sleep-onset insomnia
Research Papers
Neurofeedback in ADHD and insomnia: Vigilance stabilization through sleep spindles and circadian networks
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.
View Full Paper →Neuroflexibility and Sleep Onset Insomnia Among College Students: Implications for Neurotherapy
This study was designed to assess a neuroflexibility model of sleep onset insomnia among college students. Neuroflexibility refers to the ability to adjust cortical activation consistent with environmental demands. It was anticipated that good sleepers would demonstrate better feedback contingent alpha control, defined as the ability to both enhance alpha and suppress alpha, than poor sleepers. Ten good and 10 poor sleepers participated in two sessions of bidirectional alpha feedback. As predicted, good sleepers demonstrated better alpha control compared to poor sleepers, although this pattern was only partially replicated in a second session. This study provides a degree of empirical support for interventions designed to enhance neuroflexibility in the treatment of some people with sleep onset insomnia.
View Full Paper →Beta EEG activity and insomnia
To date there have been seven studies which find that beta EEG is elevated at around sleep onset and during polysomnographic sleep in patients with insomnia. These findings suggest that insomnia may be characterized by central nervous system (CNS) hyperarousal. In this article, the seven studies are critically reviewed, two theoretical perspectives on beta EEG are presented, and the concept of hyperarousal as a three component process is discussed.
View Full Paper →The use of EEG theta biofeedback in the treatment of a patient with sleep-onset insomnia
In this report, the treatment of a 42-year-old female with a complaint of chronic sleep-onset insomnia is described. Following the unsuccessful use of relaxation training, treatment consisted of 11 sessions of EEG theta rhythm (4–7 Hz) biofeedback. Theta density and five sleep indices were monitored throughout baseline, placebo, and treatment sessions. A significant increase in theta density was accompanied by reports of a decrease in sleep latency and an increase in total sleep time. This improvement was maintained after withdrawal of medication and at 3-month follow-up.
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