The occurrence of acute demyelinating encephalomyelitis after respiratory viral infection (clinical observation)

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Abstract

This article examines the development of acute demyelinating encephalomyelitis against a background of a viral infection in a clinical case. Based on the literature review, it is known that acute disseminated encephalomyelitis is an immuno-mediated single-phase inflammatory demyelinating disorder of white matter of the brain and spinal cord. It is noted that one of the proposed mechanisms of pathogenesis is that myelin autoantigens, such as myelin main protein, proteolipid protein and myelin oligodendrocyte protein, have antigenic determinants with the infecting agent. Antiviral antibodies or cell-mediated cross-reacting pathogens respond to myelin autoantigens, resulting in acute demyelinating encephalomyelitis. Acute demyelinating encephalomyelitis has been found to be associated with increased vascular permeability and accumulation of circulating immune complexes or other humoral factors that develop after exposure to a foreign antigen introduced by infection or vaccination. This process then leads to infiltration of the walls of the vessels by mononuclear cells with subsequent swelling and periodic hemorrhage. Microglia, lymphocytes, and phagocytes appear throughout the day, ultimately leading to demyelination and possible gliosis and necrosis. The degree of demyelination and subsequent glial and neural changes explain the difference between clinical features and disease prognosis. In clinical case, we have demonstrated the appearance of this disease, which developed in close temporal connection with infectious disease. Positive meningeal signs, tenderness and limited movements of the eyeballs, diplopia when viewed sideways, decreased convergence, horizontal nystagmus when viewed sideways, symptoms of oral automatism, decreased muscle strength diffuse, tendons and tendons = D, average liveliness; from the feet S> = D, average liveliness, tremor of the hands. The MRI findings, in addition to the clinical picture, helped to establish the diagnosis. As a result of this, a cure for the disappearance of a neurological deficit was achieved. Thus, this clinical case proves that disseminated encephalomyelitis proceeds by type of acute disease with rapid increase of symptoms and their subsequent regression.
呼吸道病毒感染后急性脱髓鞘性脑脊髓炎的发生(临床观察)
本文探讨急性脱髓鞘性脑脊髓炎的发展对病毒感染的背景下,在一个临床病例。通过文献综述,我们知道急性播散性脑脊髓炎是一种免疫介导的大脑和脊髓白质的单相炎性脱髓鞘疾病。本文提出的发病机制之一是髓磷脂自身抗原,如髓磷脂主蛋白、蛋白脂质蛋白和髓磷脂少突胶质细胞蛋白,与感染因子具有抗原决定因素。抗病毒抗体或细胞介导的交叉反应病原体对髓鞘自身抗原作出反应,导致急性脱髓鞘性脑脊髓炎。急性脱髓鞘性脑脊髓炎已被发现与血管通透性增加和循环免疫复合物或其他体液因子的积累有关,这些因素是在暴露于感染或疫苗接种引入的外来抗原后发生的。这一过程导致单个核细胞浸润血管壁,随后出现肿胀和周期性出血。小胶质细胞、淋巴细胞和吞噬细胞全天出现,最终导致脱髓鞘和可能的胶质细胞增生和坏死。脱髓鞘的程度和随后的胶质和神经的改变解释了临床特征和疾病预后的差异。在临床病例中,我们已经证明了这种疾病的出现,它与传染病的发展有着密切的时间联系。脑膜阳性征象,眼球压痛和运动受限,侧视复视,收敛性减弱,侧视水平眼震,口腔自动性症状,肌力弥散减弱,肌腱和肌腱= D,平均活力;从脚S> = D,平均活泼,手颤抖。核磁共振检查结果,加上临床表现,有助于确定诊断。因此,一种治愈神经缺陷消失的方法得以实现。因此,本临床病例证明,播散性脑脊髓炎按急性疾病类型进行,症状迅速加重,随后消退。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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