Time processing in schizophrenia: integrating behavioral, neurobiological, and clinical data

Timing is a fundamental neural process that underlies perception, behavior, and cognition. In schizophrenia, a chronic, heritable neuropsychiatric disorder that typically manifests in young adulthood, disruptions in time processing are increasingly recognized as contributing to the disorder’s positive, negative, and cognitive symptoms. This review examines how these timing mechanisms are altered in schizophrenia, assessing changes in both the perception of time and the timing of perception.

We provide an overview of dedicated, intrinsic, and Bayesian models of time processing and their complementary relevance to the behavioral manifestations and neurophysiological basis of timing deficits in schizophrenia. Behavioral studies reveal robust impairments in both the accuracy and precision of timing among patients with schizophrenia, and these abnormalities have been closely linked to symptoms such as hallucinations, delusions of control, and disorganized thought. Neurophysiological evidence suggests that these timing deficits may stem from dopaminergic, GABAergic, and NMDA receptor-related dysfunction, together with oscillatory and connectivity abnormalities across cortico-striatal-thalamo-cortical and cerebellar circuits.

This synthesis also lays the groundwork for exploring the broader phenomenological implications of timing disturbances in schizophrenia, proposing that such abnormalities may contribute to disturbances in agency, self–world boundaries, and the sense of reality. Integrating behavioral, neurophysiological, computational, and phenomenological findings, we outline a unified framework in which timing dysfunction acts as a central organizing principle in schizophrenia that may contribute to core symptoms. Finally, we propose future research directions, highlighting timing deficits as promising prodromal biomarkers and therapeutic targets that may open avenues for intervention beyond the reach of existing pharmacotherapy alone.

This work was supported by the Resident Research Track program in the Department of Psychiatry at the University of North Carolina School of Medicine. The graphical abstracts were created using BioRender.com. This work was supported by a Ford Foundation Postdoctoral Fellowship, a Burroughs Wellcome Fund/Revson Foundation Award, and a Simons Foundation Autism Research Initiative (SFARI) Fellows-to-Faculty Award.

These authors contributed equally: Aidin Ashoori, Amanda M. Department of Psychiatry, University of North Carolina School of Medicine, 101 Manning Drive, Chapel Hill, NC, 27514, USA Departments of Psychiatry & Behavioral Sciences and of Biomedical Engineering, Duke University, 101 Science Drive, Durham, NC, 27705, USA Department of Psychiatry & Behavioral Science, Stanford University School of Medicine, 401 Quarry Road, Stanford, CA, 94304, USA Correspondence to Aidin Ashoori, Amanda M. The authors declare no competing interest.

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