Abstract

Coolen et al.1 published valuable research exploring the existence of structural brain abnormalities by MRI studies in nonsurvivors of COVID-19. They described cortico-subcortical edematous changes suggestive of posterior reversible encephalopathy syndrome (PRES) in 1 decedent. The most accepted theory of PRES is a loss of autoregulation in cerebral blood flow—usually associated with hypertension or arterial pressure fluctuations, with a subsequent increase in vascular permeability and leakage of blood plasma and erythrocytes—producing vasogenic edema. Other theories have been proposed in the pathogenesis of PRES, but they all lead to activation and injury of the endothelium, stimulation of the immune system, and release of cytokines.2,3 SARS-CoV-2 neurotropism has been recently supported.4,5 Its invasion of the CNS is usually responsible of cytokine storms, leading to endothelium dysfunction,1,2 which might trigger the necessary pathophysiology mechanisms for PRES appearance. The patient described by Coolen et al. did not show arterial pressure abnormalities, and then, the direct virus invasion to the brain seems to be the mechanism involved in this patient. PRES pathophysiology is directly related to the posterior circulation of the brain. The posterior cerebral artery also offers blood supply to a large portion of the thalamus and the upper brainstem.1-3 As this is a reversible syndrome, the possibility of the occurrence of endothelial dysfunction in the rest of the brainstem—affecting the respiratory centers—cannot be excluded. I discussed that SARS-CoV-2 infection might partially explain the acute respiratory distress syndrome refractory to treatments, commonly found in this pandemic.5

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