The numbers are striking. Sleep disturbances, including insomnia, circadian rhythm disruptions, parasomnias, and fragmented sleep, affect up to 70 percent of individuals at clinical high risk for psychosis, and that figure climbs to roughly 80 percent in people with fully developed schizophrenia. A separate meta-analysis found that sleep disturbance prevalence hovers around 50 percent across every stage of the illness, from the at-risk state through early psychosis to chronic disease. Because psychotic disorders typically begin in adolescence or early adulthood—the median age of onset for schizophrenia spectrum disorders is 25 years, with a peak at 20.5 years—this window of vulnerability coincides precisely with the period when sleep problems are most prevalent in the general population.

The clinical stakes of early detection are considerable. The duration of untreated psychosis is positively correlated with poorer prognosis in first-episode illness, and among people identified as being at clinical high risk for psychosis, roughly 17.5 percent convert to a threshold psychotic disorder within the observation period. Sleep disturbance has been strongly and prospectively linked to increased psychotic symptoms in this high-risk group, and it is also associated with worse psychosocial functioning and a shorter time to transition from the at-risk state to full psychosis. In one large study of 688 individuals at clinical high risk, subjective sleep quality measured by the Pittsburgh Sleep Quality Index was significantly worse than in healthy controls, and terminal insomnia—waking too early and being unable to return to sleep—was reported by a quarter of patients and predicted conversion to psychosis over longitudinal follow-up.

What makes sleep such an attractive early marker is that it is observable, quantifiable, and potentially modifiable. Clinicians can assess it with quick self-report questionnaires such as the Pittsburgh Sleep Quality Index, the Insomnia Severity Index, and the Epworth Sleepiness Scale, or with objective tools including wrist-worn actigraphy and overnight polysomnography. Actigraphic markers such as reduced interdaily stability, elevated intradaily variability, and prolonged sleep onset latency serve as continuous indicators of circadian desynchronization and fragmented rest. Polysomnographic alterations—specifically reduced slow-wave sleep and shortened REM latency—may reflect underlying dysregulation in the thalamocortical circuits that govern both sleep and perception.

The neurobiological case for a shared pathway between sleep and psychosis is built on overlapping neurotransmitter systems. Dopamine and serotonin sit at the forefront: classical antipsychotic drugs that block dopaminergic receptors ameliorate sleep disturbances in schizophrenia, and atypical antipsychotics that also block serotonin 5-HT2 receptors correlate with improvement in negative symptoms. Postmortem studies of schizophrenic brains have revealed diminished muscarinic M1 and M4 receptors and reduced nicotinic receptors, particularly in the hippocampus, a region whose activity is closely tied to the REM phase of sleep. Because initial increases in dopaminergic activity during psychotic events may secondarily alter cholinergic signaling—and cholinergic disruption in turn reshapes sleep architecture by shortening REM latency—the same circuitry appears to underpin both phenomena.

At the synaptic level, the review highlights a convergence between sleep regulation and the neurodevelopmental trajectory toward psychosis. Adolescence and early adulthood constitute a critical window for brain maturation, during which the balance between synaptic formation and elimination becomes particularly vulnerable. One of the best-replicated neuronal hallmarks in people at clinical high risk is a reduction in mismatch negativity, an event-related brain potential that reflects NMDA receptor-dependent auditory echoic memory and short-term plasticity. Recent work combining EEG, MRI, and biomarker measurements in 303 high-risk individuals found that more deficient mismatch negativity amplitudes were associated with higher salivary cortisol and pro-inflammatory cytokine levels—but only in those who converted to psychosis within two years. Because both mismatch negativity generation during wakefulness and slow-wave sleep oscillations depend on intact NMDA receptor signaling and thalamocortical dendritic spine density, excessive synaptic pruning during adolescence could plausibly disrupt both domains simultaneously, creating a feedback loop in which fragmented sleep further erodes daytime sensory processing.

