Accurate vestibulo-ocular reflex (VOR) measurement requires control of extravestibular suppressive factors such as visual fixation. Although visual fixation is the dominant suppressor and has been extensively studied, the mechanisms underlying suppression from nonvisual factors of attention and auditory stimulation are less clear. It has been postulated that the nonvisual suppression of the VOR is the result of one of two mechanisms: (1) activation of auditory reception areas excites efferent pathways to the vestibular nuclei, thus inhibiting the VOR or (2) cortical modulation of the VOR results from directed attention, which implies a nonmodality-specific process. The purpose of this research was to determine if the VOR is affected by the intensity level and/or type of speech stimulus. A repeated measures design was used. The experiment was single-blinded. Participants included 17 adults (14 females, three males) between the ages of 18-34 years who reported normal oculomotor, vestibular, neurological, and musculoskeletal function. Each participant underwent slow harmonic acceleration testing in a rotational chair. VOR gain was assessed at 0.02, 0.08, and 0.32 Hz in quiet (baseline). VOR gain was also assessed at each frequency while a forward running speech stimulus (attentional) or a backward running speech stimulus (nonattentional) was presented binaurally via insert earphones at 42, 62, and 82 dBA. The order of the conditions was randomized across participants. VOR difference gain was calculated as VOR gain in the auditory condition minus baseline VOR gain. To evaluate auditory efferent function, the medial olivocochlear reflex (MOCR) was assayed using transient-evoked otoacoustic emissions (right ear) measured in the presence and absence of broadband noise (left ear). Contralateral acoustic reflex thresholds were also assessed using a broadband noise elicitor. A three-way repeated measures analysis of variance was conducted to evaluate the effect of frequency, intensity level, and speech type on VOR difference gain. Correlations were conducted to determine if difference gain was related to the strength of the MOCR and/or to the acoustic reflex threshold. The analysis of variance indicated that VOR difference gain was not significantly affected by the intensity level or the type of speech stimulus. Correlations indicated VOR difference gain was not significantly related to the strength of the MOCR or the acoustic reflex threshold. The results were in contrast to previous research examining the effect of auditory stimulation on VOR gain as auditory stimulation did not produce VOR suppression or enhancement for most of the participants. Methodological differences between the studies may explain the discrepant results. The removal of an acoustic target from space to attend to may have prevented suppression or enhancement of the VOR. Findings support the hypothesis that VOR gain may be affected by cortical modulation through directed attention rather than due to activation of efferent pathways to the vestibular nuclei.