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COVID-19 Infection Changed P300 Latency in Patients With Psychosis: A Retrospective Cohort Study
Xiaofeng Jiang1, Shunqi Qiu2, Weiwei Wang1
1The Seventh People's Hospital Affiliated Mental Health Center, Medical College of Shaoxing University Shaoxing Zhejiang China.
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, p = 0.002, partial η² = 0.687). Latency peaked at T3 (338.77 ms), significantly increased from T1 (335.75 ms; mean difference [MD] = 3.02 ms, 95% CI [0.24, 5.80], p = 0.030, Cohen's d = 0.85). At T4 (337.68 ms), latency remained elevated versus T1 (MD = 1.93 ms, 95% CI [0.25, 3.62], p = 0.020). In subgroup analysis, no significant effects of gender (p = 0.184), antipsychotic dose (p = 0.947), or interactions were found. Illness duration showed potential influence, warranting further study.
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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