ArticleFrontiers in neuroimaging2026
Differential deficits in pattern- versus flash-visual evoked potentials in schizophrenia: relationship to subcortical visual systems, pulvinar nucleus and cognition.
Article in Frontiers in neuroimaging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: The human subcortical visual system is divided into distinct magnocellular, parvocellular and koniocellular pathways, which contribute differentially to specific aspects of early visual processing. Schizophrenia is associated with deficits in early-visual processing, especially involving N-methyl-D-aspartate receptor (NMDAR)-mediated non-linear gain within the subcortical magnocellular visual system. Nevertheless, methods for investigating the pathophysiological consequences remain limited. Flash-VEP can be obtained using either transient (tVEP) or steady-state (ssVEP) approaches. Flash stimuli also induce sustained reduction ("blocking") of the posterior alpha rhythm. Red (vs. white) flash stimuli selectively suppress activity in magnocellular-recipient layers of primary visual cortex. Here, we investigated flash-VEP responses in schizophrenia, with emphasis on the potential utility for assessing selective pathophysiological involvement of the magnocellular and koniocellular pathways. Methods: We obtained flash-VEP from 28 healthy control and 27 schizophrenia participants to white and red stimuli across a range of stimulation rates, and pattern-VEP from 29 control and 22 schizophrenia participants. A subset (17 control/15 schizophrenia) participated in both studies. We also obtained fMRI to 6-Hz white and red stimuli in an additional sample of 14 control and 14 schizophrenia participants. fMRI analyses focused on both visual cortex and inferior pulvinar nucleus. Results: Schizophrenia participants showed increased flash-tVEP responses ( Conclusion: The findings reinforce the importance of subcortical visual dysfunction as a driver of impaired neurocognition in schizophrenia and provide a scalable mechanism for assessment of early-visual dysfunction within the clinical setting. Deficit patterns are consistent with concepts of impaired magnocellular and koniocellular visual function affecting both thalamocortical and retinotectal system function in schizophrenia.
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