Aerial hearing thresholds and detection of hearing loss in male California sea lions (Zalophus californianus) using auditory evoked potentials

Auditory evoked potential (AEP) measurements are useful for describing the variability of hearing among individuals in marine mammal populations, an important consideration in terms of basic biology and the design of noise mitigation criteria. In this study, hearing thresholds were measured for 16 male California sea lions at frequencies ranging from 0.5 to 32 kHz using the auditory steady state‐response (ASSR), a frequency‐specific AEP. Audiograms for most sea lions were grossly similar to previously reported psychophysical data in that hearing sensitivity increased with increasing frequency up to a steep reduction in sensitivity between 16 and 32 kHz. Average thresholds were not different from AEP thresholds previously reported for male and female California sea lions. Two sea lions from the current study exhibited abnormal audiograms: a 26‐yr‐old sea lion had impaired hearing with a high‐frequency hearing limit (HFHL) between 8 and 16 kHz, and an 8‐yr‐old sea lion displayed elevated thresholds across most tested frequencies. The auditory brainstem responses (ABRs) for these two individuals and an additional 26‐yr‐old sea lion were aberrant compared to those of other sea lions. Hearing loss may have fitness implications for sea lions that rely on sound during foraging and reproductive activities.     

Brain-stem auditory evoked potentials in the common marmoset (Callithrix jacchus)

Brain-stem auditory evoked potentials (BAEPs) were recorded in 10 common marmosets (Callithrix jacchus) to investigate the effects of recording electrode configurations, stimulus rate, and stimulus frequency on BAEP wave forms and peak latencies. Tone burst stimulations were used to evaluate the effects of pure tone on BAEP wave forms. Five positive peaks superimposed on positive and negative slow potentials were identified in the BAEP recorded at the linkage between the vertex and the dorsal base of the ear ipsilateral to a monaural stimulus. When the reference electrode was placed at the ipsilateral mastoid or the neck, the amplitudes of positive and negative slow potentials and the incidence of wave I increased. There were no significant changes in peak latencies of BAEP waves with changes in stimulus rate from 5 to 20/s. It was possible to record the BAEPs in response to tone burst stimulations at frequencies extending from 0.5 to 99 kHz. Wave I appeared apparently at high stimulus frequencies; while waves III to V, at low frequencies. Wave II was recorded at frequencies ranging from 0.5 to 99 kHz and comprised a superposition of 2 or 3 potentials.     

Logarithmic display of auditory evoked potentials

Auditory evoked potentials (AEP) can be simultaneously recorded on-line as a succession of 11 waves, through a single input channel of a mini-computer. Since the response waves differ widely in frequency, a computing routine has been developed to display the whole response pattern in a single picture. Based upon a non-linear samples reduction of the digitized response, this routine allows a logarithmic transformation of the time axis. The method improves the identification of the AEP components and provides an objective estimate of the central auditory pathway for both neurophysiological and neuroclinical studies.     

Brain-stem auditory evoked potentials and brain death

BAEP records were obtained from 30 brain-dead patients. Three BAEP patterns were observed: (1) no identifiable waves (73.34%), (2) an isolated bilateral wave I (16.66%) and (3) an isolated unilateral wave I (10%). When wave I was present, it was always significantly delayed. Significant augmentation of wave I amplitude was present bilaterally in one case and unilaterally in another. On the other hand, in serial records from 3 cases wave I latency tended to increase progressively until this component disappeared. During the same period. wave I amplitude fluctuations were observed. A significant negative correlation was found for wave I latency with heart rate and body temperature in 1 case. Two facts might explain the progressive delay and disappearance of wave I in brain-dead patients: a progressive hypoxic-ischaemic dysfunction of the cochlea and the eight nnerve plus hypothermia, often present in brain-dead patients. Then the incidence of wave I preservation reported by different authors in single BAEP records from brain-dead patients might depend on the moment at which the evoked potential study was done in relation to the onset of the clinical state. It is suggested that, although BAEPs provide an objective electrophysiological assessment of brain-stem function, essential for BD diagnosis, this technique could be of no value for this purpose when used in isolation.     

