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Acute delirium and other neuropsychiatric symptoms have frequently been reported in COVID-19 patients and are variably referred to as acute encephalopathy, COVID-19 encephalopathy, SARS-CoV-2 encephalitis, or steroid-responsive encephalitis. COVID-19 specific biomarkers of cognitive impairment are currently lacking, but there is some evidence that SARS-CoV-2 could preferentially and directly target the frontal lobes, as suggested by behavioral and dysexecutive symptoms, fronto-temporal hypoperfusion on MRI, EEG slowing in frontal regions, and frontal hypometabolism on 18F-FDG-PET imaging. We suggest that an inflammatory parainfectious process targeting preferentially the frontal lobes (and/or frontal networks) could be the underlying cause of these shared clinical, neurophysiological, and imaging findings in COVID-19 patients. We explore the biological mechanisms and the clinical biomarkers that might underlie such disruption of frontal circuits and highlight the need of standardized diagnostic procedures to be applied when investigating patients with these clinical findings. We also suggest the use of a unique label, to increase comparability across studies.

Original publication

DOI

10.3233/JAD-210008

Type

Journal article

Journal

J Alzheimers Dis

Publication Date

2021

Volume

81

Pages

75 - 81

Keywords

Biomarkers, COVID-19, SARS-CoV-2, delirium, frontal lobe, Acute Febrile Encephalopathy, Biomarkers, COVID-19, Delirium, Electroencephalography, Frontal Lobe, Humans, Magnetic Resonance Imaging, Nerve Net, SARS-CoV-2, Virulence