Mismatch Negativity and P300 in Children With Attention-Deficit/Hyperactivity Disorder (ADHD): A Comparative Event-Related Potential Study Using Healthy Siblings as Controls

TL;DR

This study found that children with ADHD have delayed and weaker brain responses to sounds compared to healthy siblings, suggesting differences in attention and cognitive processing.

Contribution

The study compares ERP components in ADHD children and healthy siblings, highlighting potential neurophysiological markers for ADHD.

Findings

ADHD children showed significantly prolonged MMN and P300 latencies compared to controls.

P300 amplitudes were significantly reduced in ADHD children at the Fz electrode site.

No correlation was found between ERP variables and ADHD behavioral severity scores.

Abstract

Aim and background: Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that involves attention, impulse control, and/or executive function difficulties. Knowledge of the neural bases underlying ADHD is essential for developing accurate diagnostic and treatment methods. This study assessed cognitive dysfunction in children with ADHD with respect to endophenotypic traits of event-related potentials (ERPs), specifically the mismatch negativity (MMN) and P300 components, and compared them to those of healthy siblings. These ERP components serve as neurophysiological markers of pre-attentive and attentive cognitive processes, respectively.

Materials and methods: This observational cross-sectional study was conducted at Lady Hardinge Medical College, New Delhi, India, from November 2016 to January 2021. The study group comprised 18 children diagnosed with ADHD, who were compared to 10 healthy siblings serving as controls. ERPs were recorded using the SCHWARZER TOPAS EMG neurophysiological system (Schwarzer GmbH, Munich, Germany), which was triggered via a PC running the stimulus delivery software during an oddball paradigm of auditory stimuli. Post hoc pairwise comparisons across different electrode locations were used to evaluate the MMN and P300 components relative to their delays and amplitudes. Independent t-tests were used to assess differences in MMN and P300 latency and amplitude between the groups, with Cohen's d calculated to assess effect size.

Results: Children with ADHD showed significantly prolonged latencies and reduced amplitudes in both the MMN and P300 components compared to their healthy controls. For example, MMN latency at Fz was 231.83±12.69 ms in the ADHD group and 196.60±11.53 ms in controls (P < 0.05), showing a strong effect size of 2.66, indicating a substantial difference between the two groups. In addition, there was a significant difference in the amplitude of P300 at the Fz site (µV) between ADHD children (4.28 ± 1.84) and controls (11.20 ± 3.29; p < 0.0001), with a large effect size of 2.98, favoring the control group. There were no correlations between Connors' ADHD Rating Scale subscores and any of the ERP variables.

Conclusion: These results indicate that children with ADHD demonstrate significant neurophysiological differences in MMN and P300 components compared to their healthy siblings. While ERPs show potential as objective and quantifiable markers of cognitive dysfunction in ADHD, their utility as standalone diagnostic indices remains limited, especially given this study's small sample size and absence of correlation with behavioral severity. Larger studies are needed to confirm and extend these findings before ERPs can be reliably used in clinical diagnostics for ADHD.

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