Towards an Integrative Account of Potential Mechanisms Mediating the Path From Sleep Dysfunction to Hallucinations

Sleep dysfunction and hallucinatory experiences are bidirectionally related, with the strongest path leading from poor sleep to hallucinations. This narrative review examines mechanisms across four levels: phenomenology, psychology, neural networks, and neurophysiology. Stress is a well-supported mediator, with sleep manipulation studies in non-clinical populations showing its role. Sleep loss also affects nervous system inflammation, altering brain connectivity involved in hallucinations. Lived-experience accounts reveal three novel mechanisms—source monitoring, mental resilience, and reasoning skills—that are impacted by sleep loss, though the full causal chain requires further testing. Priorities include testing stress as a mediator in clinical populations and experimentally examining these novel mediators.

Study at a glance

Abstract

BACKGROUND: Sleep dysfunction shares a bidirectional relationship with hallucinatory experiences, with the strongest path from sleep dysfunction to the occurrence of hallucinatory experiences. This review aimed to identify potential mechanisms through which sleep dysfunction leads to hallucinations. STUDY DESIGN: A narrative review was conducted across 4 levels of explanation: phenomenology (via lived-experience accounts), psychology, neural networks, and neurophysiology. STUDY RESULTS: Relatively few studies have directly tested underlying mechanisms linking sleep dysfunction to hallucinations, particularly at the levels of neural networks and neurophysiology. There is good support for stress as a mediator between sleep dysfunction and hallucinations. Stress was a plausible mechanism across levels of explanation and was supported by sleep manipulation studies in non-clinical populations. Inflammation of the nervous system is affected by sleep loss, which in turn impacts the brain connectivity underpinning hallucinatory experiences. Lived-experience accounts identified 3 novel mechanisms, all of which are meaningful to people with lived experience of hallucinations: source monitoring, mental resilience, and reasoning skills. Quantitative studies show these mechanisms are impacted by sleep loss, but the full causal path from sleep dysfunction to hallucinations via these mechanisms requires testing. CONCLUSIONS: Key priorities for future research are to (1) test stress as a mediator in clinical populations experiencing hallucinations, with stress assessed across the levels of explanation simultaneously; (2) carry out experimental tests of novel potential mediators identified in this review (eg, source monitoring, inflammation, prefrontal cortical networks); and (3) identify potential moderators that might explain individual differences in the lived-experience accounts of the effect of sleep dysfunction on hallucinations.