COVID-19 neuropsychiatric repercussions: Current evidence on the subject.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has affected the entire world, causing the coronavirus disease 2019 (COVID-19) pandemic since it was first discovered in Wuhan, China in December 2019. Among the clinical presentation of the disease, in addition to fever, fatigue, cough, dyspnea, diarrhea, nausea, vomiting, and abdominal pain, infected patients may also experience neurological and psychiatric repercussions during the course of the disease and as a post-COVID-19 sequelae. Thus, headache, dizziness, olfactory and gustatory dysfunction, cerebrovascular disorders, neuromuscular abnormalities, anxiety, depression, and post-traumatic stress disorder can occur both from the infection itself and from social distancing and quarantine. According to current evidence about this infection, the virus has the ability to infect the central nervous system (CNS) via angiotensin-converting enzyme 2 (ACE2) receptors on host cells. Several studies have shown the presence of ACE2 in nerve cells and nasal mucosa, as well as transmembrane serine protease 2, key points for interaction with the viral Spike glycoprotein and entry into the CNS, being olfactory tract and blood-brain barrier, through hematogenous dissemination, potential pathways. Thus, the presence of SARS-CoV-2 in the CNS supports the development of neuropsychiatric symptoms. The management of these manifestations seems more complex, given that the dense parenchyma and impermeability of brain tissue, despite protecting the brain from the infectious process, may hinder virus elimination. Still, some alternatives used in non-COVID-19 situations may lead to worse prognosis of acute respiratory syndrome, requiring caution. Therefore, the aim of this review is to bring more current points related to this infection in the CNS, as well as the repercussions of the isolation involved by the pandemic and to present perspectives on interventions in this scenario.