Abstract
Background: Visual sensory processing deficits are consistently observed in schizophrenia, with clear amplitude reduction of the visual evoked potential (VEP) during the initial 50–150 ms of processing. Similar deficits are seen in unaffected first-degree relatives and drug-naïve first-episode patients, pointing to these deficits as potential endophenotypic markers. Schizophrenia is also associated with deficits in neural plasticity, implicating dysfunction of both glutamatergic and GABAergic systems. Here, we sought to understand the intersection of these two domains, asking whether short-term plasticity during early visual processing is specifically affected in schizophrenia.Methods: Brief periods of monocular deprivation (MD) induce relatively rapid changes in the amplitude of the early VEP – i.e., short-term plasticity. Twenty patients and 20 non-psychiatric controls participated. VEPs were recorded during binocular viewing, and were compared to the sum of VEP responses during brief monocular viewing periods (i.e., Left-eye + Right-eye viewing).Results: Under monocular conditions, neurotypical controls exhibited an effect that patients failed to demonstrate. That is, the amplitude of the summed monocular VEPs was robustly greater than the amplitude elicited binocularly during the initial sensory processing period. In patients, this “binocular effect” was absent.Limitations: Patients were all medicated. Ideally, this study would also include first-episode unmedicated patients.Conclusion: These results suggest that short-term compensatory mechanisms that allow healthy individuals to generate robust VEPs in the context of MD are not effectively activated in patients with schizophrenia. This simple assay may provide a useful biomarker of short-term plasticity in the psychotic disorders and a target endophenotype for therapeutic interventions.
Highlights
Visual sensory processing deficits have been consistently documented in schizophrenia using the visual evoked potential (VEP) method [1,2,3,4,5,6,7]
This study would include first-episode unmedicated patients. These results suggest that short-term compensatory mechanisms that allow healthy individuals to generate robust VEPs in the context of monocular deprivation (MD) are not effectively activated in patients with schizophrenia
This simple assay may provide a useful biomarker of short-term plasticity in the psychotic disorders and a target endophenotype for therapeutic interventions
Summary
Visual sensory processing deficits have been consistently documented in schizophrenia using the visual evoked potential (VEP) method [1,2,3,4,5,6,7]. The relationship of visual sensory deficits to genetic liability was further emphasized in a pair of studies linking them to specific risk haplotypes for schizophrenia on the dysbindin gene (DTNBP1) [13] and the nitric oxide synthasase-1 gene (NOS1) [14]. Taken together, these studies point to early visual sensory processing deficits as a potentially valuable tool in early detection efforts and to the possibility that this biomarker might expand our abilities to identify children at risk during the prodromal stages of the disorder [15, 16]. We sought to understand the intersection of these two domains, asking whether short-term plasticity during early visual processing is affected in schizophrenia
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