Temperature-dependent hysteresis in somatosensory and auditory evoked potentials

Fourteen adult patients undergoing open heart surgery under induced hypothermia had median nerve, short-latency somatosensory evoked potentials (SSEPs) recorded during cooling (from 36°C to 19°C) and subsequent rewarming. Similar data on another group of patients who had brain-stem auditory evoked potentials (BAEPs) were also analyzed. Hypothermia produced increased latencies of the major SSEP and BAEP components and the latencies returned to normal with subsequent warming. The temperature-latency relationship during the cooling phase was significantly different from that during the warming phase. For SSEP components the temperature-latency relationship was linear during cooling and curvilinear during warming, whereas for BAEP it was curvilinear both during cooling and warming. Furthermore, the regression curves were different during the two phases of temperature manipulation, particularly for temperatures below 30°C both for SSEP and BAEP components. At the onset of warming there was an initial exaggerated warming response on the evoked potential (EP) latencies and amplitude of the EP components. The temperature-latency regression curves were uniformly less steep during the warming phase compared to those during cooling. These findings suggest the existence of hysteresis in the relationship between temperature and EP latencies. The latencies at a given temperature below 30°C depend on whether that temperature is reached during cooling or during warming.     

Brainstem auditory evoked potentials in the rabbit.

Eight white New Zealand rabbits were submitted to auditory stimulation in order to obtain normative BAEP parameters. A monaural alternating 0.1 ms click stimulation at 20 Hz, 90 dB was used. Two series of 1000 responses were averaged (10 ms time-base, 160-3000 Hz band-pass) and highly reproducible peaks were obtained. Peaks P1, P2, P3, P4 were obtained in all ipsilateral recordings, whereas peak P5 was detectable in only 6 animals. In contralateral recordings P1 was absent and the following peaks were similar to those of ipsilateral recordings. Normative values of absolute and interpeak latencies, peak amplitudes and amplitude ratios were obtained. The procedure was repeated 24 hours after basal recordings and measures of test-retest variability were obtained.     

Physiology-based modeling of cortical auditory evoked potentials

Evoked potentials are the transient electrical responses caused by changes in the brain following stimuli. This work uses a physiology-based continuum model of neuronal activity in the human brain to calculate theoretical cortical auditory evoked potentials (CAEPs) from the model’s linearized response. These are fitted to experimental data, allowing the fitted parameters to be related to brain physiology. This approach yields excellent fits to CAEP data, which can then be compared to fits of EEG spectra. It is shown that the differences between resting eyes-open EEG and standard CAEPs can be explained by changes in the physiology of populations of neurons in corticothalamic pathways, with notable similarities to certain aspects of slow-wave sleep. This pilot study demonstrates the ability of our model-based fitting method to provide information on the underlying physiology of the brain that is not available using standard methods.     

Event-related auditory evoked potentials and multiple sclerosis

Long latency event-related auditory evoked potentials, particularly the P300 wave, constitute an objective electrophysiological index of cognitive function. For this reason, these potentials have been studied in a series of 101 patients with multiple sclerosis (MS), classified according to McAlpine's criteria into definite, probable and possible cases. The patients were also classified as depressed or non-depressed according to the DSM-III and Research Diagnostic Criteria. They were also subjected to a battery of psychometric tests.In the patient population the N200 and P300 latencies were increased, as were the P200 latencies, when compared with a control population. This electrophysiological pattern had previously been observed in other conditions characterised by subcortical lesions. Partial correlations (at constant disease duration) between the disability score and the cognitive deficit were found to be significant. Patients with an increased P300 latency had a greater disability and the P300 latency was significantly correlated with the duration of the illness.The N200 and P300 latencies were increased in depressed MS subjects, but this increase did not reach the level of significance. Depression was more frequent in the more severely handicapped patients. This suggests that the origin of the depression seen in multiple sclerosis is only partly organic, and that it is one of the factors contributing to the subcortical cognitive deficit in multiple sclerosis.Progressive forms of the disease exhibited the most profound cognitive deficit, and the most marked increase in P300 latency.     

Brainstem auditory evoked potentials (BAEPs), pathology of wave IV

In a group of 134 consecutive patients with brainstem symptomatology wave IV was bilaterally absent in 69%. Bilateral absence of this wave can be considered as a normal state. Only absence of wave IV on one side with its presence on the other side was appraised as pathologic. Asymmetries of the latency and amplitude could not be taken into consideration because of the lack of normative data for this wave. Computer tomography showed in our pathologic cases lesions in the pons, oblongata and cerebellum. The clinical semiology was extensive and multiform pointing in 84% to a pontine origin, in 16% to a lesion of the midbrain or oblongata. A possible lesion of the pons was in accordance with its functional anatomy as well as with the supposed origin of wave IV (superior olivar complex, lateral lemniscal nucleus). In 62% of cases the pathology of wave IV was present without impairment of auditory functions. The pathology of wave IV was considered as little sensitive and little specific.     

