Selective visuoconstructional impairment following mild COVID-19 with inflammatory and neuroimaging correlation findings

Author:

de Paula Jonas Jardim,Pereira de Paiva Rachel Elisa Rodrigues,e Silva Nathália Gualberto Souza,Rosa Daniela Valadão,de Souza Duran Fabio Luis,Coimbra Roney Santos,de Souza Costa Danielle,Dutenhefner Pedro Robles,Dutra Oliveira Henrique Soares,Camargos Sarah Teixeira,Mendes Vasconcelos Herika Martins,de Oliveira Carvalho Nara,da Silva Juliana Batista,Silveira Marina Bicalho,Malamut Carlos,Oliveira Derick Matheus,Molinari Luiz Carlos,de Oliveira Danilo Bretas,Januário José Nélio,Silva Luciana Costa,De Marco Luiz Armando,Magalhães Queiroz Dulciene Maria de,Meira Wagner,Busatto Geraldo,Miranda Débora Marques,Romano-Silva Marco AurélioORCID

Abstract

ABSTRACTPeople recovered from COVID-19 may still present complications including respiratory and neurological sequelae. In other viral infections, cognitive impairment occurs due to brain damage or dysfunction caused by vascular lesions and inflammatory processes. Persistent cognitive impairment compromises daily activities and psychosocial adaptation. Some level of neurological and psychiatric consequences were expected and described in severe cases of COVID-19. However, it is debatable whether neuropsychiatric complications are related to COVID-19 or to unfoldings from a severe infection. Nevertheless, the majority of cases recorded worldwide were mild to moderate self-limited illness in non-hospitalized people. Thus, it is important to understand what are the implications of mild COVID-19, which is the largest and understudied pool of COVID-19 cases. We aimed to investigate adults at least four months after recovering from mild COVID-19, which were assessed by neuropsychological, ocular and neurological tests, immune markers assay, and by structural MRI and 18FDG-PET neuroimaging to shed light on putative brain changes and clinical correlations. In approximately one-quarter of mild-COVID-19 individuals, we detected a specific visuoconstructive deficit, which was associated with changes in molecular and structural brain imaging, and correlated with upregulation of peripheral immune markers. Our findings provide evidence of neuroinflammatory burden causing cognitive deficit, in an already large and growing fraction of the world population. While living with a multitude of mild COVID-19 cases, action is required for a more comprehensive assessment and follow-up of the cognitive impairment, allowing to better understand symptom persistence and the necessity of rehabilitation of the affected individuals.

Publisher

Cold Spring Harbor Laboratory

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