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在对严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染前后自主神经功能进行对比分析时,证明新型冠状病毒肺炎(COVID-19)后出现新发或恶化的汗腺功能。

Demonstrating new-onset or worsened sudomotor function post-COVID-19 on comparative analysis of autonomic function pre-and post-SARS-CoV-2 infection.

作者信息

Varma-Doyle Aditi, Villemarette-Pittman Nicole R, Lelorier Paul, England John

机构信息

Louisiana State University Health Sciences Center, New Orleans School of Medicine, Department of Neurology, New Orleans, LA, USA.

Massachusetts General Hospital, Harvard Medical School, Department of Neurology, Boston, MA, USA.

出版信息

eNeurologicalSci. 2023 Mar;30:100445. doi: 10.1016/j.ensci.2023.100445. Epub 2023 Jan 26.

Abstract

BACKGROUND

Autonomic dysfunction including sudomotor abnormalities have been reported in association with SARS-CoV-2 infection.

OBJECTIVE

There are no previous studies that have compared autonomic function objectively in patients pre- and post- SARS-CoV-2 infection.We aimed to identify if SARS-CoV-2 virus is triggering and/or worsening dysautonomia by comparing autonomic function tests in a group of patients pre-and post-SARS-CoV-2 infection.

DESIGN/METHODS: Six participants were enrolled and divided into two groups. The first group of 4 participants reported worsened autonomic symptoms post-SARS-CoV-2 infection. These individuals had their first autonomic test prior to COVID-19 pandemic outbreak (July 2019-December 2019). Autonomic function testing was repeated in these participants, 6 months to 1-year post-SARS-CoV-2 infection (June 2021).The second group of 2 participants reported new-onset autonomic symptoms post-COVID-19 infection and were also tested within 6 months post-SARS-CoV-2 infection.All participants had mild COVID-19 infection per WHO criteria. They had no evidence of large fiber neuropathy as demonstrated by normal neurophysiological studies (EMG/NCS). They were all screened for known causes of autonomic dysfunction and without risk factors of hypertension/hyperlipidemia, thyroid dysfunction, diabetes/prediabetes, vitamin deficiencies, history of HIV, hepatitis, or syphilis, prior radiation or chemical exposure or evidence of monoclonal gammopathy, or autoimmune condition.

RESULTS

Participants were female (age: 21-37y) and all endorsed orthostatic intolerance (6/6). Gastrointestinal symptoms (⅚), new-onset paresthesias, (3/6), and sexual dysfunction (2/6) were reported. Parasympathetic autonomic function remained stable 6-months to 1-year post-COVID-19 infection and no parasympathetic dysfunction was demonstrated in participants with new-onset dysautonomia symptoms. Postural orthostatic tachycardia was noted in half of the patients, being observed in one patient pre- SARS-CoV-2 infection and persisting post-SARS-CoV-2 infection; while new-onset postural tachycardia was observed in 1/3rd of patients. Sympathetic cholinergic (sudomotor) dysfunction was demonstrated in ALL participants. Worsened, or new-onset, sudomotor dysfunction was demonstrated in those with mild or normal sudomotor function on pre-COVID-19 autonomic testing.

CONCLUSIONS

Sympathetic adrenergic and cholinergic dysautonomia probably account for some of the symptoms of Long COVID-19. Sudomotor dysfunction was demonstrated as consistently worsened or new-sequelae to COVID-19 infection. COVID-19 may be responsible for triggering new-onset or worsened small-fiber neuropathy in this sample, supporting previously reported studies with similar findings. However, the findings in our study are preliminary, and studies with larger sample size are needed to confirm these observations.

摘要

背景

包括汗腺运动异常在内的自主神经功能障碍已被报道与严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染有关。

目的

此前尚无研究对SARS-CoV-2感染患者感染前后的自主神经功能进行客观比较。我们旨在通过比较一组SARS-CoV-2感染患者感染前后的自主神经功能测试,确定SARS-CoV-2病毒是否引发和/或加重自主神经功能障碍。

设计/方法:招募了6名参与者并分为两组。第一组4名参与者报告称SARS-CoV-2感染后自主神经症状加重。这些个体在2019年冠状病毒病疫情爆发前(2019年7月至12月)进行了首次自主神经测试。在这些参与者中,于SARS-CoV-2感染后6个月至1年(2021年6月)重复进行自主神经功能测试。第二组2名参与者报告称2019年冠状病毒病感染后出现新发自主神经症状,并且也在SARS-CoV-2感染后6个月内进行了测试。所有参与者根据世界卫生组织标准均为轻度2019年冠状病毒病感染。神经生理学研究(肌电图/神经传导速度)显示正常,他们没有大纤维神经病变的证据。他们均接受了已知自主神经功能障碍病因的筛查,且无高血压/高脂血症、甲状腺功能障碍、糖尿病/糖尿病前期、维生素缺乏、人类免疫缺陷病毒病史、肝炎或梅毒、既往放疗或化学暴露或单克隆丙种球蛋白病证据或自身免疫性疾病的危险因素。

结果

参与者均为女性(年龄:21 - 37岁),且均认可体位性不耐受(6/6)。报告有胃肠道症状(5/6)、新发感觉异常(3/6)和性功能障碍(2/6)。2019年冠状病毒病感染后6个月至1年,副交感神经自主功能保持稳定,新发自主神经功能障碍症状的参与者未表现出副交感神经功能障碍。一半的患者出现体位性直立性心动过速,其中1例患者在SARS-CoV-2感染前出现,SARS-CoV-2感染后持续存在;而1/3的患者出现新发体位性心动过速。所有参与者均表现出交感胆碱能(汗腺运动)功能障碍。在2019年冠状病毒病自主神经测试中汗腺运动功能轻度或正常的参与者中,表现出汗腺运动功能恶化或新发。

结论

交感肾上腺素能和胆碱能自主神经功能障碍可能是长期2019年冠状病毒病部分症状的原因。汗腺运动功能障碍表现为2019年冠状病毒病感染后持续恶化或新出现的后遗症。在本样本中,2019年冠状病毒病可能导致新发或加重小纤维神经病变,支持此前报道的类似研究结果。然而,我们研究的结果是初步的,需要更大样本量的研究来证实这些观察结果。

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