自主神经功能在sars - cov -2感染前后的比较分析表明,新发或加重的sudymotor功能

Q3 Neuroscience eNeurologicalSci Pub Date : 2023-03-01 DOI:10.1016/j.ensci.2023.100445
Aditi Varma-Doyle , Nicole R. Villemarette-Pittman , Paul Lelorier , John England
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引用次数: 3

摘要

自主神经功能障碍包括sudymotor异常已被报道与SARS-CoV-2感染有关。目的以往没有研究客观比较SARS-CoV-2感染前后患者的自主神经功能。我们的目的是通过比较一组感染SARS-CoV-2前和后患者的自主神经功能测试,确定SARS-CoV-2病毒是否触发和/或加重自主神经紊乱。设计/方法6名参与者被分为两组。第一组4名参与者报告了sars - cov -2感染后自主神经症状恶化。这些人在2019冠状病毒病大流行(2019年7月至2019年12月)之前进行了首次自主测试。在这些参与者中,在sars - cov -2感染后6个月至1年(2021年6月)重复进行自主功能测试。第二组2名参与者报告了covid -19感染后新发的自主神经症状,并在sars - cov -2感染后6个月内进行了检测。根据世卫组织标准,所有参与者均为轻度COVID-19感染。正常神经生理检查(EMG/NCS)显示,患者无大纤维神经病变。他们都进行了自主神经功能障碍的已知原因筛查,并且没有高血压/高脂血症、甲状腺功能障碍、糖尿病/前驱糖尿病、维生素缺乏、HIV、肝炎或梅毒病史、既往辐射或化学暴露或单克隆γ病或自身免疫性疾病的证据等危险因素。结果参与者均为女性(年龄21-37岁),6/6均为直立不耐受。胃肠道症状(⅚)、新发感觉异常(3/6)和性功能障碍(2/6)均有报道。副交感神经自主神经功能在covid -19感染后6个月至1年保持稳定,新发自主神经异常症状的参与者未出现副交感神经功能障碍。半数患者体位性站立性心动过速,其中1例在SARS-CoV-2感染前和SARS-CoV-2感染后持续存在;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功能障碍。在covid -19前自主神经检测中,那些sudommotor功能轻度或正常的患者表现出加重或新发的sudommotor功能障碍。结论交感肾上腺素能性和胆碱能性植物神经异常可能是新冠肺炎的部分症状。Sudomotor功能障碍被证明为COVID-19感染的持续恶化或新后遗症。COVID-19可能是该样本中引发新发或恶化的小纤维神经病变的原因,这支持了先前报道的具有类似发现的研究。然而,我们的研究结果是初步的,需要更大样本量的研究来证实这些观察结果。
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Demonstrating new-onset or worsened sudomotor function post-COVID-19 on comparative analysis of autonomic function pre-and post-SARS-CoV-2 infection

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.

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来源期刊
eNeurologicalSci
eNeurologicalSci Neuroscience-Neurology
CiteScore
3.50
自引率
0.00%
发文量
45
审稿时长
62 days
期刊介绍: eNeurologicalSci provides a medium for the prompt publication of original articles in neurology and neuroscience from around the world. eNS places special emphasis on articles that: 1) provide guidance to clinicians around the world (Best Practices, Global Neurology); 2) report cutting-edge science related to neurology (Basic and Translational Sciences); 3) educate readers about relevant and practical clinical outcomes in neurology (Outcomes Research); and 4) summarize or editorialize the current state of the literature (Reviews, Commentaries, and Editorials). eNS accepts most types of manuscripts for consideration including original research papers, short communications, reviews, book reviews, letters to the Editor, opinions and editorials. Topics considered will be from neurology-related fields that are of interest to practicing physicians around the world. Examples include neuromuscular diseases, demyelination, atrophies, dementia, neoplasms, infections, epilepsies, disturbances of consciousness, stroke and cerebral circulation, growth and development, plasticity and intermediary metabolism. The fields covered may include neuroanatomy, neurochemistry, neuroendocrinology, neuroepidemiology, neurogenetics, neuroimmunology, neuroophthalmology, neuropathology, neuropharmacology, neurophysiology, neuropsychology, neuroradiology, neurosurgery, neurooncology, neurotoxicology, restorative neurology, and tropical neurology.
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