Why do we sleepwalk? A noradrenergic hypothesis of NREM sleep parasomnias.

Disorders of arousal (DOA), including sleepwalking, sleep terrors, and confusional arousals, are characterized by complex behaviors emerging from non-rapid eye movement (NREM) sleep. Although these conditions are defined by abnormal arousal, their neurobiological basis remains poorly understood, and the contribution of neuromodulatory systems, particularly the locus coeruleus-noradrenaline (LC-NA) system, has received limited attention. Here, we present a hypothesis-driven conceptual framework integrating existing evidence from neurophysiology, neuroimaging, autonomic regulation, and genetics. The LC-NA is organized into partially segregated modules projecting to distinct cortical and subcortical targets with different kinetics. We propose that under conditions such as sleep deprivation or stress, these modules become asynchronously engaged due to use-dependent fatigue. Motor- and limbic-projecting ensembles reactivate more readily, while prefrontal-projecting neurons remain functionally disengaged. This imbalance produces asynchronous cortical arousal, allowing complex motor and emotional behaviors to occur without full cognitive integration. This framework generates testable predictions and conceptualizes DOA as manifestations of arousal instability during NREM sleep, driven by intrinsic modular LC dynamics that modulate transitions between sleep and wakefulness. More broadly, it provides insight into how disrupted neuromodulatory coordination affects the integration of conscious states.