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Cervical and cortical somatosensory evoked potentials (SEP) following electrical stimulation of the median nerve and blink reflexes (BR) following electrical stimulation of the supraorbital nerve were recorded in 30 normal subjects aged 20-49 years. Subjects aged 40-49 had longer SEP latencies than subjects aged 20-39 years. A total of 29 slightly affected patients with multiple sclerosis (MS) aged 26-49 years, including four patients without clinical signs (suspected MS) and 19 patients with signs indicating only one lesion (possible MS) were examined by low-rate random-stimulated brain stem auditory (BAEP), checkerboard pattern-reversal visual evoked potentials (VEP), SEP and BR. Abnormal recordings by at least one of the examinations were found in all but three patients, and by all four tests in five patients. In patients with definite or probably MS, demonstration of clinically recognized or subclinical lesions was of minor diagnostic value, in contrast to the importance such findings had in patients with suspected or possible MS. Silent lesions were shown by at least one of the tests in the four suspected and in 13 of the possible MS patients, so these 17 patients could be transferred to a more certain diagnostic category. This reclassification was most often due to the BAEP recording. In patients with spinal signs, the combination of BAEP and VEP recording was sufficiently efficient. In patients with optic neuritis a combination of BAEP and SEP was preferred. No abnormal recordings were found in 15 normal subjects examined by all four tests.
Our previous studies found that electroacupuncture at the right Zhongzhu acupoint (TE3) can enhance auditory recovery in rats with noise-induced hearing loss. Here, we investigated the changes in auditory brainstem response (ABR) and long late latency (LLR) evoked potential to explain the mechanisms of electroacupuncture at TE3. The auditory evoked potentials were recorded, including ABR and LLR, at baseline and on day 3 (D3), D5, and D8 after baseline. The 2-Hz electroacupuncture at the right TE3 was applied on D3, D4, and D5 in the electroacupuncture group but not in the control group. In ABR, compared with the control group, the latency shift of waves I (0.298 ± 0.033 vs -0.045 ± 0.057 ms), III (0.718 ± 0.038 vs -0.163 ± 0.130 ms), and V (1.160 ± 0.082 vs -0.207 ± 0.138 ms) on D3 (all p < 0.01) and of wave V (0.616 ± 0.433 vs -0.352 ± 0.209 ms, p < 0.05) on D5 was greater in the electroacupuncture group than that in the control group. Moreover, the interpeak latency shift of I-III (0.420 ± 0.041 vs -0.118 ± 0.177 ms) and I-V (0.863 ± 0.088 vs -0.162 ± 0.156 ms) on D3 (both p < 0.05) and of III-V (0.342 ± 0.193 vs -0.190 ± 0.110 ms) and I-V (0.540 ± 0.352 vs -0.343 ± 0.184 ms) on D5 (both p < 0.05) was greater in the electroacupuncture group than that in the control group. In LLR, the latency shift of P0 was greater in the electroacupuncture group than in the control group on D3 (3.956 ± 2.975 vs -1.178 ± 1.358 ms, p < 0.01) and D5 (2.200 ± 1.889 vs -0.311 ± 1.078 ms, p < 0.05). These findings indicate that electroacupuncture at the right TE3 can modulate the neuroplasticity of the central auditory pathway, including the brain stem and the primary and secondary auditory cortex.
We investigated the effect of pulse duration (PD) and interphase-gap (IPG) on the electrically-evoked auditory brain stem response (EABR) and viiith nerve compound action potential (ECAP) of deafened guinea pigs in order to test the hypothesis that the extent of change in these neural responses is affected by the histological status of the auditory nerve. Fifteen guinea pigs were deafened by co-administration of kanamycin and furosemide. Animals were acutely implanted with an 8-band electrode array at 1, 4 or 12 weeks following deafening. EABR and ECAP input/output functions were recorded in response to charge balanced biphasic current pulses. We determined the change in current required to equalize; (i) the EABR amplitude when the duration of the current pulse was doubled (104-208 micros/phase); and (ii) the EABR and ECAP amplitudes when the IPG was increased from 8 to 58 micros using a 104 micros/phase current pulse. Following the completion of each experiment the cochleae were examined quantitatively for spiral ganglion neuron survival. As expected, the current level required to evoke an EABR with equal amplitude was lower when the animal was stimulated with current pulses of 208 compared with 104 micros/phase. Moreover, the current level required to evoke EABR/ECAPs with equal amplitude was lower when current pulses had an IPG of 58 versus 8 micros. Importantly, there was a reduction in the magnitude of this effect with greater neural loss; the reduced efficacy of changing both PD and IPG on these electrically-evoked potentials was statistically correlated with neural survival. These results may provide a tool for investigating the contribution of auditory nerve survival to clinical performance among cochlear implant subjects.
