Increased intra-participant variability in children with autistic spectrum disorders: evidence from single-trial analysis of evoked EEG.
paper
Cited
Public
- Authors
- Milne, Elizabeth
- Year
- 2011
- Journal
- Frontiers in psychology
- PMID
- 21716921
- DOI
- 10.3389/fpsyg.2011.00051
- PMCID
- PMC3110871
Intra-participant variability in clinical conditions such as autistic spectrum disorder (ASD) is an important indicator of pathophysiological processing. The data reported here illustrate that trial-by-trial variability can be reliably measured from EEG, and that intra-participant EEG variability is significantly greater in those with ASD than in neuro-typical matched controls. EEG recorded at the scalp is a linear mixture of activity arising from muscle artifacts and numerous concurrent brain processes. To minimize these additional sources of variability, EEG data were subjected to two different methods of spatial filtering. (i) The data were decomposed using infomax independent component analysis, a method of blind source separation which un-mixes the EEG signal into components with maximally independent time-courses, and (ii) a surface Laplacian transform was performed (current source density interpolation) in order to reduce the effects of volume conduction. Data are presented from 13 high functioning adolescents with ASD without co-morbid ADHD, and 12 neuro-typical age-, IQ-, and gender-matched controls. Comparison of variability between the ASD and neuro-typical groups indicated that intra-participant variability of P1 latency and P1 amplitude was greater in the participants with ASD, and inter-trial Ξ±-band phase coherence was lower in the participants with ASD. These data support the suggestion that individuals with ASD are less able to synchronize the activity of stimulus-related cell assemblies than neuro-typical individuals, and provide empirical evidence in support of theories of increased neural noise in ASD.
Current source density (CSD) and IC scalp maps. CSD maps (left panel) are plotted at the time when P1 amplitude was highest. The electrode selected for analysis is indicated by the black dot. IC scalp maps (right panel) are stationary, and therefore constant across the time-course. [(A) = TD, (B) = ASD].
Single-trial amplitude from the raw EEG, CSD interpolated data, and back-projected IC data. Each colored trace on the y-axis indicates amplitude across the time-course of a single-trial (red = +ve, blue = βve as shown on colormap). The blue trace below each figure is the average of the single-trials.
Estimates of variability averaged across group. [(A) (normalized)] measures of peak variability. The left graph shows mean variation in the amplitude of the P1 peak, the middle graph shows mean variation in the latency of the P1 peak, and the right graph shows the mean maximum ITPC between 100 and 170 ms. [(B) (normalized)] median absolute deviation in amplitude across trials at each time-point, averaged across participant groups. (C) ITPC at each time-point, averaged across participant groups. The black lines on the x-axis of plots (B) and (C) indicate time-points of group difference (p < 0.05). P1 amplitude is shown in plots (D) and (E). (D) P1 amplitude calculated from the ERP peak, and the SD of the single-trial P1 peaks. (E) P1 amplitude calculated as the median of the single-trial P1 peaks, and the median absolute deviation of the single-trial P1 peaks. Bars represent Β±1 SE.
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