RT Journal Article
SR Electronic
T1 Presentations and mechanisms of CNS disorders related to COVID-19
JF Neurology - Neuroimmunology Neuroinflammation
JO Neurol Neuroimmunol Neuroinflamm
FD Lippincott Williams & Wilkins
SP e923
DO 10.1212/NXI.0000000000000923
VO 8
IS 1
A1 Marta Bodro
A1 Yaroslau Compta
A1 Raquel Sánchez-Valle
YR 2021
UL http://nn.neurology.org/content/8/1/e923.abstract
AB Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the coronavirus disease 2019 (COVID-19) pandemic. In addition to severe respiratory symptoms, there are a growing number of reports showing a wide range of CNS complications in patients with COVID-19. Here, we review the literature on these complications, ranging from nonspecific symptoms to necrotizing encephalopathies, encephalitis, myelitis, encephalomyelitis, endotheliitis, and stroke. We postulate that there are several different mechanisms involved in COVID-19–associated CNS dysfunction, particularly activation of inflammatory and thrombotic pathways and, in a few patients, a direct viral effect on the endothelium and the parenchyma. Last, critically ill patients frequently present with protracted cognitive dysfunction in the setting of septic encephalopathy likely due to multifactorial mechanisms. Further studies are needed to clarify the relative contribution of each of these mechanisms, but available data suggest that CNS complications in COVID-19 are rare and probably not directly caused by the virus.ACE=angiotensin-converting enzyme; ADEM=acute disseminated encephalomyelitis; AQP4=aquaporin 4; COVID-19=coronavirus disease 2019; ECMO=extracorporeal membrane oxygenation; ICU=intensive care unit; IL=interleukin; IVIg=IV immunoglobulin; MOG=myelin oligodendrocyte glycoprotein; SARS-CoV-2=severe acute respiratory syndrome coronavirus 2; SIRS=systemic inflammatory response syndrome; TNF=tumor necrosis factor