When two pure tones of slightly different frequencies are delivered simultaneously to the two ears, is generated a beat whose frequency corresponds to the frequency difference between them. That beat is known as acoustic beat. If these two tones are presented one to each ear, they still produce the sensation of the same beat, although no physical combination of the tones occurs outside the auditory system. This phenomenon is called binaural beat. In the present study, we explored the potential contribution of binaural beats to the enhancement of specific electroencephalographic (EEG) bands, as previous studies suggest the potential usefulness of binaural beats as a brainwave entrainment tool. Additionally, we analyzed the effects of binaural-beat stimulation on two psychophysiological measures related to emotional arousal: heart rate and skin conductance. Beats of five different frequencies (4.53 Hz -theta-, 8.97 Hz -alpha-, 17.93 Hz -beta-, 34.49 Hz -gamma- or 57.3 Hz -upper-gamma) were presented binaurally and acoustically for epochs of 3 min (Beat epochs), preceded and followed by pink noise epochs of 90 s (Baseline and Post epochs, respectively). In each of these epochs, we analyzed the EEG spectral power, as well as calculated the heart rate and skin conductance response (SCR). For all the beat frequencies used for stimulation, no significant changes between Baseline and Beat epochs were observed within the corresponding EEG bands, neither with binaural or with acoustic beats. Additional analysis of spectral EEG topographies yielded negative results for the effect of binaural beats in the scalp distribution of EEG spectral power. In the psychophysiological measures, no changes in heart rate and skin conductance were observed for any of the beat frequencies presented. Our results do not support binaural-beat stimulation as a potential tool for the enhancement of EEG oscillatory activity, nor to induce changes in emotional arousal.

The results of this study indicate the effectiveness of Forbrain® in modifying the speech of its users. It is suggested that Forbrain® works as an altered auditory feedback device. It may hence be used as a clinical device in speech therapy clinics, yet further studies are warranted to test its usefulness in clinical groups.

The frequency-following response (FFR) is an auditory evoked potential (AEP) that follows the periodic characteristics of a sound. Despite being a widely studied biosignal in auditory neuroscience, the neural underpinnings of the FFR are still unclear. Traditionally, FFR was associated with subcortical activity, but recent evidence suggested cortical contributions which may be dependent on the stimulus frequency. We combined electroencephalography (EEG) with an inhibitory transcranial magnetic stimulation protocol, the continuous theta burst stimulation (cTBS), to disentangle the cortical contribution to the FFR elicited to stimuli of high and low frequency. We recorded FFR to the syllable /ba/ at two fundamental frequencies (Low: 113 Hz; High: 317 Hz) in healthy participants. FFR, cortical potentials, and auditory brainstem response (ABR) were recorded before and after real and sham cTBS in the right primary auditory cortex. Results showed that cTBS did not produce a significant change in the FFR recorded, in any of the frequencies. No effect was observed in the ABR and cortical potentials, despite the latter known contributions from the auditory cortex. Possible reasons behind the negative results include compensatory mechanisms from the non-targeted areas, intraindividual variability of the cTBS effectiveness, and the particular location of our target area, the primary auditory cortex.

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It is not known how Auditory‐Evoked Responses (AERs) comprising Middle Latency Responses (MLRs) and Long Latency Responses (LLRs) are modulated by stimulus intensity and inter‐stimulus interval (ISI) in an unpredictable auditory context. Further, intensity and ISI effects on MLR and LLR have never been assessed simultaneously in the same humans. To address this important question, thirty participants passively listened to a random sequence of auditory clicks of three possible intensities (65, 75, and 85 dB) at five possible ISI ranges (0.25 to 0.5 s, 0.5 to 1 s, 1 to 2 s, 2 to 4 s, 4 to 8 s) over four to seven one‐hour sessions while EEG was recorded. P0, Na, Pa, Nb, and Pb MLR peaks and N1 and P2 LLR peaks were measured. MLRs P0 (p = .005), Pa (p = .021), and Pb (p = <.001) were modulated by intensity, while only MLR Pb (p = <.001) was modulated by ISI. LLR N1 and P2 were modulated by both intensity and ISI (all p values < .001). Intensity and ISI interacted at Pb, N1, and P2 (all p values < .001), with greater intensity effects at longer ISIs and greater ISI effects at louder intensities. Together, these results provide a comprehensive picture of intensity and ISI effects on AER across the entire thalamocortical auditory pathway, while controlling for stimulus predictability. Moreover, they highlight P0 as the earliest MLR response sensitive to stimulus intensity and Pb (~50 ms) as the earliest cortical response coding for ISIs above 250 ms and showing an interdependence between intensity and ISI effects.