SARS-CoV-2 could pass the blood-brain barrier (BBB) because inflammatory cytokines induce BBB instability or via monocytes.

SARS-CoV-2 is known to penetrate the olfactory mucosa, causing loss of smell, and may enter the brain, migrating from the cribriform plate along the olfactory tract 2 or through vagal or trigeminal pathways however, definitive evidence for this is lacking. These insults induce new-onset or re-exacerbation of preexisting NPs.

Moreover, systemic inflammation leads to decreased monoamines and trophic factors and activation of microglia, resulting in increased glutamate and N-methyl- d-aspartate (NMDA) 3 and excitotoxicity ( Figure). Follow-ups conducted in Germany and the United Kingdom found post–COVID-19 NPs in 20% to 70% of patients, even in young adults, and lasting months after respiratory symptoms resolved, 1 suggesting brain involvement persists.Įntering through angiotensin-converting enzyme 2 receptors, 2 SARS-CoV-2 can damage endothelial cells leading to inflammation, thrombi, and brain damage. 1, 2 These present before, during, and after respiratory symptoms and are unrelated to respiratory insufficiency, 1 suggesting independent brain damage. Some patients present with anosmia, cognitive and attention deficits (ie, brain fog), new-onset anxiety, depression, psychosis, seizures, and even suicidal behavior. Respiratory and gastrointestinal symptoms are accompanied by short- and long-term neuropsychiatric symptoms (NPs) and long-term brain sequelae. Shared Decision Making and CommunicationĬOVID-19 has resulted in more than 120 million cases and 2.6 million deaths to date.Scientific Discovery and the Future of Medicine.

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