The neuronal mechanisms of NDE are poorly understood (Peinkhofer, Dreier & Kondziella, 2019). Nelson and colleagues previously proposed the concept that rapid eye movement (REM) sleep intrusion and REM related out-of-body experiences could occur at the time of a life-threatening event and might explain many elements of NDE (Nelson et al., 2006; Nelson, Mattingly & Schmitt, 2007). REM sleep is defined by rapid and random saccadic eye movements, loss of muscle tone, vivid dreaming, and cortical activation as revealed by desynchronization of the scalp electroencephalography (EEG). REM state features can intrude into wakefulness, both in healthy individuals and patients with narcolepsy. This may cause visual and auditory hallucinations at sleep onset (hypnagogic) or upon awakening (hypnopompic) and muscle atonia with sleep paralysis and cataplexy (Scammell, 2015). According to the hypothesis of Nelson and colleagues, danger provokes the arousal of neural pathways that, when stimulated, are known to generate REM-associated responses. This was interpreted as a “diathesis stress model” (Nelson et al., 2006; Long & Holden, 2007). In this model, an unusually sensitive arousal system (i.e. the diathesis), as evidenced by the experience of REM intrusion, would predispose people to NDE in situations of stress and danger. To test their hypothesis, Nelson and colleagues conducted a survey comparing a group of individuals with self-reported NDE and an age- and sex-matched control group (Nelson et al., 2006). The results suggested that episodes of REM intrusion are more common in individuals with NDE.