Better than sham? A double-blind placebo-controlled neurofeedback study in primary insomnia.

See Thibault et al. (doi:10.1093/awx033) for a scientific commentary on this article.Neurofeedback training builds upon the simple concept of instrumental conditioning, i.e. behaviour that is rewarded is more likely to reoccur, an effect Thorndike referred to as the 'law of effect'. In the case of neurofeedback, information about specific electroencephalographic activity is fed back to the participant who is rewarded whenever the desired electroencephalography pattern is generated. If some kind of hyperarousal needs to be addressed, the neurofeedback community considers sensorimotor rhythm neurofeedback as the gold standard. Earlier treatment approaches using sensorimotor-rhythm neurofeedback indicated that training to increase 12-15 Hz sensorimotor rhythm over the sensorimotor cortex during wakefulness could reduce attention-deficit/hyperactivity disorder and epilepsy symptoms and even improve sleep quality by enhancing sleep spindle activity (lying in the same frequency range). In the present study we sought to critically test whether earlier findings on the positive effect of sensorimotor rhythm neurofeedback on sleep quality and memory could also be replicated in a double-blind placebo-controlled study on 25 patients with insomnia. Patients spent nine polysomnography nights and 12 sessions of neurofeedback and 12 sessions of placebo-feedback training (sham) in our laboratory. Crucially, we found both neurofeedback and placebo feedback to be equally effective as reflected in subjective measures of sleep complaints suggesting that the observed improvements were due to unspecific factors such as experiencing trust and receiving care and empathy from experimenters. In addition, these improvements were not reflected in objective electroencephalographic-derived measures of sleep quality. Furthermore, objective electroencephalographic measures that potentially reflected mechanisms underlying the efficacy of neurofeedback such as spectral electroencephalographic measures and sleep spindle parameters remained unchanged following 12 training sessions. A stratification into 'true' insomnia patients and 'insomnia misperceivers' (subjective, but no objective sleep problems) did not alter the results. Based on this comprehensive and well-controlled study, we conclude that for the treatment of primary insomnia, neurofeedback does not have a specific efficacy beyond unspecific placebo effects. Importantly, we do not find an advantage of neurofeedback over placebo feedback, therefore it cannot be recommended as an alternative to cognitive behavioural therapy for insomnia, the current (non-pharmacological) standard-of-care treatment. In addition, our study may foster a critical discussion that generally questions the effectiveness of neurofeedback, and emphasizes the importance of demonstrating neurofeedback efficacy in other study samples and disorders using truly placebo and double-blind controlled trials.

Enhancing sleep quality and memory in insomnia using instrumental sensorimotor rhythm conditioning.

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 abundant during sleep, and overlaps with the sleep spindle frequency band. In the present pilot study we tested whether instrumental conditioning of SMR during wakefulness can enhance sleep and cognitive performance in insomnia. Twenty-four subjects with clinical symptoms of primary insomnia were tested in a counterbalanced within-subjects-design. Each patient participated in a SMR- as well as a sham-conditioning training block. Polysomnographic sleep recordings were scheduled before and after the training blocks. Results indicate a significant increase of 12-15 Hz activity over the course of ten SMR training sessions. Concomitantly, the number of awakenings decreased and slow-wave sleep as well as subjective sleep quality increased. Interestingly, SMR-training enhancement was also found to be associated with overnight memory consolidation and sleep spindle changes indicating a beneficial cognitive effect of the SMR training protocol for SMR "responders" (16 out of 24 participants). Although results are promising it has to be concluded that current results are of a preliminary nature and await further proof before SMR-training can be promoted as a non-pharmacological approach for improving sleep quality and memory performance.

Susceptibility to declarative memory interference is pronounced in primary insomnia.

Sleep has been shown to stabilize memory traces and to protect against competing interference in both the procedural and declarative memory domain. Here, we focused on an interference learning paradigm by testing patients with primary insomnia (N = 27) and healthy control subjects (N = 21). In two separate experimental nights with full polysomnography it was revealed that after morning interference procedural memory performance (using a finger tapping task) was not impaired in insomnia patients while declarative memory (word pair association) was decreased following interference. More specifically, we demonstrate robust associations of central sleep spindles (in N3) with motor memory susceptibility to interference as well as (cortically more widespread) fast spindle associations with declarative memory susceptibility. In general the results suggest that insufficient sleep quality does not necessarily show up in worse overnight consolidation in insomnia but may only become evident (in the declarative memory domain) when interference is imposed.

Event-related activity and phase locking during a psychomotor vigilance task over the course of sleep deprivation.

There is profound knowledge that sleep restriction increases tonic (event-unrelated) electroencephalographic (EEG) activity. In the present study we focused on time-locked activity by means of phasic (event-related) EEG analysis during a psychomotor vigilance task (PVT) over the course of sleep deprivation. Twenty healthy subjects (10 male; mean age ± SD: 23.45 ± 1.97 years) underwent sleep deprivation for 24 h. Subjects had to rate their sleepiness hourly (Karolinska Sleepiness Scale) and to perform a PVT while EEG was recorded simultaneously. Tonic EEG changes in the δ (1-4 Hz), θ (4-8 Hz) and α (8-12 Hz) frequency range were investigated by power spectral analyses. Single-trial (phase-locking index, PLI) and event-related potential (ERP) analyses (P1, N1) were used to examine event-related changes in EEG activity. Subjective sleepiness, PVT reaction times and tonic EEG activity (delta and theta spectral power) significantly increased over the night. In contrast, event-related EEG parameters decreased throughout sleep deprivation. Specifically, the ERP component P1 diminished in amplitude, and delta and theta PLI estimates decreased progressively over the night. It is suggested that event-related EEG measures (such as the amplitude of the P1 and especially delta/theta phase-locking) serve as a complimentary method to track the deterioration of attention and performance during sleep loss. As these measures actually reflect the impaired response to specific events rather than tonic changes during sleep deprivation they are a promising tool for future sleep research.