Les manifestations neurologiques associées au COVID-19 sont fréquentes et variées. Alors que des symptômes non spécifiques tels que des céphalées, des vertiges, des douleurs et des myalgies sont décrits dans 2 à 30 % des cas, on retrouve des atteintes neurologiques plus sévères chez 8 à 13 % des patients hospitalisés. Il s’agit d’atteintes neurologiques centrales ou périphériques, avec au premier plan des encéphalopathies, des accidents vasculaires cérébraux mais également des encéphalites et des syndromes de Guillain–Barré. Les troubles du goût et de l’odorat, assez caractéristiques du COVID-19, touchent quant à eux 34 à 86 % des patients. À l’heure actuelle, les mécanismes en cause dans ces atteintes neurologiques sont imparfaitement compris. Les études autopsiques mettent en lumière le possible rôle du sepsis et de l’hypoxie, de l’infection/dysfonction endothéliale, de l’inflammation et d’atteintes immunomédiées. Le rôle pathogène direct du virus sur le parenchyme cérébral reste quant à lui incertain.

The COVID-19 pandemic highlighted the existence of neurological manifestations associated with SARS-CoV-2 infection. The aim of this review was to summarize the prevalence and the range of neurological manifestations associated with COVID-19, and to expose the main hypotheses about the pathogenic pathways based on available neuropathological studies.

Articles have been identified by searches of PubMed and Google scholar up to November 15, 2020, using a combination of COVID-19 and neurology search terms and adding relevant references in the articles.

Nonspecific neurological symptoms such as headache, dizziness, pain and myalgia, have been reported in 2 to 30% of COVID-19 hospitalized patients. More severe neurological diseases affected 8 to 13% of COVID-19 hospitalized patients including various central or peripheral manifestations. Among central nervous system involvement, encephalopathy and cerebrovascular disease – especially ischemic stroke – were the most frequent, followed by encephalitis, myelitis, meningitis, and posterior reversible encephalopathy syndrome. Guillain–Barré syndrome and variants were the most common form of peripheral nervous system involvement, followed by critical illness neuromyopathy, plexopathy, polyneuropathy, oculomotor neuropathy, and Tapia syndrome. Encephalopathy, ischemic stroke and encephalitis occurred 6 to 12days in median after the first signs of COVID-19, while Guillain–Barré syndrome occured later, at 15 to 23days in median. Taste and smell disorders affected 34 to 86% of patients and occurred 3.5days in median after the onset of infection. Pathogenic pathways of nervous system involvement in COVID-19 remain poorly understood. Neuropathological studies highlighted the possible role of sepsis and hypoxia, endothelial infection/dysfunction, inflammation and immune-mediated disease. While the presence of SARS-CoV-2 in the brain was confirmed in some COVID-19 patients, there were no definite evidence to support its direct pathogenicity on brain parenchyma.

Neurological involvement in COVID-19 is frequent and includes various manifestations. Most of them are encephalopathies and strokes, probably linked to viral sepsis, hypoxia and/or endotheliitis. A wide range of post-infectious disorders was also reported, such as encephalitis and Guillain–Barré syndrome. To date no studies demonstrated definite evidence of a direct pathogenicity of SARS-CoV-2 on brain.