The medial nucleus of the trapezoid body (MNTB) is an important source of inhibition during the computation of sound location. It transmits fast and precisely timed action potentials at high frequencies; this requires an efficient calcium clearance mechanism, in which plasma membrane calcium ATPase 2 (PMCA2) is a key component. Deafwaddler (dfw2J ) mutant mice have a null mutation in PMCA2 causing deafness in homozygotes (dfw2J /dfw2J ) and high-frequency hearing loss in heterozygotes (+/dfw2J ). Despite the deafness phenotype, no significant differences in MNTB volume or cell number were observed in dfw2J homozygous mutants, suggesting that PMCA2 is not required for MNTB neuron survival. The MNTB tonotopic axis encodes high to low sound frequencies across the medial to lateral dimension. We discovered a cell size gradient along this axis: lateral neuronal somata are significantly larger than medially located somata. This size gradient is decreased in +/dfw2J and absent in dfw2J /dfw2J The lack of acoustically driven input suggests that sound-evoked activity is required for maintenance of the cell size gradient. This hypothesis was corroborated by selective elimination of auditory hair cell activity with either hair cell elimination in Pou4f3 DTR mice or inner ear tetrodotoxin (TTX) treatment. The change in soma size was reversible and recovered within 7 days of TTX treatment, suggesting that regulation of the gradient is dependent on synaptic activity and that these changes are plastic rather than permanent.NEW & NOTEWORTHY Neurons of the medial nucleus of the trapezoid body (MNTB) act as fast-spiking inhibitory interneurons within the auditory brain stem. The MNTB is topographically organized, with low sound frequencies encoded laterally and high frequencies medially. We discovered a cell size gradient along this axis: lateral neurons are larger than medial neurons. The absence of this gradient in deaf mice lacking plasma membrane calcium ATPase 2 suggests an activity-dependent, calcium-mediated mechanism that controls neuronal soma size.
Changes in central auditory processing due to aging in normal-hearing elderly patients, as well as age-related hearing loss, are often associated with difficulties in speech processing, especially in unfavorable acoustic environments. Speech processing depends on the perception of temporal and spectral features, and for this reason can be assessed by recordings of phase-locked neural activity when synchronized to transient and periodic sound stimuli frequency-following responses (FFRs). An electronic search of the PubMed and Web of Science databases was carried out in July 2019. Studies that evaluated the effects of age-related hearing loss on components of FFRs were included. Studies that were not in English, studies performed on animals, studies with cochlear implant users, literature reviews, letters to the editor, and case studies were excluded. Our search yielded 6 studies, each of which included 30 to 94 subjects aged between 18 and 80 years. Latency increases and significant amplitude reduction of the onset, offset, and sloop V/A components of FFRs were observed. Latency and amplitude impairment of the fundamental frequency, first formant, and high formants were related to peripheral sensorineural hearing loss in the elderly population. Conclusions: Temporal changes in FFR tracing were related to the aging process. Hearing loss also impacts the envelope fine structure, producing poorer speech comprehension in noisy environments. More research is needed to understand aspects related to hearing loss and cognitive aspects common to the elderly.
