Effect of white noise "masking" on vestibular evoked potentials recorded using different stimulus modalities.

Short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses (L-VsEPs) are initiated in the otolith organs (saccule and utricle). Some of the saccule afferents have been reported to respond not only to linear acceleration, but also to high intensity acoustic stimuli. If so, the L-VsEP recorded from the saccule (elicited with the stimulus orientated relative to the head so as to optimally activate the saccule, i.e. stimulus in the vertical plane, Z-VsEP) should be reduced during high intensity broad band noise (BBN) "masking". Conversely, the utricular afferents have been reported to be less auditory-sensitive. Therefore, an L-VsEP which is mainly utricular in origin (stimulus in the horizontal plane, X-VsEP) should be less affected by this noise "masking". This was investigated in rats by recording X-VsEPs and Z-VsEPs and angular VsEPs (A-VsEPs), originating in the lateral semi-circular canals, before, during and after exposure to short duration, high intensity (113 dB SPL) BBN. This intensity completely masked auditory nerve evoked responses. The Z-VsEP did appear to be slightly more affected by the noise "masking" than the X-VsEP, implying the presence of more auditory-sensitive elements in the saccule. The A-VsEP was also affected by the BBN. The overall effect was relatively small (on average, 10-25% depression of the first wave of the different VsEPs). The responses showed recovery 5 min later.     

Origins of the short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses

OBJECTIVE: To verify the vestibular origin of the short latency (t < 12.5 msec) vestibular evoked potentials (VsEPs) in response to linear acceleration impulses (L-VsEPs) and to differentiate between the contributions of the otolith organs and the semi-circular canals (SCCs) to their initiation. DESIGN AND METHODS: L-VsEPs (stimulus intensity, 3 g; rise time, 1.0 to 1.5 msec) were recorded in fat sand rats (Psammomys obesus) before and after unilateral labyrinthectomy, plugging of the SCCs in the remaining ear, and bilateral labyrinthectomy. Auditory nerve brainstem evoked responses (ABRs) and VsEPs to angular acceleration impulses (A-VsEPs) were also recorded. Wave amplitudes and latencies were statistically analyzed (MANOVA, repeated t-tests). RESULTS: In the intact animal, the linear VsEPs consisted of 5 to 6 waves, several mV in amplitude, with short latencies. The latency of the first wave was 2.0 msec. These waves were abolished after bilateral labyrinthectomy. Before and after plugging of the SCCs, linear acceleration VsEP wave latencies did not change, although amplitudes were slightly reduced. Similar results were obtained with respect to ABRs recorded from the same ear. Angular acceleration VsEPs were abolished after SCC plugging. CONCLUSIONS: These and other results confirm that the linear VsEPs are compound action potentials of the vestibular pathway, the first wave is the response of the vestibular nerve, and they are initiated mainly in the otolith organs.     

Correlations between psychophysical magnitude estimates and simultaneously obtained auditory nerve, brain stem and cortical responses to click stimuli in man.

Responses from the auditory nerve, brain stem auditory nuclei and cortex, as well as subjective responses to click stimuli at 10 intensities, were recorded simultaneously in the same human subjects. For various measures of the responses, the power-law exponents of their intensity functions were calculated, along with their statistical significances. The electrophysiological and psycho-physical functions were compared for similarity. On average, the exponents of the intensity functions of amplitudes of the auditory nerve and earlier brain stem responses were highly significant, showing similarity across subjects and similarity with the exponents of the subjective estimates. However, a closer examination proved this similarity to be superficial, since magnitude estimates showed an appreciable intersubject and intersession variability while the auditory nerve and brain stem responses were approximately constant. All other electric response measures either had exponents which were not significant or showed even poorer correlation with the subjective response. It is proposed that the type of electrical activity recorded in this study may not be the proper set of neural parameters which give rise to the loudness estimate.     

Contribution of changes in click rate and intensity on diagnosis of multiple sclerosis by brainstem auditory evoked potentials

Brainstem auditory evoked potentials (BAEPs) were recorded in 51 patients with different degrees of certainty with respect to multiple sclerosis (MS): Definite, probable and possible ( McAlpine et al. 1972). Click stimuli were presented at various intensities and rates which were thought to stress the auditory pathways. The main types of abnormal BAEP traces were the absence of some of the brainstem waves (in the presence of a normal audiogram), prolonged brainstem transmission time (BTT) and abnormal amplitude ratio. In the definite MS group, average BTT was prolonged and average amplitude ratio was more than two standard deviations greater than the corresponding parameter in the normal group. The stressful manoeuvres of increasing click repetition rate and lowering click intensity increased the degree of abnormality of BAEP traces. There was no case in which the response to standard click stimuli (75 dB HL, 10 or 20 per sec) showed a normal trace while increasing the stimulus repetition rate and/or decreasing intensity showed a pathological response. The pathophysiology of BAEP traces in MS is discussed.     

