S170 REM – Dreaming – Emotions: The neurophysiology of nightmare disorder

Abstract

Objectives Nightmares are intense and highly unpleasant mental experiences that occur usually – but not exclusively – during late-night Rapid Eye Movement (REM) sleep and often provoke abrupt awakenings.The underlying mechanism of nightmare disorder was only scarcely investigated and remains poorly understood. The most influential model of nightmare disorder that provided a common framework fortrauma-related and non-traumatic (idiopathic) nightmares was introduced by Levin and Nielsen (2007). One of the main assumptions of the model is that nightmares reflect unsuccessful fear-extinction processes during (REM) sleep due to a dysfunctional brain network comprising fronto-limbic structures. Consequently, amygdalar over-activation and inefficient (prefrontal) inhibition lead to the emotional intensification of dreaming and hyperarousal during sleep. Nevertheless, sleep quality and emotional regulation in nightmare sufferers was mainly examined by questionnaire-based studies. Methods We have performed a series of quantitative EEG analyses based on the polysomnographic data of young (non-ptsd) nightmare sufferers and matched controls. Moreover, in a subsequent study we investigated emotional habituation to arousing images after a night of polysomnographically monitored sleep in a group of nightmare sufferers and matched controls. Emotional reactivity was quantified by subjective evaluations and psychophysiological measures (HRV, SCR). Results In line with questionnaire-based findings, we found that nightmare sufferers are characterized by fragmented sleep, reduced Slow Wave Sleep (SWS), enhanced microarousals during NREM sleep and heightened wake-like oscillations during REM sleep. Furthermore, arousal-related cortical activity coupled with attenuated parasympathetic regulation were evidenced in nightmare sufferers specifically during NREM to REM transitions. Discussion Given that the neural network underlying emotional memory processing is highly active during REM periods, and REM sleep seems to be intimately related to fear memory processing, our findings might indirectly support Levin and Nielsen’s assumption of disrupted REM-dependent fear-extinction in nightmare disorder. Nevertheless, the association between impaired emotional regulation and altered sleep physiology remains to be investigated. Conclusions In our experiments we aimed to directly test Levin and Nielsen’s fear-extintion model of nightmare disorder and to relate impaired emotional regulation to specific sleep EEG features. We conclude that examining nightmare disorder by such integrative approach would shed more light on the enigma of REM sleep and emotional memory processing. Significance Our research could shed more light on the mechanism of nightmare formation, propagate the professional knowledge of nightmare disorder, and facilitate the development of effective, evidence-based treatment procedures.