This paper describes audiologic, electrophysiologic, and medical test results for a now 10-year-old girl who has had 45 episodes of reversible, sudden sensorineural hearing loss over the last 8 years. Episodes have lasted from 6 to 72 hours and often have been accompanied by a mild illness. Acoustic immittance measures have been consistent with normal middle-ear function with the exception of absent ipsilateral and contralateral acoustic reflexes. Mechanically evoked perioral reflex activity was markedly asymmetric following lower lip stimulation. The asymmetry of R1 activation between right and left side lower lip inputs raises questions about the integrity of central connections within the brain stem, including internuncial pathways coursing between trigeminal sensory relay nuclei and the facial motor nucleus. An electrocochleographic evaluation revealed cochlear microphonic but absent or markedly abnormal whole nerve action potentials. Auditory brainstem responses (ABR) have been either absent or poorly formed and significantly delayed, regardless of hearing sensitivity. Middle and late auditory evoked potentials were essentially normal. Both transient-evoked and distortion-product otoacoustic emissions were present regardless of peripheral auditory sensitivity. All medical tests have been essentially normal. Although no definitive diagnosis has been reached, beta blockers have been used with some success. Taken together, these data document a very unusual case of fluctuating hearing loss. The electrocochleographic and otoacoustic emission data suggest that the outer hair cells are functioning normally and that the loss is not cochlear in origin.(ABSTRACT TRUNCATED AT 250 WORDS)
Polymorphisms in the δ-aminolevulinic acid dehydratase (ALAD) and the vitamin D receptor (VDR) genes may modify lead metabolism and neurotoxicity. Two cohorts of children were examined for hearing [pure-tone audiometry (PTA), brain stem auditory evoked potentials (BAEP)], acoustic otoemission (transient emission evoked by a click) and blood-lead concentrations (B-Pb). The children were genotyped for polymorphisms in ALAD and VDR. The median B-Pbs were 55 and 36μg/L in the two cohorts (merged cohort 45μg/L). B-Pb was significantly associated with impaired hearing when tested with PTA (correlation coefficient rS=0.12; P<0.01), BAEP (rS=0.18; P<0.001) and otoemission (rS=-0.24; P<0.001). VDR significantly modified the lead-induced effects on PTA. Carriers of the VDR alleles BsmI B, VDR TaqI t and VDR FokI F showed greater toxic effects on PTA, compared to BsmI bb, VDR TaqI TT and VDR FokI ff carriers. No significant interaction was found for ALAD. Lead impairs hearing functions in the route from the cochlea to the brain stem at low-level exposure, and polymorphisms in VDR significantly modify these effects.
Sense of presence has been often explored in the context of virtual reality (VR) and immersive visual technologies; however, standardized and objective measures of the sense of presence have been difficult to find. Studies attempting to find physiological correlates of sense presence using electroencephalography (EEG) have reported mixed results. In the present study, we used brain event-related potentials (ERPs) elicited by auditory stimuli to identify an objective physiological index of sense of presence during VR, attempting to replicate the findings of previous studies and explain the heterogeneity of results reported in the literature. Participants in our experiment were asked to experience an immersive virtual environment using a modern head-mounted display while passively hearing task-irrelevant frequent standard and infrequent deviant tones as in a classic auditory oddball paradigm. Subsequently, they were asked to complete a battery of questionnaires aimed to estimate their sense of presence during the VR. EEG and questionnaire data from three-seventh participants were analyzed. ERP components evoked by the auditory stimuli were then analyzed. Late ERP components (after 450 ms from stimulus onset) registered over central brain areas were associated with the sense of presence as measured with questionnaires, while earlier components were not associated with presence. The use of different questionnaires and the content of the VR environment may both be a plausible explanation for heterogeneous results as reported in previous studies. The present study showed that late ERP components recorded over the central brain may represent good electrophysiological correlates of the subjective sense of presence.
Progressive sensorineural hearing loss is the most common form of acquired hearing impairment in the human population. It is also highly prevalent in inbred strains of mice, providing an experimental avenue to systematically map genetic risk factors and to dissect the molecular pathways that orchestrate hearing in peripheral sensory hair cells. Therefore, we ascertained hearing function in the inbred long sleep (ILS) and inbred short sleep (ISS) strains. Using auditory-evoked brain stem response (ABR) and distortion product otoacoustic emission (DPOAE) measurements, we found that ISS mice developed a high-frequency hearing loss at twelve weeks of age that progressed to lower frequencies by 26 weeks of age in the presence of normal endocochlear potentials and unremarkable inner ear histology. ILS mice exhibited milder hearing loss, showing elevated thresholds and reduced DPOAEs at the higher frequencies by 26 weeks of age. To map the genetic variants that underlie this hearing loss we computed ABR thresholds of 63 recombinant inbred stains derived from the ISS and ILS founder strains. A single locus was linked to markers associated with ISS alleles on chromosome 10 with a highly significant logarithm of odds (LOD) score of 15.8. The 2-LOD confidence interval spans approximately 4 Megabases located at position 54-60 Mb. This locus, termed sensorineural hearing loss 1 (Snhl1), accounts for approximately 82% of the phenotypic variation. In summary, this study identifies a novel hearing loss locus on chromosome 10 and attests to the prevalence and genetic heterogeneity of progressive hearing loss in common mouse strains.
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