Ana Luiza Menezes Santana Bezerra, Amanda Menezes Morgado, Esther Barbosa Gonçalves Felix, Francisco Marcos Bezerra Cunha, Modesto Rolim Neto* and Ana Luíza de Aguiar Rocha Martin
Understanding the SARS-CoV-2 pathophysiology regarding neural system contamination and damage is necessary for clinical and therapeutic approaches, which may reduce the damage caused by the disease. In this regard, it is important to highlight that, besides the direct effect on neurons, the inflammatory state caused by a dysregulation of the immune system due to infection are both factors responsible for neurological phenomena of the disease. The presence of the virus in the bloodstream, its ability to directly penetrate the NS through peripheral nerves and the weakening of the blood-brain barrier are added to the tropism of SARS-CoV-2 by ACE-2 receptors, which favours the appearance of brain manifestations, associated with metabolic complications in the autoimmune processes induced by viral clinical condition. It is essential to remember that the cerebrovascular events have been increasingly reported in infected patients and are associated with the hypercoagulability caused by the disease. The activation of the coagulation cascade and deregulation of physiological anticoagulant mechanisms, such as protein C system and the disintegration of fibrin, are possible causes of this hypercoagulable state present in COVID-19. Even though it is still not evident whether the impairment of the nervous system is a result of direct infection by SARS-CoV-2 or of a diffuse inflammatory process affecting various organs and systems generating multiple manifestations, including those of the nervous system, we highlight that the quantity of drugs administered in intensive care units also can interfere with neurological conditions.
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