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.Health Care Economics, Insurance, Payment.Clinical Implications of Basic Neuroscience.Challenges in Clinical Electrocardiography.
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