Three patients with non-REM parasomnias experienced episodes of Cotard delusion—believing they were dead or dying and unable to perceive their bodies as their own. These nihilistic mentations occurred during confusional arousals from sleep and were accompanied by panic. EEG source analysis indicated right-hemispheric hypoactivity during the episodes. The authors argue that aberrant activation of the salience network and default mode network—two major intrinsic networks of wakefulness—underlies these states. Such dreamlike mentations are rarely remembered and likely underreported, but can cause significant distress and worsen clinical outcomes if unaddressed.
Patients with idiopathic REM Sleep Behavior Disorder (iRBD) and those with Non-Rapid Eye Movement Parasomnia (NREMP) differ not only in the content of their morning dream recalls but also in the structural organization of those recalls. iRBD patients were more likely to recall dreams and had more white dreams (feeling of having dreamt without memory). Speech graph analysis revealed that iRBD dream reports had stable, linear sequential structures, while NREMP dream reports were more recursive and less stable, with higher graph connectivity scores. These findings suggest distinct underlying mechanisms for dream recall in these two sleep disorders.
A 7-year history of vivid, immersive dreaming perceived as continuous with waking life, accompanied by persistent dream-reality confusion, is described in a younger individual. The patient engaged in reality-testing behaviors and reported significant cognitive fatigue. Video-polysomnography confirmed REM sleep without atonia and a dream re-enactment episode. Neuropsychiatric evaluation ruled out dissociative or psychotic disorders, and no neurodegenerative disease was observed. The case suggests a potentially distinct, non-neurodegenerative REM parasomnia phenotype, highlighting the need to expand current classifications to capture cognitive and metacognitive dimensions of REM sleep disorders. Potential mechanisms involving melanin-concentrating hormone signaling are discussed.
Nightmare disorder involves not only REM sleep but also altered NREM sleep physiology. In a retrospective case-control study of 26 adults with nightmare disorder and 32 controls, those with nightmare disorder showed reduced frontal slow-oscillation–spindle coupling, while delta–spindle coupling remained normal, resulting in lower coupling dominance. Stage-adjusted K-complex density across the first 6 hours of sleep was also lower in the nightmare disorder group. These findings suggest that nightmare disorder involves changes in NREM sleep microarchitecture, not just REM sleep, and warrant prospective confirmation.