Pathomorphological brain changes due to coronavirus disease 2019 (COVID-19)

Aim: To investigate the pathomorphological changes in the brains of individuals who died from complications of coronavirus disease (COVID-19) and to identify the neuropathological features associated with COVID-19. Materials and methods. A morphological study was conducted on autopsy material from 78 individuals who died due to complications of COVID-19 between March 2020 and April 2021. Histological examinations of various brain regions – including the cortex, white matter, basal ganglia, hippocampus, brainstem, and cerebellum – were performed using both morphological and immunohistochemical methods. Monoclonal antibodies were used to detect astrocytes (GFAP, Thermo Scientific), microglia (CD68, Clone Ab-4, Thermo Scientific), and T-lymphocytes (CD3, Clone SP7, Thermo Scientific). Histological evaluation and microphotography were carried out using a Leica DM750 universal optical microscope (Leica Microsystems GmbH). Results. It was found that brain damage in hospitalized patients with SARS-CoV-2 infection was associated with older age, disease severity, and comorbidities. In cases of severe COVID-19 with neurological deficits, neurovascular incidents were accompanied by ischemic infarction, venous sinus thrombosis, and intracerebral hemorrhage. Hypoxic-ischemic encephalopathy was histologically characterized by degeneration and partial loss of neurons, microglial activation with the formation of numerous microglial nodules in the cortex around hypoxically altered neurons, in the white matter, perivascularly, and in perivascular spaces throughout different parts of the brain, reactive astrogliosis with a positive immunohistochemical marker GFAP, and perivascular infiltration by T-lymphocytes. Conclusions. Since SARS-CoV-2 has a broad tissue tropism, both respiratory and extrapulmonary complications can occur. The neuropathological features and findings in the studied cases with a severe course included neuronal degeneration, microglial activation, infiltration by CD3-positive T-lymphocytes, reactive astrogliosis, and, in some cases, macroscopic abnormalities such as fresh and old ischemic infarctions and hemorrhages.