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<p>Research suggests that ADHD is characterized by dominant Default-Mode Network (DMN) and diminished Task Positive Network (TPN) activity, which has been linked to detrimentally affecting attention and executive task-dependent functioning. Interventions targeting this DMN-TPN interplay may be clinically important in ameliorating ADHD symptoms. This hypothesis was explored using frequency and spatial domains of 33-channel EEG data as an index of the EEG-DMN. Specifically, tonic EEG power spectra measures and Low Resolution Brain Electromagnetic Tomography (LORETA) analysis during resting-state eyes-open and eyes-closed were examined in 54 ADHD patients versus 16 healthy-controls. Furthermore, the effects of a 12-week Mindfulness-Based Cognitive Therapy (MBCT) programme were observed in the same ADHD patient sample, with 30 patients randomly allocated to MBCT and 24 to wait-list control. Significantly reduced power across EEG spectra, and increased activation of the medial ventral prefrontal cortex (mvPFC) indexed via LORETA, was observed in ADHD patients compared to healthy controls. MBCT-related increase in β-power, and increased LORETA current density of the precuneus, was observed. These findings suggest the clinical utility of considering the basal brain state in ADHD within the wider perspective of cortical hypoactivity. MBCT-related elevated β-power viably connects to enhanced cortical alertness/activation and arousal of the DMN, conceivably aiding the more efficient regulation of the DMN-TPN interplay. Increased precuneus activation, a central region of the DMN, may reflect altered intrinsic baseline activity relevant to more adaptive regulation of DMN–TPN dynamics, associated with attentional control and executive processes. Further understanding of the EEG DMN-TPN dynamic within ADHD may present neural markers of inattention and executive functioning, further to elucidating a working mechanism of MBCT in its treatment.</p>

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Electrocortical Indices of Default Mode Network-Related Activity in ADHD and Modulation Through Mindfulness-Based Cognitive Therapy

  • 期刊论文

  • 发表日期：

    2026年6月26日

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  • Poppy L.A. Schoenberg,
  • Reza M. Zargar,
  • Sevket Hepark

摘要

Research suggests that ADHD is characterized by dominant Default-Mode Network (DMN) and diminished Task Positive Network (TPN) activity, which has been linked to detrimentally affecting attention and executive task-dependent functioning. Interventions targeting this DMN-TPN interplay may be clinically important in ameliorating ADHD symptoms. This hypothesis was explored using frequency and spatial domains of 33-channel EEG data as an index of the EEG-DMN. Specifically, tonic EEG power spectra measures and Low Resolution Brain Electromagnetic Tomography (LORETA) analysis during resting-state eyes-open and eyes-closed were examined in 54 ADHD patients versus 16 healthy-controls. Furthermore, the effects of a 12-week Mindfulness-Based Cognitive Therapy (MBCT) programme were observed in the same ADHD patient sample, with 30 patients randomly allocated to MBCT and 24 to wait-list control. Significantly reduced power across EEG spectra, and increased activation of the medial ventral prefrontal cortex (mvPFC) indexed via LORETA, was observed in ADHD patients compared to healthy controls. MBCT-related increase in β-power, and increased LORETA current density of the precuneus, was observed. These findings suggest the clinical utility of considering the basal brain state in ADHD within the wider perspective of cortical hypoactivity. MBCT-related elevated β-power viably connects to enhanced cortical alertness/activation and arousal of the DMN, conceivably aiding the more efficient regulation of the DMN-TPN interplay. Increased precuneus activation, a central region of the DMN, may reflect altered intrinsic baseline activity relevant to more adaptive regulation of DMN–TPN dynamics, associated with attentional control and executive processes. Further understanding of the EEG DMN-TPN dynamic within ADHD may present neural markers of inattention and executive functioning, further to elucidating a working mechanism of MBCT in its treatment.