Neurofeedback in ADHD and insomnia: Vigilance stabilization through sleep spindles and circadian networks

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Abstract

Highlights

▽ ADHD is characterized by delayed circadian phase resulting in sleep onset insomnia. ▽ Circadian advancing treatments result in vigilance stabilization by activation of the locus coerulues. ▽ Neurofeedback results in increased sleep spindle density, which stabilizes vigilance via the locus coerulues. ▽ Future clinical trials in ADHD should consider using follow-up assessments as their primary endpoint.

In this review article an overview of the history and current status of neurofeedback for the treatment of ADHD and insomnia is provided. Recent insights suggest a central role of circadian phase delay, resulting in sleep onset insomnia (SOI) in a sub-group of ADHD patients. Chronobiological treatments, such as melatonin and early morning bright light, affect the suprachiasmatic nucleus. This nucleus has been shown to project to the noradrenergic locus coeruleus (LC) thereby explaining the vigilance stabilizing effects of such treatments in ADHD. It is hypothesized that both Sensori-Motor Rhythm (SMR) and Slow-Cortical Potential (SCP) neurofeedback impact on the sleep spindle circuitry resulting in increased sleep spindle density, normalization of SOI and thereby affect the noradrenergic LC, resulting in vigilance stabilization. After SOI is normalized, improvements on ADHD symptoms will occur with a delayed onset of effect. Therefore, clinical trials investigating new treatments in ADHD should include assessments at follow-up as their primary endpoint rather than assessments at outtake. Furthermore, an implication requiring further study is that neurofeedback could be stopped when SOI is normalized, which might result in fewer sessions.

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