Erdoğan Tuğba, Koçer Belgin, Şen Sedat, Balcı Belgin Petek, Terzi Murat
Gazi University School of Medicine, Department of Neurology, Ankara, Turkey.
Ondokuz Mayıs University School of Medicine, Department of Neurology, Samsun, Turkey.
Noro Psikiyatr Ars. 2023 Jan 13;60(3):223-230. doi: 10.29399/npa.28142. eCollection 2023.
To describe the parainfectious or postinfectious effects of COVID-19 infection on the first demyelinating presentation of Multiple Sclerosis and tumefactive demyelinating lesion (TDL) developing with Longitudinally Extensive Transverse Myelitis (LETM).
We present six patients who presented with a first CNS demyelination event or whose demyelinating lesions had aggravated after COVID-19 infection between May and December 2020. Nasopharyngeal swab SARS-CoV-2 PCR positivity was detected in five cases and cerebrospinal fluid (CSF) PCR was positive in one. The symptoms, neurological signs, radiological and CSF findings of the cases were examined.
A 24-year-old woman presented with LETM aggravated by COVID-19, accompanied by a newly developed open-ring enhanced TDL. Four patients were diagnosed with the first presentation of MS, and one presented with clinically isolated syndrome according to the McDonald 2017 criteria. The interval between SARS-CoV-2 infection and the onset of clinical symptoms ranged from 4-93 days. All of the cases present with pyramidal or brain stem findings and have high brain and/or spinal MRI load. This suggests the moderate activity of CNS demyelinating disease after COVID-19 infection.
Based on this case series, all these first demyelinating events suggested that COVID-19 infection might trigger or exacerbate CNS demyelinating disease. SARS-CoV-2 plays a role in the clinical onset of Multiple Sclerosis. Active delayed demyelination developed within the first three months. This can be explained by COVID-triggered neuroimmune response that had been latent, and the initiation of the active disease process began with triggering or aggravation of the lesions in MRI. Multiple Sclerosis should be maintained during the COVID-19 pandemic.
描述新型冠状病毒肺炎(COVID-19)感染对多发性硬化首次脱髓鞘表现以及伴纵向广泛横贯性脊髓炎(LETM)的瘤样脱髓鞘病变(TDL)的感染后或感染后效应。
我们报告了2020年5月至12月期间6例在COVID-19感染后出现首次中枢神经系统脱髓鞘事件或脱髓鞘病变加重的患者。5例患者鼻咽拭子严重急性呼吸综合征冠状病毒2(SARS-CoV-2)聚合酶链反应(PCR)检测呈阳性,1例脑脊液(CSF)PCR检测呈阳性。对这些病例的症状、神经体征、影像学和脑脊液检查结果进行了检查。
一名24岁女性出现因COVID-19加重的LETM,并伴有新出现的开环强化TDL。4例患者被诊断为首次出现多发性硬化,1例根据2017年麦克唐纳标准诊断为临床孤立综合征。SARS-CoV-2感染与临床症状出现的间隔时间为4至93天。所有病例均有锥体束或脑干表现,且脑和/或脊髓磁共振成像(MRI)负荷较高。这表明COVID-19感染后中枢神经系统脱髓鞘疾病处于中度活动状态。
基于该病例系列,所有这些首次脱髓鞘事件表明COVID-19感染可能触发或加重中枢神经系统脱髓鞘疾病。SARS-CoV-2在多发性硬化的临床发病中起作用。在最初三个月内出现了活动性延迟脱髓鞘。这可以用COVID触发的潜伏神经免疫反应来解释,并且活动性疾病过程的启动始于MRI中病变的触发或加重。在COVID-19大流行期间应持续关注多发性硬化。