Diagnostic role of brain-stem auditory evoked potentials in neurobrucellosis

Evoked potential audiometry and brain-stem auditory evoked potentials were evaluated in 15 patients with systemic brucellosis in whom brucella meningitis was suspected clinically. In 8 patients cerebrospinal fluid (CSF) was abnormal with high brucella titre, and evoked potentials were abnormal in all of them. In 7 patients the CSF was normal and evoked potentials were also normal. Brain-stem auditory evoked potential abnormalities were categorised into 4 types: (1) abnormal wave I, (2) abnormal wave V, both irreversible, (3) prolonged I–III interpeak latencies, and (4) prolonged I–V interpeak latencies, both reversible. These findings are of important diagnostic value and correlate well with the clinical features, aetiopathogenesis and final outcome.     

Intensity dependence of auditory evoked potentials in behaving cats

The intensity dependence of auditory evoked potentials (AEPs) recorded epidurally over the primary (AI) and secondary (AII) areas of the auditory cortex was studied in behaving cats during wakefulness, sleep and anesthesia. Four kHz tones of 50, 60, 70, and 80 dB SPL, presented in random order every 2 ± 0.2 s by a bone conductor, elicited clear changes of the AEP amplitudes with increasing stimulus intensity, but individual components displayed different responses curves. AEP components from the AI region showed saturation of their amplitude with stimulus intensity (P13, P34) or no amplitude increase (N19), while amplitude and intensity were linearly related in the AII area. The intensity dependence of the first positive component (P12/P13) was consistently stronger for the AEP recorded from the AI than from the AII area, while later components exhibited no difference between AI and AII. During slow wave sleep, the intensity dependence of this first positive component increased in the two areas, while that of later components decreased. Pentobarbital anesthesia abolished almost all later components and depressed the intensity dependence of the first positive component both in the AI and AII area. These results indicate that (1) clear intensity dependence of AEP exists in the cat auditory cortex and (2) this intensity dependence, especially that of the first positive AEP component, shares functional similarities to the human augmenting/reducing phenomenon in the auditory modality concerning regional differences and sleep-waking cycle.     

Age-related changes in human middle latency auditory evoked potentials

We recorded middle latency auditory evoked potentials (MAEPs) in young (20–40 years) and elderly (60–80 years) subjects with normal hearing. The Pa component was prolonged in latency and markedly enhanced in amplitude in the elderly subjects. No changes were found in Na, or in the binaural interaction of the MAEP. Differences in Pa amplitude and latency were not due exclusively to changes in auditory thresholds, since they were not duplicated by changes in stimulus intensity, and persisted when MAEPs from selected young and old subjects were compared at similar SPL levels. The enhancement of Pa amplitude appears to reflect age-related central modifications in auditory processing.     

Stimulus-dependent oscillations and evoked potentials in chinchilla auditory cortex

Besides the intensity and frequency of an auditory stimulus, the length of time that precedes the stimulation is an important factor that determines the magnitude of early evoked neural responses in the auditory cortex. Here we used chinchillas to demonstrate that the length of the silent period before the presentation of an auditory stimulus is a critical factor that modifies late oscillatory responses in the auditory cortex. We used tetrodes to record local-field potential (LFP) signals from the left auditory cortex of ten animals while they were stimulated with clicks, tones or noise bursts delivered at different rates and intensity levels. We found that the incidence of oscillatory activity in the auditory cortex of anesthetized chinchillas is dependent on the period of silence before stimulation and on the intensity of the auditory stimulus. In 62.5% of the recordings sites we found stimulus-related oscillations at around 8-20 Hz. Stimulus-induced oscillations were largest and consistent when stimuli were preceded by 5 s of silence and they were absent when preceded by less than 500 ms of silence. These results demonstrate that the period of silence preceding the stimulus presentation and the stimulus intensity are critical factors for the presence of these oscillations.     

Age-dependent amplitude variation of brain-stem auditory evoked potentials

Normative amplitude values of brain-stem auditory evoked potential (BAEP) components are given for normally hearing subjects at 1, 10, 30, 50 and 70 years of age, with an intragroup age variation of only ±6 months. Under these circumstances amplitude standard deviations decreased to less than 20% of the mean values. In contrast with the reduced evolution of latency with age, BAEP amplitude (for components I–V) undergoes a greater oscillation during ontogeny. With the exception of component I, it increased markedly from 1 year to 10 years of age and decreased thereafter constantly up to 50 years, with a mean rate of 10 nV yearly. The decrease slowed down between 50 and 70 years. The amplitude differences between the subgroups are highly significant statistically (P < 0.01). Possible reasons for these changes are discussed.