ArticleHealth science reports2026
COVID-19 Infection Changed P300 Latency in Patients With Psychosis: A Retrospective Cohort Study.
Article in Health science reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- COVID-19 Infection Changed P300 Latency in Patients With Psychosis: A Retrospective Cohort Study.Health science reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aims: The COVID-19 pandemic raises concerns about neurological impacts on individuals with mental health conditions, particularly cognitive function. P300 event-related potential (ERP) latency is a validated neurophysiological marker of attention and working memory. This study aimed to quantify COVID-19's effect on P300 latency in psychiatric patients and explore associations with demographic/clinical factors (gender, antipsychotic dosage). Methods: A retrospective cohort study enrolled 19 psychiatric inpatients (13 male, 6 female; ICD-11 diagnoses: 79.2% schizophrenia). Participants underwent four auditory oddball P300 assessments: pre-infection (T1), 1 week post-infection (T2), and at ~2 months (T3), and ~3 months post-infection (T4). Latency changes were analyzed using repeated-measures ANOVA with Greenhouse-Geisser correction. Effects of gender, chlorpromazine-equivalent dose (stratified: low/medium/high) were assessed. Results: A significant main effect of time on P300 latency was observed (F(3,12) = 8.76, Conclusion: COVID-19 infection significantly prolongs P300 latency in psychiatric patients, indicating transient impairment in attentional processing and accelerating of the progression of neurodegeneration. The effect is independent of gender or medication dose, suggesting direct neurological dysfunction mechanisms. Partial recovery by T4 supports the potential reversibility of COVID-19-related cognitive deficits, with implications for monitoring rehabilitation.
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Registered trials
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