Taquet Maxime, Skorniewska Zuzanna, Zetterberg Henrik, Geddes John R, Mummery Catherine J, Chalmers James D, Ho Ling-Pei, Horsley Alex, Marks Michael, Poinasamy Krisnah, Raman Betty, Leavy Olivia C, Richardson Matthew, Elneima Omer, McAuley Hamish J C, Shikotra Aarti, Singapuri Amisha, Sereno Marco, Saunders Ruth M, Harris Victoria Claire, Houchen-Wolloff Linzy, Mansoori Parisa, Greening Neil J, Harrison Ewen M, Docherty Annemarie B, Lone Nazir I, Quint Jennifer, Greenhalf William, Wain Louise V, Brightling Christopher E, Evans Rachael E, Harrison Paul J, Koychev Ivan
Department of Psychiatry, University of Oxford, Oxford OX3 7JX, UK.
Oxford Health NHS Foundation Trust, Oxford OX3 7JX, UK.
Brain Commun. 2023 Dec 27;6(1):fcad357. doi: 10.1093/braincomms/fcad357. eCollection 2024.
A proportion of patients infected with severe acute respiratory syndrome coronavirus 2 experience a range of neuropsychiatric symptoms months after infection, including cognitive deficits, depression and anxiety. The mechanisms underpinning such symptoms remain elusive. Recent research has demonstrated that nervous system injury can occur during COVID-19. Whether ongoing neural injury in the months after COVID-19 accounts for the ongoing or emergent neuropsychiatric symptoms is unclear. Within a large prospective cohort study of adult survivors who were hospitalized for severe acute respiratory syndrome coronavirus 2 infection, we analysed plasma markers of nervous system injury and astrocytic activation, measured 6 months post-infection: neurofilament light, glial fibrillary acidic protein and total tau protein. We assessed whether these markers were associated with the severity of the acute COVID-19 illness and with post-acute neuropsychiatric symptoms (as measured by the Patient Health Questionnaire for depression, the General Anxiety Disorder assessment for anxiety, the Montreal Cognitive Assessment for objective cognitive deficit and the cognitive items of the Patient Symptom Questionnaire for subjective cognitive deficit) at 6 months and 1 year post-hospital discharge from COVID-19. No robust associations were found between markers of nervous system injury and severity of acute COVID-19 (except for an association of small effect size between duration of admission and neurofilament light) nor with post-acute neuropsychiatric symptoms. These results suggest that ongoing neuropsychiatric symptoms are not due to ongoing neural injury.
一部分感染严重急性呼吸综合征冠状病毒2的患者在感染数月后会出现一系列神经精神症状，包括认知缺陷、抑郁和焦虑。这些症状背后的机制仍然难以捉摸。最近的研究表明，在冠状病毒病（COVID-19）期间可能会发生神经系统损伤。目前尚不清楚COVID-19感染数月后持续存在的神经损伤是否导致了持续或新出现的神经精神症状。在一项针对因严重急性呼吸综合征冠状病毒2感染而住院的成年幸存者的大型前瞻性队列研究中，我们分析了感染后6个月时的神经系统损伤和星形胶质细胞激活的血浆标志物：神经丝轻链、胶质纤维酸性蛋白和总tau蛋白。我们评估了这些标志物是否与急性COVID-19疾病的严重程度以及出院后6个月和1年时的急性后神经精神症状（通过用于评估抑郁的患者健康问卷、用于评估焦虑的广泛性焦虑障碍评估、用于评估客观认知缺陷的蒙特利尔认知评估以及用于评估主观认知缺陷的患者症状问卷中的认知项目来衡量）相关。未发现神经系统损伤标志物与急性COVID-19的严重程度之间存在显著关联（除了住院时间与神经丝轻链之间存在小效应量的关联），也未发现与急性后神经精神症状存在关联。这些结果表明，持续的神经精神症状并非由持续的神经损伤所致。
