Lieke W A Hermans1, Tim R Leufkens2, Merel M van Gilst3, Tim Weysen4, Marco Ross5, Peter Anderer6, Sebastiaan Overeem7, Annemiek Vermeeren8. 1. Department of Electrical Engineering, Eindhoven University of Technology, De Zaale, Eindhoven, the Netherlands. Electronic address: l.w.a.hermans@tue.nl. 2. Brain, Behavior and Cognition Group, Philips Research, High Tech Campus 34, Eindhoven, the Netherlands; Department of Industrial Design, Eindhoven University of Technology, De Zaale, Eindhoven, the Netherlands. Electronic address: tim.leufkens@philips.com. 3. Department of Electrical Engineering, Eindhoven University of Technology, De Zaale, Eindhoven, the Netherlands; Sleep Medicine Centre Kempenhaeghe, Sterkselseweg 65, Heeze, the Netherlands. Electronic address: GilstM@kempenhaeghe.nl. 4. Brain, Behavior and Cognition Group, Philips Research, High Tech Campus 34, Eindhoven, the Netherlands. Electronic address: tim.weysen@philips.com. 5. Sleep and Respiratory Care, Philips Austria GmbH, Vienna, Austria. Electronic address: marco.ross@philips.com. 6. Sleep and Respiratory Care, Philips Austria GmbH, Vienna, Austria. Electronic address: peter.anderer@philips.com. 7. Sleep Medicine Centre Kempenhaeghe, Sterkselseweg 65, Heeze, the Netherlands; Department of Electrical Engineering, Eindhoven University of Technology, De Zaale, Eindhoven, the Netherlands. Electronic address: OvereemS@kempenhaeghe.nl. 8. Department of Neuropsychology and Psychopharmacology, Faculty of Psychology and Neuroscience, Maastricht University, Universiteitssingel 40, Maastricht, the Netherlands. Electronic address: a.vermeeren@maastrichtuniversity.nl.
Abstract
STUDY OBJECTIVE: To study sleep EEG characteristics associated with misperception of Sleep Onset Latency (SOL). METHODS: Data analysis was based on secondary analysis of standard in-lab polysomnographic recordings in 20 elderly people with insomnia and 21 elderly good sleepers. Parameters indicating sleep fragmentation, such as number of awakenings, wake after sleep onset (WASO) and percentage of NREM1 were extracted from the polsysomnogram, as well as spectral power, microarousals and sleep spindle index. The correlation between these parameters during the first sleep cycle and the amount of misperceived sleep was assessed in the insomnia group. Additionally, we made a model of the minimum duration that a sleep fragment at sleep onset should have in order to be perceived as sleep, and we fitted this model to subjective SOLs of both subject groups. RESULTS: Misperception of SOL was associated with increased percentage of NREM1 and more WASO during sleep cycle 1. For insomnia subjects, the best fit of modelled SOL with subjective SOL was found when assuming that sleep fragments shorter than 30 min at sleep onset were perceived as wake. The model indicated that healthy subjects are less sensitive to sleep interruptions and perceive fragments of 10 min or longer as sleep. CONCLUSIONS: Our findings suggest that sleep onset misperception is related to sleep fragmentation at the beginning of the night. Moreover, we show that people with insomnia needed a longer duration of continuous sleep for the perception as such compared to controls. Further expanding the model could provide more detailed information about the underlying mechanisms of sleep misperception.
STUDY OBJECTIVE: To study sleep EEG characteristics associated with misperception of Sleep Onset Latency (SOL). METHODS: Data analysis was based on secondary analysis of standard in-lab polysomnographic recordings in 20 elderly people with insomnia and 21 elderly good sleepers. Parameters indicating sleep fragmentation, such as number of awakenings, wake after sleep onset (WASO) and percentage of NREM1 were extracted from the polsysomnogram, as well as spectral power, microarousals and sleep spindle index. The correlation between these parameters during the first sleep cycle and the amount of misperceived sleep was assessed in the insomnia group. Additionally, we made a model of the minimum duration that a sleep fragment at sleep onset should have in order to be perceived as sleep, and we fitted this model to subjective SOLs of both subject groups. RESULTS: Misperception of SOL was associated with increased percentage of NREM1 and more WASO during sleep cycle 1. For insomnia subjects, the best fit of modelled SOL with subjective SOL was found when assuming that sleep fragments shorter than 30 min at sleep onset were perceived as wake. The model indicated that healthy subjects are less sensitive to sleep interruptions and perceive fragments of 10 min or longer as sleep. CONCLUSIONS: Our findings suggest that sleep onset misperception is related to sleep fragmentation at the beginning of the night. Moreover, we show that people with insomnia needed a longer duration of continuous sleep for the perception as such compared to controls. Further expanding the model could provide more detailed information about the underlying mechanisms of sleep misperception.