The Atypical GAMMA Range EEG Is NOT Explained By Developmental Delay in Young Children with Autism Spectrum Disorder

Poster Presentation
Saturday, May 4, 2019: 11:30 AM-1:30 PM
Room: 710 (Palais des congres de Montreal)
T. M. Helminen1, S. Pihlajamaa1, S. Yrttiaho1, K. Eriksson2, J. M. Leppanen1 and A. Kylliainen1, (1)Tampere University, Tampere, Finland, (2)Tampere University and Tampere University Hospital, Tampere, Finland

It has been suggested that the cortical brain activity of children with autism spectrum disorder (ASD) would show an imbalance between excitation and inhibition, which is reflected in atypically high baseline gamma activity. The previous research have showed abnormalities in gamma band activity in children with ASD when compared with typically developing children. However, there are age-related changes in gamma band activity during the development, and the developmental level of children with ASD has been shown to correlate with abnormalities in gamma band activity. Thus, it is not clear, whether the abnormalities found in previous studies could be better explained by developmental delay than ASD.


This study aimed at investigating whether the baseline gamma band EEG is atypical in children with ASD, when compared with typically developing children, and with children with developmental delay without ASD. In addition, the aim was to investigate whether the level of autistic behaviour correlates with gamma band EEG.


Fifteen children with ASD (2.5–5.3 years, developmental age 1.2–4.2 years), 16 typically developing children (TD) matched with chronological age, and 14 children with developmental delay (DD) matched with developmental age, participated in the study. The baseline EEG was recorded when the children were watching a 3 minute video, where a person was calmly building a block tower. Only segments without movements or other distractions were analyzed, based on video analysis. The gamma band activity (24.4-44.0 Hz) was analyzed in central and parietal areas, which are least likely to be contaminated by of myogenic artefacts. The level of autistic behaviour was measured with ADOS-2 and ADI-R.


The split-plot ANOVA [Brain area (2) x Group (3)] on gamma activity showed a significant main effect of Group [F(2,42)=3.276, p=.048, 𝜂𝑝2=.135]. The gamma activity was significantly higher in ASD Group, when compared to TD (p=.029) or DD group (p=.036). The gamma activity between TD and DD groups did not differ. Activity was higher on parietal than on central areas [F(1,42)=5.709, p=.021, 𝜂𝑝2=.120], but there was no interaction between brain area and the Group. The correlation between gamma activity on central brain areas and ADOS-2 comparison scores in ASD group was marginal (rs = .487, p=.066). The more autistic symptoms the child exhibited in ADOS-2, the higher was the gamma activity. No significant correlations were found between gamma activity and ADI-R scores.


The present study supports previous studies by showing that the gamma band activity is higher in children with ASD than in typically developing children. Moreover, this finding seems to be specific to autistic psychopathology and not related to developmental delay per se, as according our results, the children with ASD showed higher gamma activity also when compared to children with developmental delay but without ASD. Some indications were found that the severity of autistic symptoms might be associated with gamma band activity. These findings suggest that the gamma band activity could be considered as one potential diagnostic marker for autism.