Gamma oscillations are physiological phenomena that reflect perception and cognition, and involve parvalbumin-positive γ-aminobutyric acid-ergic interneuron function. The auditory steady-state response (ASSR) is the most robust index for gamma oscillations, and it is impaired in patients with neuropsychiatric disorders such as schizophrenia and autism. Although ASSR reduction is known to vary in terms of frequency and time, the neural mechanisms are poorly understood. We obtained high-density electrocorticography recordings from a wide area of the cortex in 8 patients with refractory epilepsy. In an ASSR paradigm, click sounds were presented at frequencies of 20, 30, 40, 60, 80, 120, and 160 Hz. We performed time-frequency analyses and analyzed intertrial coherence, event-related spectral perturbation, and high-gamma oscillations. We demonstrate that the ASSR is globally distributed among the temporal, parietal, and frontal cortices. The ASSR was composed of time-dependent neural subcircuits differing in frequency tuning. Importantly, the frequency tuning characteristics of the late-latency ASSR varied between the temporal/frontal and parietal cortex, suggestive of differentiation along parallel auditory pathways. This large-scale survey of the cortical ASSR could serve as a foundation for future studies of the ASSR in patients with neuropsychiatric disorders.

Neurofeedback through visual, auditory, or tactile sensations improves cognitive functions and alters the activities of daily living. However, some people, such as children and the elderly, have difficulty concentrating on neurofeedback for a long time. Constant stressless neurofeedback for a long time may be achieved with auditory neurofeedback using music. The primary purpose of this study was to clarify whether music-based auditory neurofeedback increases the power of the alpha wave in healthy subjects. During neurofeedback, white noise was superimposed on classical music, with the noise level inversely correlating with normalized alpha wave power. This was a single-blind, randomized control crossover trial in which 10 healthy subjects underwent, in an assigned order, normal and random feedback (NF and RF), either of which was at least 4 weeks long. Cognitive functions were evaluated before, between, and after each neurofeedback period. The secondary purpose was to assess neurofeedback-induced changes in cognitive functions. A crossover analysis showed that normalized alpha-power was significantly higher in NF than in RF; therefore, music-based auditory neurofeedback facilitated alpha wave induction. A composite category-based analysis of cognitive functions revealed greater improvements in short-term memory in subjects whose alpha-power increased in response to NF. The present study employed a long period of auditory alpha neurofeedback and achieved successful alpha wave induction and subsequent improvements in cognitive functions. Although this was a pilot study that validated a music-based alpha neurofeedback system for healthy subjects, the results obtained are encouraging for those with difficulty in concentrating on conventional alpha neurofeedback.Trial registration: 2018077NI, date of registration: 2018/11/27

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Auditory mismatch negativity (MMN) is an electrophysiological response to a deviation from regularity. This response is considered pivotal to understanding auditory processing, particularly in the pre-attentive phase. However, previous findings suggest that MMN is a product of N1 adaptation/enhancement, which reflects lower-order auditory processing. The separability of these two components remains unclear and is considered an important issue in the field of neuroscience. The aim of the present study was to spatiotemporally differentiate MMN from N1 adaptation using human electrocorticography (ECoG). Auditory evoked potentials under the classical oddball (OD) task as well as the many standards (MS) task were recorded in three patients with epilepsy whose lateral cortices were widely covered with high-density electrodes. Close observation identified an electrode at which N1 adaptation was temporally separated from MMN, whereas N1 adaptation was partially incorporated into MMN at other electrodes. Since N1 adaptation occurs in the N1 population, we spatially compared MMN with N1 obtained from the MS task instead of N1 adaptation. As a result, N1 was observed in a limited area around the Sylvian fissure adjacent to A1, whereas MMN was noted in wider areas, including the temporal, frontal, and parietal lobes. MMN was thus considered to be differentiated from N1 adaptation. The results suggest that MMN is not merely a product of the neural adaptation of N1 and instead represents higher-order processes in auditory deviance detection. These results will contribute to strengthening the foundation of future research in this field.