Changes in the auditory nerve brainstem evoked responses in a case of maple syrup urine disease

Maple syrup urine disease (MSUD) is a rare metabolic disease due to deficiency in the enzyme that breaks down branched chain amino acids. Lack of the enzyme causes accumulation of these amino acids and, if untreated, causes severe neurological damage. A case study of a 10-day old female infant, born after 40 weeks' gestation with a birthweight of 2740 g with MSUD hospitalized in the acute stage with respiratory failure and severe brain oedema is described. As part of the neurological evaluation, auditory nerve brainstem evoked response testing was conducted and revealed bilateral presence of the first wave from the auditory nerve, with no later brainstem waves. Over the course of days when her condition improved following dialysis treatment and a diet to reach balanced levels of branched chain amino acids, the later brainstem waves appeared on one side, and several weeks later they were also observed on the other side. The possible mechanisms of the reversibility of the appearance of brainstem waves in this case are discussed.     

Cochlear activation at low sound intensities by a fluid pathway

In order to assess the mechanisms responsible for cochlear activation at low sound intensities, a semi-circular canal was fenestrated in fat sand rats, and in other experiments a hole was made in the bone over the scala vestibuli of the first turn of the guinea-pig cochlea. Such holes, which expose the cochlear fluids to air, provide a sound pathway out of the cochlea which is of lower impedance than that through the round window. This should attenuate the pressure difference across the cochlear partition and thereby reduce the driving force for the base-to-apex traveling wave along the basilar membrane. The thresholds of the auditory nerve brainstem evoked responses (ABR) and of the cochlear microphonic potentials were not affected in the fenestration experiments. In addition, holes in the scala vestibuli of the first turn did not cause ABR threshold elevations. These results contribute further evidence that at low sound intensities the outer hair cells are probably not activated by a base-to-apex traveling wave along the basilar membrane. Instead it is possible that they are excited directly by the alternating condensation/rarefaction fluid pressures induced by the vibrations of the stapes footplate. The activated outer hair cells would then cause the localized basilar membrane movement.     

Functional impairment of the vestibular end organ resulting from impulse noise exposure

OBJECTIVES/HYPOTHESIS: To assess the effect of exposure t o impulse noise, known to cause damage tothe cochlea, on the vestibular part of the inner ear using short latency vestibular evoked potentials (VsEPs), which is a direct and objective test for evaluating the function of the vestibular end organs. STUDY DESIGN: Prospective animal study. METHODS: Sand rats (Psammomys obesus) underwent baseline measurements of VsEPs in response to linear and angular acceleration stimuli and measurement of the auditory nerve and brainstem evoked response (ABR). The animals were then exposed to 10 gunshots generating impulse noise at an intensity of approximately 160 dB sound pressure level (SPL). Repeat measurements of the evoked potentials were conducted 2 to 4 hours, 1 week, and 6 weeks after the exposure. The amplitude and latency of the first wave of VsEPs in response to linear and angular acceleration stimuli, reflecting the function of the otolith organs and semicircular canals respectively, were compared between baseline and post-exposure measurements, as were ABR thresholds. RESULTS: The amplitude of the first wave of the VsEPs in response to linear acceleration was significantly (P <.001) reduced and the latency significantly (P <.005) prolonged 2 to 4 hours after the exposure in comparison to baselinemeasurements. The latency prolongation persisted in follow-up measurements, whereas the amplitude showed partial recovery. The first wave of VsEPs in response to angular acceleration was unchanged long-term. ABR thresholds were elevated in the long-term by 60 dB. CONCLUSION: It seems that impulse noise not only damages the cochlea, but also causes clear functional impairment to the vestibular end organs, mainly the otolith organs.     

Susceptibility of young adult and old rats to noise-induced hearing loss

This study was designed to test whether old rats show signs of presbyacusis and whether they would be either similarly or more or less susceptible to noise-induced hearing loss than young adult rats. Old (24 months) and young adult (3-4 months) Wistar rats were exposed to a broad-band noise of 113 dB SPL for a duration of 1 h (producing temporary threshold shifts) or 3 days (12 h noise/12 h quiet; permanent shifts). Auditory brainstem response (ABR), distortion product otoacoustic emissions (DPOAEs) and transient evoked otoacoustic emissions (TEOAEs) were measured before and after exposure. At the initial recording (before exposure), old rats demonstrated a small mean ABR threshold elevation, a reduction in amplitude of wave I (WI), a shortening of WI latency and a prolongation of the interpeak interval between WI and WIV, as compared to the young rats. The old rats also demonstrated a small DPOAE amplitude reduction and a reduction of peak-to-peak amplitude in the TEOAE response 2 ms after stimulus, but no reduction in TEOAE energy content between 2 and 4 kHz. These are signs of presbyacusis in the old rats. The noise exposures caused elevations in ABR threshold and reductions in DPOAE amplitude and TEOAE energy content that were similar in both the old and young rats. Their recovery from the noise-induced loss was also similar. Thus, the results of this study show that old and young adult rats, at least when considering clinically relevant intensities and durations of noise exposure, are equally susceptible to the effects of the exposure.