P 110. Modifying sleep continuity parameters with tDCS

Abstract

The regulation of sleep onset and maintenance is a complex process with a broad clinical significance. Several regulatory brain circuits have been identified, including an ascending reticular activating system and thalamo-cortical feedback loops ( Saper et al., 2005 ). Dysfunctions in one or more of those circuits might lead to an insomnia spectrum disorder. The “hyperarousal model of insomnia” ( Riemann et al., 2010 ) postulates an increased state of arousal leading to a disturbance of sleep onset and continuity. This arousal has been demonstrated in different systems, including cordial, metabolic and brain ( Riemann et al., 2010 ). Transcranial direct-current-stimulation (tDCS) has been shown having the potential to modify excitability in the prefrontal cortex and to modulate resting-state activity ( Keeser et al., 2011 ). The aim of this study is to answer the question whether modifying cortical excitability in the prefrontal cortex via bilateral tDCS leads to a change in excitability-dependent sleep parameters like sleep onset latency and the occurrence of arousal. The hypothesis is that prefrontal bidirectional anodal stimulation leads to an increase in excitability and arousal thereby disturbing sleep continuity whereas cathodal stimulation over the same region facilitates the opposite effect. Twenty-five patients with primary insomnia (as a human model for cortical hyperarousal) and twenty-five healthy subjects (16 females, aged 40–65 years) will be included after a thorough screening process. After adaptation to the sleep laboratory conditions, each participant will undergo a baseline polysomnography and three experimental sleep laboratory nights in intervals of 7 days with a tDCS protocol (two 10 min stimulation blocks with 20 min. inter-stimulation interval, bilateral frontal montage, parieto-occipital reference electrodes, intensity of current 1 mA over each electrode ( Monte-Silva et al., 2010 )) immediately prior to polysomnographically monitored sleep (11 pm to 7 am). Three different conditions (activation, deactivation, sham) will be applied in a counterbalanced order. Outcome parameters will include sleep latency, arousal parameters during NREM and REM sleep and EEG spectral parameters. Pilot data indicate changes in the wake EEG prior to sleep after prefrontal tDCS. First sleep results of the ongoing study will be presented at the conference. The results of this study are expected to improve our understanding of the impact of prefrontal cortical activity and arousal for the onset and maintenance of sleep. Results from this study might be informative for the development of novel treatments for sleep disruptions.