Structural neuroimaging adds another layer of complexity. In a prospective study of 507 individuals at clinical high risk and 81 healthy controls, sleep disturbances measured by questionnaire significantly predicted an increased risk of conversion to psychosis. Yet no associations were found between subjective sleep quality and macrostructural gray matter volume in the thalamus, hippocampus, or cerebellum, suggesting that the relationship between sleep disruption and brain changes operates at the microstructural and functional level rather than through gross volume loss. Meanwhile, earlier work had shown that sleep disturbances in ultra-high-risk adolescents correlated negatively with bilateral thalamus volume, and that circadian rhythm fragmentation, desynchronization from the light-dark cycle, and lower daily activity predicted greater positive and negative symptoms and psychosocial impairment at one-year follow-up.

The review also examines the everyday forces that shape adolescent sleep and may amplify risk. Evening chronotype—the tendency to be a night owl—is the most prevalent pattern among young people and is associated with higher rates of insomnia, poorer sleep quality, and more mental health problems. Psychoactive substances compound the problem: caffeine, energy drinks, alcohol, and cigarettes all degrade sleep, while cannabinoid use in adolescents was linked with poorer sleep outcomes in nearly half of reported cases, and amphetamine-type stimulans used by young patients with affective or psychotic illness were associated with poorer sleep quality over the course of disease. Light exposure from smartphones and screens in the hours before bed, irregular school and university schedules that force five days of morning wake times followed by weekend recovery sleep that never fully compensates, and psychosocial stress all converge to shorten sleep and fragment its architecture. In one meta-analysis, shorter sleep time in healthy adolescents was linked to a 55 percent increase in mood deficits.

Crucially, the review argues that sleep is not just a marker but a potential therapeutic target. Cognitive behavioral therapy for insomnia, delivered in a program called SleepWell to young people at ultra-high risk for psychosis, improved sleep variables, psychiatric symptoms, and social functioning in a randomized feasibility trial. The intervention focused on three sleep domains—sleep pressure, circadian rhythm, and hyperarousal—through morning routines, light-dark exposure, and nighttime relaxation. Other approaches remain less well explored: melatonin has established efficacy for circadian rhythm treatment in schizophrenia but has never been assessed in the at-risk state, omega-3 fatty acids show promise for alleviating cognitive deficits in high-risk individuals though their effect on conversion is statistically inconclusive, and electroconvulsive therapy improved polysomnographic measures in first-episode psychosis but raises ethical questions in at-risk populations. Current guidelines recommend psychological interventions, mostly cognitive behavioral therapy, with antipsychotic drugs as a secondary option, though available data do not support antipsychotic use specifically to prevent conversion.

The authors are candid about the limitations of the evidence base. Most studies focus on the at-risk state rather than first-episode psychosis, on adolescents rather than young adults, and rely on a single method of measuring sleep. Objective actigraphy and neuroimaging investigations frequently depend on small samples without formal power calculations, while larger multicenter studies rely solely on subjective measures. Cross-study synthesis is constrained by wide age ranges and inconsistent control for confounders such as psychotropic medication and comorbid mood symptoms. Nevertheless, the core message is clear: sleep assessment is a low-cost, scalable tool that could be woven into routine evaluation of young people reporting psychotic symptoms, and future research should prioritize longitudinal, multimodal studies and personalized, sleep-centered preventive strategies. If the findings hold up, the humble sleep diary may become one of psychiatry’s most valuable early-warning instruments.

Subject of Research: Sleep disturbances as early indicators of psychotic disorders in adolescents and young adults

Article Title: Sleep disturbances as an early indicator of psychotic disorders in adolescents and young adults

Article References: Sleep disturbances as an early indicator of psychotic disorders in adolescents and young adults. (n.d.). https://doi.org/10.3389/fnsyn.2026.1949833

Image Credits: AI Generated

DOI: 10.3389/fnsyn.2026.1949833

Keywords: sleep disturbances, psychosis, clinical high risk, adolescents, young adults, schizophrenia, circadian rhythm, insomnia, cognitive behavioral therapy, neurotransmission, synaptic pruning, early intervention