According to the ''hyper-arousal" model of primary insomnia (PI), insomnia patients experience heightened physiological and cognitive arousal compared to normal people during both sleep and wakefulness. Previous studies have reported that in- somnia patients show more high frequency electroencephalogram (EEG) signals than normal people.

 

This suggests that hyper-arousal in insomnia, reflected in the high frequency EEG pattern, results in non-restorative sleep. Specifically, hyper- arousal in PI results in increased beta activity that is associated with cortical arousal, resulting in non-restorative sleep. This study aimed to verify the efficacy of a beta-decrease neurofeedback (NF) protocol for insomnia.

 

Participants were randomly assigned to an NF treatment or a wait-list control group. The NF treatment group received 10 sessions of NF (n = 5), and the wait-list control group (n = 9) group received no treatment. We compared the following parameters pre-and post-treatment, as well as 2-weeks following the final treatment: resting state EEG (eye-open, EO; eye-closed, EC), heart rate variability (HRV), sleep scales, sleep diaries, and Smart Wearable Device data.

 

Results showed significantly decreased beta power, HRV, SL (sleep latency), sleep scale scores, increased alpha power, TST (total sleep time), SE (sleep effectiveness), and sleep satisfac- tion in the wait-list control group compared with the NF group. This study is the first neurofeedback protocol using “Beta power” as a marker of neurophysiological arousal in insomnia.

 

Our findings provide new evidence for the efficacy of Beta in decreasing insomnia symptoms and add to the range of non-pharmacological insomnia intervention choices for pregnant, psychopharmacotherapy-resistant, and older people. Neurofeedback not only provides control of insomnia symptoms but also results in a decreased risk of psychological comorbidities.

 

This study found improved insomnia symptoms after only 10 sessions of NF. Fast remission of insomnia symptoms may reinforce patients’ motivations for treatment, is more cost-effective, and can result in reduced treatment times.

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.

Introduction

A non-pharmacological intervention, namely instrumental conditioning of 12–15 Hz oscillations (ISC), for improving sleep quality and memory is introduced. EEG recordings over the sensorimotor cortex show a prominent oscillatory pattern in a frequency range between 12 and 15 Hz (sensorimotor rhythm, SMR) under quiet but alert wakefulness. This frequency range is also known to be abundant during light non-rapid eye movement sleep, and is overlapping with the sleep spindle frequency band. Some early findings indicated that ISC of SMR during wakefulness can influence subsequent sleep. In the present study we intend to clarify the nature of these effects and apply neurofeedback (NFT) to insomnia patients.

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Materials and methods

Twenty-four subjects (Mean = 34.83; SD = 10.60) with clinical symptoms of primary insomnia were tested. A counterbalanced within-subjects design (19 lab visits over the course of 3–6 weeks) was adopted. Each patient participated in an ISC–NFT as well as a sham-NFT training block. Polysomnographic sleep recordings were scheduled before and after training blocks.

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Results

Data confirm a significant increase of 12–15 Hz activity over the course of the ten SMR training sessions which was also positiviely related to overnight memory consolidation changes.Number of awakenings were reduced and slow-wave sleep was increased following ISC but not following sham-NFT. In addition, subjective sleep quality was enhanced over the course of the trainings. Last but not least sleep spindles in slow-wave sleep were found to be exclusively enhanced after SMR training.

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Conclusion

Current results indicate that besides healthy individuals also people suffering from primary insomnia can experience subjective as well as objective benefits from ISC–NFT. Replication studies are yet awaited.

Since the pharmacological treatment of insomnia has the potential risk for dependence and various side effects, nonpharmacological intervention for insomnia is very important in clinical practice.

 

The neurophysiological characteristics and recent researches using quantitative EEG of insomnia suggest the insomnia as a state of CNS(central nervous system) hyperarousal. Insomnia should not be restricted to subjective sleep complaints alone because it appears to be a 24-hour disorder including daytime fatigue and decreased quality of life. The neurofeedback treatment is a self-regulation method based on the paradigm of operant conditioning.

 

The goal of this treatment modality is to normalize the functioning of the brain by inhibiting and/or reinforcing specific frequency bands of brain waves. Therefore, the neurofeedback treatment on the basis of thalamocortical mechanisms which play an important role in sleep and arousal might be a useful treatment modality for the insomnia in the future.

 

In this paper the authors suggest the clinical applications of neurofeedback for the treatment of insomnia and further clinical researches about its therapeutic effects in insomnia.

Insomnia is a significant sleep disorder in today's society and has multiple psychological, physical, general health, and occupational implications.

 

Common treatments for insomnia include pharmacotherapy, cognitive behavior therapy, and over-the-counter products. These treatments have varying degrees of efficacy and/or potential side effects.

 

Based on the neurocognitive model of insomnia whereby persistent sensory and cognitive processing may disturb sleep, neurofeedback is a potential nonpharmacological treatment.

 

Based on the limited but positive research in the area, neurofeedback may be considered as a promising tool for treating insomnia.