Auditory Evoked Potentials Peak Research Articles

Differential effects of isoflurane on auditory and visually evoked potentials in the cat.

Evoked potentials can be used as an intraoperative monitoring measure in neurological surgery. Auditory evoked potentials (AEPs), or specifically brainstem auditory evoked responses (BAERs), are known for being minimally affected by anesthetics, while visually evoked potentials (VEPs) are presumed to be unreliable and easily affected by anesthetics. While many anesthesia trials or intraoperative recordings have provided evidence in support of these hypotheses, the comparisons were always made between AEPs and VEPs recorded sequentially, rather than recorded at the same time. Although the logistics of improving data comparability of AEPs and VEPs may be a challenge in clinical settings, it is much more approachable in animal models to measure AEPs and VEPs as simultaneously as possible. Five cats under dexmedetomidine sedation received five, 10-min blocks of isoflurane with varying concentrations while click-evoked AEPs and flash-evoked VEPs were recorded from subdermal electrodes. We found that, in terms of their waveforms, (1) short-latency AEPs (BAERs) were the least affected while middle-latency AEPs were dramatically altered by isoflurane, and (2) short-latency VEPs was less persistent than that of short-latency AEPs, while both middle- and long-latency VEPs were largely suppressed by isoflurane and, in some cases, completely diminished. In addition, the signal strength in all but the middle-latency AEPs was significantly suppressed by isoflurane. We identified multiple AEP or VEP peak components demonstrating suppressed amplitudes and/or changed latencies by isoflurane. Overall, we confirmed that both cat AEPs and VEPs are affected during isoflurane anesthesia, as in humans.

Ephrin A2 protein expression in the regeneration and plasticity of cochlear hair cells in chicken following kanamycin ototoxicity.

The results from this study showed that the thresholds of brainstem auditory-evoked potentials peak following 10 successive days of intramuscular injection of Roman chickens with kanamycin, starting 3 days after birth. Fluorescence immunohistochemistry analysis revealed few ganglion cells positively labeled for Ephrin A2 in the cochlea of experimental chickens from 2 days before until 7 days after the last kanamycin injection. The number of Ephrin A2-positive ganglion cell bodies was increased at 15 days after the last injection and was similar to that in normal chickens at 30 days following the cessation of kanamycin treatment. These experimental findings indicate that Ephrin A2 protein expression in the acoustic ganglia is synchronized with the connection damage and regeneration of cochlear hair cells after kanamycin exposure. Ephrin A2 may play an important role in the regeneration and plasticity of cochlear hair cells in the chick cochlea following kanamycin ototoxicity.

Does oxygen deficit to the cerebral blood flow caused by subdural hematoma and/or increased intracranial pressure affect the variations in auditory evoked potentials in white New Zealand rabbits?

The experiment entails surgically placing two subarachnoid bolts and a subdural balloon through the skull of white New Zealand rabbits. One bolt is used to raise the intracranial pressure (ICP) by continuously infusing lactated Ringer's solution (LRS) into the subarachnoid space to maintain the desired level of ICPs, and the second bolt is to monitor the ICP. A subdural balloon is inflated with a known volume of LRS to simulate a subdural hematoma condition. Using various levels of ICP and/or different sizes of balloons, auditory evoked potentials (AEPs) were recorded from a rabbit. The results indicate that a major correlation of changes in AEP peak latencies is due to mechanical forces of a mass (inflated balloon simulating a hematoma) on the brain matter rather than increased ICP. The AEP peak latencies are relatively insensitive to an increase in ICP without the simulated intracranial hematoma. This study provides evidence that oxygen deficit to the cerebral blood flow caused by deformation of certain parts of the brain could be identified using AEPs.

Plasticity in the adult human central auditory system: evidence from late-onset profound unilateral deafness

Experience-related changes in central nervous system (CNS) activity have been observed in the adult brain of many mammalian species, including humans. In humans, late-onset profound unilateral deafness creates an opportunity to study plasticity in the adult CNS consequent to monaural auditory deprivation. CNS activity was assessed by measuring long-latency auditory evoked potentials (AEPs) recorded from teens and adults with late-onset (post-childhood) profound unilateral deafness. Compared to monaurally stimulated normal-hearing subjects, the AEPs recorded from central electrode sites located over auditory cortical areas showed significant increases in inter-hemispheric waveform cross-correlation coefficients, and in inter-hemispheric AEP peak amplitude correlations. These increases provide evidence of substantial changes from the normal pattern of asymmetrical (contralateral>ipsilateral amplitude) and asynchronous (contralateral earlier than ipsilateral) central auditory system activation in the normal-hearing population to a much more symmetrical and synchronous activation in the unilaterally deaf. These cross-sectional analyses of AEP data recorded from the unilaterally deaf also suggest that the changes in cortical activity occur gradually and continue for at least 2 years after the onset of hearing loss. Analyses of peak amplitude correlations suggest that the increased inter-hemispheric symmetry may be a consequence of changes in the generators producing the N 1 (approximately 100 ms peak latency) potential. These experience-related changes in central auditory system activity following late-onset profound unilateral deafness thus provide evidence of the presence and the time course of auditory system plasticity in the adult brain.

