Pathogenesis of nervous system lesions and clinical syndromes of the new coronavirus infection COVID-19

Based on the analysis of literature data, the issues of neurological complications after the new coronavirus infection COVID-19 are highlighted. There is little evidence for a direct mechanism for the neuroinvasiveness and neurotoxicity of the SARS-CoV-2 virus. Various mechanisms of coronavirus penetration into the brain are discussed - anterograde and retrograde, neuronal spread, transcriptional and hematogenous pathways. Retrograde/anterograde transport and transsynaptic transfer of the virus have been confi rmed by in vitro studies. Penetration of the virus into the central nervous system is also possible by spreading through peripheral nerves, for example, along the vagus nerve, which innervates the lungs and intestines. There are several possible mechanisms for the spread of SARS-CoV-2 across the blood-brain barrier: circulation of viral particles in the bloodstream, viral transcytosis through endothelial cells of blood vessels and capillaries, infection of leukocytes by viruses and transfer of viruses through the blood-brain barrier. Hypoxia caused by cytokine storm and respiratory distress lead to disruption of brain metabolism and the development of neurological complications. Aim. Analysis of literature data on the study of early and long-term manifestations of neurological disorders and diseases during a new coronavirus infection, postCovid syndrome (long COVID-19), as well as after vaccination. Results. Among the large number of nervous system disorders, there are five main types with long-term neurological complications associated with COVID-19: 1) encephalopathy with delirium/psychosis; 2) inflammatory syndromes of the central nervous system; 3) ischemic strokes; 4) peripheral neuropathies, in particular Guillain–Barre syndrome and brachial plexopathies; 5) other disorders of the central nervous system.