Comparative Analysis of Cortical Auditory Evoked Potential in Cochlear Implant Users.

OBJECTIVES: The primary goal of the study was to investigate electrical cortical auditory evoked potentials (eCAEPs) at maximum comfortable level (MCL) and 50% MCL on three cochlear implant (CI) electrodes and compare them with the acoustic CAEP (aCAEPs), in terms of the amplitude and latency of the P1-N1-P2 complex. This was achieved by comparing the eCAEP obtained with the method described and stimulating single electrodes, via the fitting software spanning the cochlear array and the aCAEP obtained using the HEARLab system at four speech tokens. DESIGN: Twenty MED-EL (MED-EL Medical Electronics, Innsbruck, Austria) CI adult users were tested. CAEP recording with HEARLab System was performed with speech tokens /m/, /g/, /t/, and /s/ in free field, presented at 55 dB SPL. eCAEPs were recorded with an Evoked Potential device triggered from the MAX Programming Interface (MED-EL Medical Devices) with 70 msec electrical burst at 0.9 Hz at the apical (1), middle (6), and basal (10 or 11) CI electrode at their MCL and 50% MCL. RESULTS: CAEP responses were recorded in 100% of the test subjects for the speech token /t/, 95% for the speech tokens /g/ and /s/, and 90% for the speech token /m/. For eCAEP recordings, in all subjects, it was possible to identify N1 and P2 peaks when stimulating the apical and middle electrodes. This incidence of detection decreased to an 85% chance of stimulation at 50% MCL on the same electrodes. A P1 peak was less evident for all electrodes. There was an overall increase in latency for stimulation at 50% MCL compared with MCL. There was a significant difference in the amplitude of adjacent peaks (P1-N1 and N1-P2) for 50% MCL compared with MCL. The mean of the maximum cross-correlation values were in the range of 0.63 to 0.68 for the four speech tokens. The distribution of the calculated time shift, where the maximum of the cross-correlation was found, was distributed between the speech tokens. The speech token /g/ had the highest number of valid cross-correlations, while the speech token /s/ had the lowest number. CONCLUSIONS: This study successfully compared aCAEP and eCAEP in CI users. Both acoustic and electrical P1-N1-P2 recordings obtained were clear and reliable, with good correlation. Latency increased with decreasing stimulation level, while amplitude decreased. eCAEP is potentially a better option to verify speech detection at the cortical level because it (1) uses direct stimulation and therefore creates less interference and delay of the sound processor and (2) creates more flexibility with the recording setup and stimulation setting. As such, eCAEP is an alternative method for CI optimization.

Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to noise-induced hearing loss associated with plasma hyperhomocysteinemia.

Betaine-homocysteine S-methyltransferases (BHMTs) are methionine cycle enzymes that remethylate homocysteine; hence, their malfunction leads to hyperhomocysteinemia. Epidemiologic and experimental studies have revealed a correlation between hyperhomocysteinemia and hearing loss. Here, we have studied the expression of methionine cycle genes in the mouse cochlea and the impact of knocking out the Bhmt gene in the auditory receptor. We evaluated age-related changes in mouse hearing by recording auditory brainstem responses before and following exposure to noise. Also, we measured cochlear cytoarchitecture, gene expression by RNA-arrays and quantitative RT-PCR, and metabolite levels in liver and plasma by HPLC. Our results indicate that there is an age-dependent strain-specific expression of methionine cycle genes in the mouse cochlea and a further regulation during the response to noise damage. Loss of Bhmt did not cause an evident impact in the hearing acuity of young mice, but it produced higher threshold shifts and poorer recovery following noise challenge. Hearing loss was associated with increased cochlear injury, outer hair cell loss, altered expression of cochlear methionine cycle genes, and hyperhomocysteinemia. Our results suggest that BHMT plays a central role in the homeostasis of cochlear methionine metabolism and that Bhmt2 up-regulation could carry out a compensatory role in cochlear protection against noise injury in the absence of BHMT.-Partearroyo, T., Murillo-Cuesta, S., Vallecillo, N., Bermúdez-Muñoz, J. M., Rodríguez-de la Rosa, L., Mandruzzato, G., Celaya, A. M., Zeisel, S. H., Pajares, M. A., Varela-Moreiras, G., Varela-Nieto, I. Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to noise-induced hearing loss associated with plasma hyperhomocysteinemia.