The efficacy of auditory brainstem responses (ABRs), middle-latency responses (MLRs), and slow cortical potentials (SCPs) has been evaluated in 40 patients with multiple sclerosis (MS). ABRs and MLRs were averaged to clicks and SCPs to 1-kHz tone bursts of 70-dB nHL intensity. ABR, MLR, and SCP abnormalities were detected in 65.0, 42.5, and 30.0% of the sample, respectively. The combined sensitivity of ABRs and MLRs amounted to 80.0%, of ABRs and SCPs to 75.0%, and of MLRs and SCPs to 60.0%. The joint aptitude of all three responses equalled 87.5%. All three responses were capable to detect MS in seven of nine patients, failing to display neurological signs of brainstem lesion. The responses were also abnormal in three of five subjects with negative magnetic resonance imaging. It is concluded that the combined application of ABRs, MLRs, and SCPs promotes both detecting and confirming MS loci.

Auditory brainstem responses (ABRs), middle latency responses (MLRs), and slow cortical potentials (SCPs) were registered in normal-hearing adults to trains of low-frequency signals delivered binaurally on a background of a continuous masking noise. Two stimulus conditions, labelled as S0M0 and S pi M0 paradigms, respectively, were systematically compared. In the S0M0 paradigm, both the signals and the masker were in-phase at two ears. In the S pi M0 paradigm, the signals were out-of-phase at two ears, while the masker was in-phase. The psychoacoustic release from masking in S pi M0 vs. S0M0 paradigms was regularly accompanied by an increase in amplitudes and a shortening in peak latencies of the SCPs. In contrast, no differences were evidenced between the S0M0 and the S pi M0 paradigms with respect to the ABRs and the MLRs. Considering the generation loci of the studied electric responses, it is concluded that the binaural psychoacoustic phenomenon, referred to as the masking level difference, is operated primarily at the cortical level.

Auditory brainstem responses, middle-latency responses, and slow cortical potentials (ABRs, MLRs, SCPs) were recorded in 21 epileptic patients before and during treatment with carbamazepine (CBZ). The peak-latencies, interpeak intervals, and amplitudes were estimated and evaluated statistically. CBZ monotherapy resulted in prolongation of peak latencies of ABR waves I, III, and V as well as of interpeak intervals I-III and I-V. A significant increase in the peak-latencies of MLR components Na, Pa, and Nb and of interpeak intervals V-Pa and Na-Nb was also observed along with the systematic NaPa amplitude reduction. CBZ also prolonged the peak-latencies of SCP components P1 and N1. Based on the obtained results, we suggest that CBZ exerts suppressive influences both on modally specific (lemniscal) and modally nonspecific (extralemniscal) auditory structures.

ABR recordings were made on 31 normal-hearing subjects and 253 patients with sensorineural hearing loss (86 patients with unilateral hearing loss, 61 patients with asymmetrical hearing loss, 34 patients with symmetrical hearing loss, 55 patients with noise-induced hearing loss and 17 patients in the late chronic stage of Menière's disease). In the patient group with unilateral hearing loss, the mean interpeak interval (IPI) I-V was significantly shorter than in normal-hearing subjects. The interaural IPI differences provide a sharp criterion for early detection of acoustic neuroma. The calculation of the 95%-limits (means + 1.96 SD) showed that in patients with normal hearing or with unilateral or symmetrical hearing loss an interaural difference in the IPII-V greater than 0.2 ms has to be considered as an indication of a neuroma or any other brainstem abnormality. In patients with asymmetrical or with noise-induced hearing loss, the limit is 0.3 ms. In contrast to the frequently recommended interaural wave V latency difference criterion, the interaural IPI difference criterion requires no correction for audiogram differences.

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