This study analyses the spontaneous electroencephalogram (EEG) brain activity of 14 children diagnosed with Autism Spectrum Disorder (ASD) compared to 18 children with normal development, aged 5–11 years. (i) Power Spectral Density (PSD), (ii) variability across trials (coefficient of variation: CV), and (iii) complexity (multiscale entropy: MSE) of the brain signal analysis were computed on the resting state EEG. PSD (0.5–45 Hz) and CV were averaged over different frequency bands (low-delta, delta, theta, alpha, low-beta, high-beta and gamma). MSE were calculated with a coarse-grained procedure on 67 time scales and divided into fine, medium and coarse scales. In addition, significant neurophysiological variables were correlated with behavioral performance data (Kaufman Brief Intelligence Test (KBIT) and Autism Spectrum Quotient (AQ)). Results show increased PSD fast frequency bands (high-beta and gamma), higher variability (CV) and lower complexity (MSE) in children with ASD when compared to typically developed children. These results suggest a more variable, less complex and, probably, less adaptive neural networks with less capacity to generate optimal responses in ASD children.

The present study showed a higher amplitude for the late N1 and the PINV with reference to both the prediction performed in auditory paradigms of higher abstraction and the unexpected breaking of the extracted rules. Additionally, both components were modulated depending on the local probability, which would suggest that they are continuously being updated by the previous stimulus history.

The auditory mismatch negativity (MMN) has been considered a preattentive index of auditory processing and/or a signature of prediction error computation. This study tries to demonstrate the presence of an MMN to deviant trials included in complex auditory stimuli sequences, and its possible relationship to predictive coding. Additionally, the transfer of information between trials is expected to be represented by stimulus-preceding negativity (SPN), which would possibly fit the predictive coding framework. To accomplish these objectives, the EEG of 31 subjects was recorded during an auditory paradigm in which trials composed of stimulus sequences with increasing or decreasing frequencies were intermingled with deviant trials presenting an unexpected ending. Our results showed the presence of an MMN in response to deviant trials. An SPN appeared during the intertrial interval and its amplitude was reduced in response to deviant trials. The presence of an MMN in complex sequences of sounds and the generation of an SPN component, with different amplitudes in deviant and standard trials, would support the predictive coding framework.

This study examines spontaneous activity in children aged 3-11 years with Specific Language Impairment (SLI) using electroencephalogram (EEG). We compared SLI diagnosed children with a normo-development group (ND). Signal complexity Multiscale Entropy (MSE) and parameterized Spectral Power Density (FOOOF) were analyzed, decomposing the PSD into its aperiodic (AP, proportional to 1/fx) and periodic (P) components. The results show increases in complexity across scales in both groups. Although topographic distributions were similar, children with SLI exhibited higher lateralized exponent parameter values in both hemispheres, along with an increased AP component over a broad frequency range (13–45 Hz) in medial regions. The P component shows differences in brain activity according to frequency and region. At 9–12 Hz, ND presents greater central-anterior activity, whereas in SLI, it is posterior-central. At 33–36 Hz, anterior activity is greater in SLI than in ND. At 37–45 Hz, SLI shows greater activity than ND, with a specific increase in the left, medial, and right regions at 41–45 Hz. These findings suggest alterations in the excitatory-inhibitory balance and impaired intra and interhemispheric connectivity, indicating difficulties in neuronal modulation possibly associated with the cognitive and linguistic characteristics of SLI.