SWS and SWA are thought to be reflective of sleep depth and to play a central role in sleep maintenance and restorative sleep functions. Individuals with insomnia have also been reported to have less slow wave activity (SWA lower spectral power in the delta frequency range), with a shift towards elevated high frequency EEG activity, a potential physiological marker of increased cortical arousal. For instance, it is estimated that people with chronic insomnia spend 20 minutes less in SWS per night compared to good sleepers. Insomnia is notably linked to prolonged sleep onset latency, short total sleep time, numerous nocturnal awakenings, poor sleep efficiency and low amounts of SWS. Whether such auditory stimulation can potentiate slow waves in people with insomnia symptoms remains to be tested.įurthermore, sleep architecture and quantitative EEG measures undergo significant alterations in many people with insomnia.
Recent findings show that carefully timed auditory stimulation can increase sleep slow waves.
Novel devices which can be used in the field over multiple days now enable longer term monitoring of EEG features such as sleep slow waves to assess not only inter-individual variability, but also intra-individual variability, a phenomenon of high importance to assess the stability of slow wave abnormalities in insomnia subtypes. Some individuals with insomnia show low levels of slow wave sleep (SWS). Extensive work is still being deployed to better delineate the multiple subtypes of insomnia, and major gains are to be made using multi-domain physiological monitoring to deepen our understanding of this heterogeneous disease. Insomnia is estimated to be the most prevalent sleep disorder, with nearly 10% of the general population meeting diagnostic criteria.
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