Rahmawati Putu Lohita, Tini Kumara, Susilawathi Ni Made, Wijayanti I A Sri, Samatra Dpg Purwa
Department of Neurology, Udayana University, Sanglah General Hospital, Denpasar, Bali, Indonesia.
Department of Neurology, Udayana University, Udayana University Hospital, Bali, Indonesia.
J Clin Neurol. 2021 Apr;17(2):155-163. doi: 10.3988/jcn.2021.17.2.155.
Coronavirus disease 2019 (COVID-19) can reportedly manifest as an acute stroke, with most cases presenting as large vessel ischemic stroke in patients with or without comorbidities. The exact pathomechanism of stroke in COVID-19 remains ambiguous. The findings of previous studies indicate that the most likely underlying mechanisms are cerebrovascular pathological conditions following viral infection, inflammation-induced endothelial dysfunction, and hypercoagulability. Acute endothelial damage due to inflammation triggers a coagulation cascade, thrombosis propagation, and destabilization of atherosclerosis plaques, leading to large-vessel occlusion and plaque ulceration with concomitant thromboemboli, and manifests as ischemic stroke. Another possible mechanism is the downregulation of angiotensin-converting enzyme 2 as the target action of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). Acute stroke management protocols need to be modified during the COVID-19 pandemic in order to adequately manage stroke patients with COVID-19.
据报道，2019冠状病毒病（COVID-19）可表现为急性中风，大多数病例表现为有或无合并症患者的大血管缺血性中风。COVID-19中风的确切发病机制仍不明确。先前研究结果表明，最可能的潜在机制是病毒感染后的脑血管病理状况、炎症诱导的内皮功能障碍和高凝状态。炎症引起的急性内皮损伤触发凝血级联反应、血栓形成和动脉粥样硬化斑块不稳定，导致大血管闭塞和斑块溃疡并伴有血栓栓塞，表现为缺血性中风。另一种可能的机制是严重急性呼吸综合征冠状病毒2（SARS-CoV-2）作为靶作用使血管紧张素转换酶2下调。在COVID-19大流行期间，需要修改急性中风管理方案，以便对COVID-19中风患者进行充分管理。
