Theta EEG oscillatory activity and auditory change detection.

The mismatch negativity is an electrophysiological marker of auditory change detection in the event-related brain potential and has been proposed to reflect an automatic comparison process between an incoming stimulus and the representation of prior items in a sequence. There is evidence for two main functional subcomponents comprising the MMN, generated by temporal and frontal brain areas, respectively. Using data obtained in an MMN paradigm, we performed time-frequency analysis to reveal the changes in oscillatory neural activity in the theta band.

Functional neural dynamics underlying auditory event-related N1 and N1 suppression response.

Presenting tone triplets of identical stimuli preceded by silent intervals of 30 s produces a series of three N1 averaged event-related potentials (ERPs), the first being of greater amplitude (non-suppressed N1) than the second and third ones (suppressed N1). Maximal statistically independent components (ICs) of single-trial multi-electrode scalp EEG responses to triplets were obtained by ICA algorithm, and then each IC was searched for underlying brain structures by LORETA inverse solution, and for oscillatory contributions by time-frequency analysis. Non-suppressed N1 cortical mechanisms were broken down into five ICs, grouped in two time-windows (early-onset and late-onset) involving the participation of temporal, frontal and parietal structures, and sub-serving EEG oscillatory contributions of power enhancement and putative phase concentration of mainly theta, alpha and low beta bands.

Modulation of spectral power and of phase resetting of EEG contributes differentially to the generation of auditory event-related potentials.

Nowadays, the mechanisms involved in the genesis of event-related potentials (ERPs) are a matter of debate among neuroscientists. Specifically, the debate lies in whether ERPs arise due to the contribution of a fixed-polarity and fixed-latency superimposed neuronal activity to background electroencephalographic oscillations (evoked model) and/or due to a partial phase synchronization of the ongoing EEG (oscillatory model). The participation of the two mechanisms can be explored by the spectral power modulation and phase coherence of scalp EEG rhythms, respectively.