Aug 2026· Expert Review of Neurotherapeutics· Vol 26, pp.
1-20
· 0 citations· 140 references
Medicine
TL;DR
The bidirectional relationship between sleep dysfunction and psychosis, the shared biological mechanisms underlying both, the utility of sleep assessment as an early warning marker for relapse, and the current gaps in sleep-targeted intervention evidence are examined.
Abstract
INTRODUCTION
Psychosis is increasingly understood as a disorder of brain systems that are also central to sleep regulation. Indeed, sleep disturbances are both highly prevalent in psychotic disorders and are likely to contribute to the emergence and maintenance of psychotic experiences.
AREAS COVERED
This narrative review, based on a comprehensive search of MEDLINE/PubMed, Embase, PsycINFO, and Web of Science (March 2026), examines the bidirectional relationship between sleep dysfunction and psychosis, the shared biological mechanisms underlying both, the utility of sleep assessment as an early warning marker for relapse, and the current gaps in sleep-targeted intervention evidence.
EXPERT OPINION
Sleep dysfunction constitutes a transdiagnostic pathway to psychosis, with varying temporal profiles across diagnoses: organic and substance-induced psychoses emerge acutely over hours to days with rapid reversibility; mood- and trauma-related psychoses develop subacutely over days to weeks; schizophrenia spectrum disorders show insidious onset over years with chronic persistence. Across these presentations, disturbances in sleep continuity, architecture, and circadian regulation may act as mechanistic drivers rather than epiphenomena, interacting with disorder-specific vulnerabilities to shape the timing, severity, and course of psychosis. Translating this understanding into practice requires routine sleep-circadian assessment from the earliest clinical stages, integration of scalable interventions into transdiagnostic care pathways, and recognition of sleep as both a clinically relevant outcome and a stratification variable in future psychosis trials. This framework positions sleep-circadian dysfunction not only as a marker of risk and progression, but also as a promising modifiable target for prevention, early intervention, and relapse reduction across psychotic disorders.
The association between sleep-related phenomena and psychosis has received increasing attention in recent years, as sleep disturbances (e.g., insomnia) have shown robust associations with psychotic symptoms. However, the role of other, more specific sleep processes in psychosis remains unclear, despite their potential importance as symptom-related correlates. Particularly, phenomena such as dreaming and hypnagogic experiences may share certain phenomenological features with hallucination-like experiences. Given that both sleep and psychosis involve complex neural systems, examining their neurobiological correlates may help clarify their potential relationships. Therefore, in this review, we summarize the literature on the potential connections between different sleep processes and psychosis from both conceptual and neurological perspectives. Current evidence suggests that anterior cingulate and frontal regions may be relevant to some sleep disturbances, dreaming-related processes, and psychosis-related abnormalities. However, given the broad and non-specific functions of these regions, such overlap should be interpreted cautiously. Overall, neurobiological evidence directly linking sleep-related processes to psychosis remains limited. We then conclude by highlighting current gaps in knowledge, particularly regarding the role of other sleep processes, and outlining directions for future research.
Zhiyu Cui, Linlin Fan· Progress in Neuro-psychophar...· 0 citations
Current understanding of the clinical features, etiological factors, biological mechanisms, and pharmacological management of schizophrenia is summarized, while emerging therapeutic targets that may guide future research and drug development are outlined.
Vaishnavi S. Solav, A. Wankhade, V. Paithankar et al.· Research Journal of Pharmaco...· 0 citations
Anxiety and depressive disorders impose a heavy global burden. Although sleep disturbances have traditionally been regarded as secondary symptoms of these conditions, converging evidence now implicates circadian rhythm disruption as a core pathophysiological mechanism rather than a mere epiphenomenon. This review systematically explores the circadian system and constructs an integrated framework linking disruption to the synergistic dysregulation of multiple pathways and subsequent emotional/sleep abnormalities. We systematically examine five key mechanistic pathways: the SCN-limbic circuit, HPA axis, immune inflammation, neurotransmitter plasticity, and the gut-brain axis. Furthermore, we define actionable subtypes of disruption, summarize chronotherapies (e.g., light therapy, melatonin), and analyze current controversies regarding causality. Finally, we propose future directions, including multi-omics sampling and personalized intervention algorithms. By integrating evidence linking circadian disruption to anxiety/depression, this paper highlights its central mechanistic value, providing theoretical support for precision psychiatry and the integration of circadian medicine.