Of Kittens and Kids: Altered Cortical Maturation following Profound Deafness and Cochlear Implant Use

Profoundly deaf children who use a cochlear implant (CI) provide a unique opportunity to investigate the effects of auditory sensory deprivation on the maturing human central nervous system. Previous results suggest that children fitted with a CI show evidence of altered auditory cortical maturation, based on evoked potentials. This altered maturation was characterized by both latency delays and morphological changes in the cortical auditory evoked potentials (AEPs). Based on prolonged P₁ latencies compared to age-matched normal-hearing (NH) peers, these data suggested a delayed maturation nearly equivalent to the period of deafness. However, rates of maturation for this AEP peak were essentially the same in NH and CI children. This suggests that, given enough time, the AEPs of CI children would assume the characteristic morphology found in older NH teens and NH adults. However, the data also indicated a substantial alteration of the typical set of obligatory P₁-N_1b-P₂ peaks, specifically related to the absence of the N₁ potential. Recent analyses of more extensive sets of longitudinal and cross-sectional data indicate that even after many years of implant use, the AEPs of CI users in their late teens remain very different from those of their NH peers. The P₁ peak latency remains prolonged and P₁ amplitude remains much larger in CI users than in age-matched NH teens. These findings suggested that age-related changes in the P₁ peak are completed by 12 years of age. In addition, the normal N_1b peak fails to emerge in virtually all of the CI children tested in our laboratory. A major new interpretation of the abnormal maturation of AEP waveforms in CI children is presented. It is based on direct evidence showing that a persistent immaturity of the superficial layer axons has persistent negative effects on the generation of the N_1b and, consequently, on the morphology of the AEPs. A comparison of scalp-recorded AEPs from implanted children with local field potentials measured from the cortical surface in deaf white kittens suggests the effects of deafness and CI use are similar across these mammalian species. For both species, a period of profound deafness followed by CI stimulation reveals a substantial immaturity in cortical activation even after a period of electrical stimulation by the CI.

Maturation of human central auditory system activity: evidence from multi-channel evoked potentials

Objective: The purpose of this study was to evaluate central auditory system maturation based on detailed data from multi-electrode recordings of long-latency auditory evoked potentials (AEPs). Methods: AEPs were measured at 30 scalp-electrode locations from 118 subjects between 5 and 20 years of age. Analyses focused on age-related latency and amplitude changes in the P 1, N 1b, P 2, and N 2 peaks of the AEPs generated by a brief train of clicks presented to the left ear. Results: Substantial and unexpected changes that extend well into adolescence were found for both the amplitude and latency of the AEP components. While the maturational changes in latency followed a pattern of gradual change, amplitude changes tended to be more abrupt and step-like. Age-related latency decreases were largest for the P 1 and N 1b peaks. In contrast, P 2 latency did not change significantly and the N 2 peak increased in latency as a function of age. Abrupt changes in P 1, P 1-N 1b, and N 2 peak amplitude (also RMS amplitude) were observed around age 10 at the lateral electrode locations C3 and C4, but not at the midline electrodes Cz and Fz. These changes in amplitude coincided with a sharp increase and plateau in AEP peak and RMS amplitude variability from 9 to 11 years of age. Conclusions: These analyses demonstrated that the observed pattern of AEP maturation depends on the scalp location at which the responses are recorded. The distinct maturational time courses observed for individual AEP peaks support a model of AEP generation in which activity originates from two or more at least partly independent central nervous system pathways. A striking parallel was observed between previously reported maturational changes in auditory cortex synaptic density and, in particular, the age-related changes in P 1 amplitude. The results indicate that some areas of the brain activated by sound stimulation have a maturational time course that extends into adolescence. Maturation of certain auditory processing skills such as speech recognition in noise also has a prolonged time course. This raises the possibility that the emergence of adult-like auditory processing skills may be governed by the same maturing neural processes that affect AEP latency and amplitude.

Auditory evoked brain potentials as a function of interstimulus interval in adults with Down's syndrome.

Auditory-evoked potentials (AEP) to repeated binaural tone pips of several interstimulus intervals (ISIs) greater than or equal to 1 s were recorded from the vertex of young adults with Down's syndrome (DS; trisomy 21) and normal young adults. The following results were obtained: (1) AEP amplitudes, as well as one latency measure, of both experimental groups increased with the lengthening of ISI. (2) AEP peak latencies of the DS group were longer than AEP peak latencies of the normal group for all the ISIs employed. (3) AEP amplitudes of the DS group tended to be larger than AEP amplitudes of the normal group. These findings are discussed in relationship to issues of attention.