Rua Catarina, Raman Betty, Rodgers Christopher T, Newcombe Virginia F J, Manktelow Anne, Chatfield Doris A, Sawcer Stephen J, Outtrim Joanne G, Lupson Victoria C, Stamatakis Emmanuel A, Williams Guy B, Clarke William T, Qiu Lin, Ezra Martyn, McDonald Rory, Clare Stuart, Cassar Mark, Neubauer Stefan, Ersche Karen D, Bullmore Edward T, Menon David K, Pattinson Kyle, Rowe James B
Wolfson Brain Imaging Centre, University of Cambridge, Cambridge CB2 0QQ, UK.
University of Cambridge Centre for Parkinson-plus, University of Cambridge, Cambridge CB2 0QQ, UK.
Brain. 2024 Dec 3;147(12):4121-4130. doi: 10.1093/brain/awae215.
Post-mortem studies have shown that patients dying from severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection frequently have pathological changes in their CNS, particularly in the brainstem. Many of these changes are proposed to result from para-infectious and/or post-infection immune responses. Clinical symptoms such as fatigue, breathlessness, and chest pain are frequently reported in post-hospitalized coronavirus disease 2019 (COVID-19) patients. We propose that these symptoms are in part due to damage to key neuromodulatory brainstem nuclei. While brainstem involvement has been demonstrated in the acute phase of the illness, the evidence of long-term brainstem change on MRI is inconclusive. We therefore used ultra-high field (7 T) quantitative susceptibility mapping (QSM) to test the hypothesis that brainstem abnormalities persist in post-COVID patients and that these are associated with persistence of key symptoms. We used 7 T QSM data from 30 patients, scanned 93-548 days after hospital admission for COVID-19 and compared them to 51 age-matched controls without prior history of COVID-19 infection. We correlated the patients' QSM signals with disease severity (duration of hospital admission and COVID-19 severity scale), inflammatory response during the acute illness (C-reactive protein, D-dimer and platelet levels), functional recovery (modified Rankin scale), depression (Patient Health Questionnaire-9) and anxiety (Generalized Anxiety Disorder-7). In COVID-19 survivors, the MR susceptibility increased in the medulla, pons and midbrain regions of the brainstem. Specifically, there was increased susceptibility in the inferior medullary reticular formation and the raphe pallidus and obscurus. In these regions, patients with higher tissue susceptibility had worse acute disease severity, higher acute inflammatory markers, and significantly worse functional recovery. This study contributes to understanding the long-term effects of COVID-19 and recovery. Using non-invasive ultra-high field 7 T MRI, we show evidence of brainstem pathophysiological changes associated with inflammatory processes in post-hospitalized COVID-19 survivors.
尸检研究表明,死于严重急性呼吸综合征冠状病毒(SARS-CoV-2)感染的患者中枢神经系统(CNS)常有病理变化,尤其是脑干。许多此类变化被认为是由感染期和/或感染后免疫反应所致。2019冠状病毒病(COVID-19)康复出院的患者经常报告疲劳、气短和胸痛等临床症状。我们认为这些症状部分归因于关键神经调节性脑干核团的损伤。虽然在疾病急性期已证实脑干受累,但MRI上长期脑干变化的证据尚无定论。因此,我们使用超高场(7T)定量磁化率成像(QSM)来检验这一假设,即COVID-19康复患者存在持续的脑干异常,且这些异常与关键症状的持续存在有关。我们使用了30例患者的7T QSM数据,这些患者在因COVID-19入院93 - 548天后接受扫描,并将其与51名无COVID-19感染史的年龄匹配对照者进行比较。我们将患者的QSM信号与疾病严重程度(住院时间和COVID-19严重程度量表)、急性疾病期间的炎症反应(C反应蛋白、D-二聚体和血小板水平)、功能恢复情况(改良Rankin量表)、抑郁(患者健康问卷-9)和焦虑(广泛性焦虑障碍-7)进行关联分析。在COVID-19幸存者中,脑干的延髓、脑桥和中脑区域的磁共振磁化率增加。具体而言,延髓下部网状结构以及苍白和 obscurus中缝核的磁化率增加。在这些区域,组织磁化率较高的患者急性疾病严重程度更差、急性炎症标志物水平更高,且功能恢复明显更差。本研究有助于理解COVID-19的长期影响和康复情况。通过使用非侵入性超高场7T MRI,我们展示了COVID-19康复出院幸存者中与炎症过程相关的脑干病理生理变化的证据。