脑血管疾病和 SARS-CoV-2 患者的神经心理学和实验室参数分析与无 SARS-CoV-2 患者的比较

V.V. Marshtupa, T.I. Nasonova
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引用次数: 0

摘要

背景。严重急性呼吸系统综合征 2 型冠状病毒(SARS-CoV-2,原名 2019-nCoV)是 2019 年冠状病毒病(COVID-19)的病原体,最早在中国武汉被报道。然而,它也会传染给人类,并通过感染者之间的密切接触或相对简单的传播机制(空气传播)在全球迅速传播。据了解,COVID-19 几乎会影响人体的所有系统。初步报告显示,高血压可能是易感染 SARS-CoV-2、COVID-19 病程更严重以及 COVID-19 死亡率增加的危险因素。据估计,1%-3% 的 COVID-19 患者会出现短暂性脑缺血发作,其频率与其他冠状病毒感染(SARS-CoV-1 和 MERS-CoV)相似。与 COVID-19 相关的缺血性中风的病因尚不清楚,但之前的研究表明,炎症细胞因子风暴可能会导致高凝状态和内皮损伤。我们认为 COVID-19 与神经系统并发症密切相关,因为有一些潜在的因素可以引起这些并发症。材料和方法对 111 名感染 SARS-CoV-2 的患者(n = 71)和无 SARS-CoV-2 病史的患者(n = 40)的脑血管疾病进行了分析。研究的主题是神经心理学和实验室指标。研究采用了以下方法:心理测量--贝克焦虑量表、汉密尔顿抑郁评分量表、疲劳评估量表;神经心理学--迷你精神状态检查、蒙特利尔认知评估、额叶评估电池;临床--神经系统状态;检测 COVID-19 RNA 的聚合酶链反应;统计方法。研究结果在患有短暂性脑缺血发作和缺血性脑卒中且神经功能缺损程度较轻且患有 COVID-19 的患者中,红细胞沉降率、白细胞、分段中性粒细胞均有升高,而在所有患有脑血管疾病且患有 COVID-19 的患者中,C 反应蛋白均有升高,其中缺血性脑卒中患者的升高更为显著。所有患有 COVID-19 的亚组中,D-二聚体和纤维蛋白原均有所增加,其中缺血性中风患者的含量更高。此外,在这一亚组中,降钙素原指数也超过了正常值,这表明 COVID-19 病程的严重程度与合并感染有关。缺血性中风患者的神经心理测试数据显示,SARS-CoV-2 导致的神经功能缺损程度很轻,但蒙特利尔认知评估得分却有所下降,这表明这些患者的认知能力发生了轻微变化。经常出现危机的高血压患者和有轻微神经功能缺损的缺血性中风患者的焦虑水平高于参考值,其中未患 COVID-19 的患者略占多数。由此可见,根据脑血管疾病以及是否感染 SARS-CoV-2 病毒,实验室和神经心理学参数在三个亚组中均存在差异,因此有可能开发出更合适的诊断方法,以预测 COVID-19 的病程和预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Analysis of neuropsychological and laboratory parameters in patients with cerebrovascular disease and SARS-CoV-2 compared to those without SARS-CoV-2
Background. Severe acute respiratory syndrome сoronavіrus 2 (SARS-CoV-2, formerly known as 2019-nCoV) is the cause of coronavirus disease 2019 (COVID-19), and was first reported in Wuhan, China. However, it is also contagious to humans and spreads rapidly around the world through close contact between infected people or through a relatively simple transmission mechanism (airborne transmission). COVID-19 is known to affect almost all systems of the human body. Initial reports suggest that hypertension may be a risk factor for susceptibility to SARS-CoV-2 infection, a more severe course of COVID-19, and increased mortality associated with COVID-19. It is estimated that 1–3 % of COVID-19 patients experience transient ischemic attacks with a frequency similar to other coronavirus infections (SARS-CoV-1 and MERS-CoV). The cause of ischemic stroke associated with COVID-19 is unknown, but previous studies have suggested that an inflammatory cytokine storm may cause hypercoagulation and endothelial damage. We see that COVID-19 is closely related to neurological complications because there are potential factors that can cause them. Materials and methods. Cerebrovascular diseases were analyzed in 111 patients infected with SARS-CoV-2 (n = 71) and those without a history of SARS-CoV-2 (n = 40). The subject of the study was neuropsychological and laboratory indicators. The following methods were used: psychometric — Beck Anxiety Inventory, Hamilton Depression Rating Scale, Fatigue Assessment Scale; neuropsychological — Mini-Mental State Examination, Montreal Cognitive Assessment, Frontal Assessment Battery; clinical — neurological status; polymerase chain reaction to detect COVID-19 RNA; statistical methods. Results. In patients who suffered transient ischemic attack and ischemic stroke with a minimal neurological deficit and COVID-19, there were elevations in the erythrocyte sedimentation rate, leukocytes, segmented neutrophils, while an increase in C-reactive protein was noted in all participants with cerebrovascular disease and COVID-19, with more significant levels among those with ischemic stroke. All subgroups with COVID-19 showed an increase in D-dimer and fibrinogen with higher content in patients after ischemic stroke. Also in this subgroup, the procalcitonin index exceeded the norm, which indicates the severity of the course of COVID-19 with the addition of co-infection. Data of neuropsychological tests in patients with ischemic stroke with a minimal neurological deficit with SARS-CoV-2 revealed a decrease in the Montreal Cognitive Assessment score, indicating mild cognitive changes in these patients. The level of anxiety in patients with hypertension with frequent crises and ischemic stroke with a minimal neurological deficit was above the reference values, with a slight predominance in patients who did not have COVID-19. It follows that both laboratory and neuropsychological parameters differed in three subgroups depending on cerebrovascular disease, as well as the presence and absence of SARS-CoV-2, which makes it possible to develop more appropriate diagnostic methods in order to predict the course and outcome of COVID-19.
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