Jiao Yuan, Jing Zhang, Menghui Yu et al.· Frontiers in Psychiatry· 0 citations
Bipolar disorder (BD) is a highly complex, chronic psychiatric illness marked by episodic disturbances of mood. While historically conceptualized as a disorder of neurotransmitter imbalance, converging evidence suggests it is better understood as a disorder of dynamic dysregulation across multiple interacting systems, including genetic and epigenetic vulnerability, HPA axis dysregulation, mitochondrial/metabolic dysfunction, immune activation, circadian disruption, and gut-brain axis disturbances. These systems comprise a hierarchically organized, bidirectionally coupled feedback network that is responsible for the oscillatory mood states that define the disorder. Here, it’s proposed that a specific, testable, integrative model in which genetic/epigenetic vulnerabilities lead to destabilization of HPA axis regulation, which then leads to mitochondrial bioenergetic dysfunction (the central integrative node of the cascade), which then, through its interaction with immune activation and gut-brain signaling, causes the excitation-inhibition imbalance underlying the clinical presentation of mood-state transitions. From this model, three empirically tractable predictions are made: that co-occurring inflammatory/metabolic/circadian dysregulation will constitute a biological subtype with earlier onset, more rapid cycling, and a more negative response to lithium; that neuroendocrine/metabolic disturbances will prospectively precede rather than simply co-occur with mood-state transitions; and that interventions targeting the metabolic-inflammatory interface will produce mood-stabilizing effects whose magnitude correlates with baseline biological severity rather than symptom severity. Throughout, the importance of state-dependence, trait-level features, and medication confounds is discussed. Finally, translational implications for metabolic stratification, circadian-focused intervention, and gut-brain modulation are outlined.
Y. Muhammad· Frontiers in Integrative Neu...· 0 citations
Sleep disturbances are a common, heterogeneous comorbidity of autism spectrum disorder (ASD). This systematic review updates the field on sleep in ASD over 2022–2026, with attention to how the evidence has evolved. Eighty-nine studies met inclusion criteria. Sleep disturbance remained more prevalent in autistic individuals than in typically developing peers (47–84%), confirmed by actigraphic and polysomnographic measures. The most distinctive recent advance is in sleep microstructure: spindles, slow-oscillation–spindle coupling, and oscillatory EEG features are emerging as candidate neurophysiological markers. Behavioural and parent-mediated programmes remain the most consistent intervention evidence, while pharmacological trials produced largely null effects; neuromodulation, microbiota-targeted, and physical-activity interventions are preliminary but expanding. The question of whether individuals with ASD sleep worse than peers appears largely settled. Future priorities are harmonized objective sleep protocols, adequately powered trials in emerging intervention categories, and broader inclusion of adults with ASD, who remain markedly under-represented.
M. Veneruso, Antonella Barbieri, G. Silvestrini et al.· Current Sleep Medicine Repor...· 0 citations
Sleep disturbance is one of the most common and clinically important features of depressive disorders. Although it has traditionally been viewed as a secondary symptom of depression, growing evidence indicates that sleep disturbance plays an active role in both the development and persistence of depressive illness. Longitudinal and experimental studies demonstrate that insomnia, poor sleep quality, and circadian rhythm disruption increase vulnerability to depression, are associated with greater symptom severity, and elevate the risk of relapse. Conversely, depressive disorders disrupt sleep regulation through characteristic changes in sleep architecture, circadian misalignment, and maladaptive sleep related behaviors, creating a self reinforcing cycle between sleep disturbance and mood dysregulation. Shared mechanisms underlying this bidirectional relationship include alterations in monoaminergic neurotransmission, hypothalamic pituitary adrenal axis activation, circadian rhythm disruption, inflammatory processes, and impaired emotional regulation. Clinical evidence further suggests that interventions targeting sleep, particularly cognitive behavioral therapy for insomnia and chronotherapeutic approaches, can reduce depressive symptoms and improve treatment outcomes when integrated into standard depression care. This narrative review synthesizes current evidence on the bidirectional relationship between sleep disturbance and depression and highlights its implications for clinical practice and future research.
Muhammad Sanan, Sun Yao, Nicha Wareesawetsuwan et al.· World Journal of Psychiatry· 0 citations
