• Maria C Barbosa-Silva, Maiara N Lima, Denise Battaglini, Chiara Robba, Paolo Pelosi, RoccoPatricia R MPRMLaboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.National Institute of Science and Technology for Regenerative Medicine, Rio de Janeiro, Ri, and Tatiana Maron-Gutierrez.
• Laboratory of Immunopharmacology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Fiocruz, Av. Brasil, 4365, Pavilhão 108, sala 45, Manguinhos, Rio de Janeiro, RJ, 21040-360, Brazil.
• Crit Care. 2021 Jul 6; 25 (1): 236236.

AbstractInfectious diseases may affect brain function and cause encephalopathy even when the pathogen does not directly infect the central nervous system, known as infectious disease-associated encephalopathy. The systemic inflammatory process may result in neuroinflammation, with glial cell activation and increased levels of cytokines, reduced neurotrophic factors, blood-brain barrier dysfunction, neurotransmitter metabolism imbalances, and neurotoxicity, and behavioral and cognitive impairments often occur in the late course. Even though infectious disease-associated encephalopathies may cause devastating neurologic and cognitive deficits, the concept of infectious disease-associated encephalopathies is still under-investigated; knowledge of the underlying mechanisms, which may be distinct from those of encephalopathies of non-infectious cause, is still limited. In this review, we focus on the pathophysiology of encephalopathies associated with peripheral (sepsis, malaria, influenza, and COVID-19), emerging therapeutic strategies, and the role of neuroinflammation.

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