in cVEMPs elicited by long TBs may result from the involvement of two different pathways with different dynamics or a single pathway with quick adaptation in the activity along the vestibulo-collic arc. Excitatory activity following the period of inhibition may represent rebound activity at the motor unit level.
Effects of acoustic stimulus duration on cervical vestibular evoked myogenic potentials: A neurophysiological and modeling study
MAURO, Alessandro;PRIANO, LORENZO
Last
2016-01-01
Abstract
Abstract OBJECTIVE: To analyze and model the effects of acoustic stimulus duration on cervical vestibular evoked myogenic potentials (cVEMPs). DESIGN: Subjects with normal hearing and no vestibular or cervical disorders were tested using 1 kHz tone bursts (TBs) of different durations to evoke cVEMPs from the ipsilateral sternocleidomastoid muscle. VEMP modeling was performed in Labview. RESULTS: The increase in TB duration initially resulted in a non-linear increase in cVEMP amplitude, followed by more complex cVEMP modifications that were mainly related to the appearance of a new wave (nX) that interfered with n23. With long TBs there were two distinct negative peaks with an identical threshold, suggesting a common vestibular nature. A two-level inhibition model qualitatively accounted for the two distinct negative peaks. However, good fitting of the cVEMP waveform required a multi-level model that included an excitatory phase after the inhibitory period. CONCLUSIONS: The two negative components (n23 and nX) observed in cVEMPs elicited by long TBs may result from the involvement of two different pathways with different dynamics or a single pathway with quick adaptation in the activity along the vestibulo-collic arc. Excitatory activity following the period of inhibition may represent rebound activity at the motor unit level.
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