18F-FDG brain PET hypometabolism in post-SARS-CoV-2 infection: substrate for persistent/delayed disorders?

Purpose Several brain complications of SARS-CoV-2 infection have been reported. It has been moreover speculated that this neurotropism could potentially cause a delayed outbreak of neuropsychiatric and neurodegenerative diseases of neuroinflammatory origin. A propagation mechanism has been proposed...

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Veröffentlicht in:	European journal of nuclear medicine and molecular imaging 2021-02, Vol.48 (2), p.592-595
Hauptverfasser:	Guedj, E, Million, M, Dudouet, P, Tissot-Dupont, H, Bregeon, F, Cammilleri, S, Raoult, D
Format:	Artikel
Sprache:	eng
Schlagworte:	Amygdala Anosmia Biomarkers Brain Brain stem Cardiology Cerebellum Cognitive ability Cortex (cingulate) Disorders Epithelium Human health and pathology Hypometabolism Hypothalamus Imaging Inflammation Life Sciences Medicine Medicine & Public Health Medulla oblongata Mental disorders Neurodegenerative diseases Neurology Neurotropism Nuclear Medicine Olfaction disorders Olfactory bulb Olfactory epithelium Oncology Orthopedics Parahippocampal gyrus Pons Positron emission tomography Radiology Severe acute respiratory syndrome coronavirus 2 Short Communication Signs and symptoms Smell Substrates Thalamus Viral diseases
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Zusammenfassung:	Purpose Several brain complications of SARS-CoV-2 infection have been reported. It has been moreover speculated that this neurotropism could potentially cause a delayed outbreak of neuropsychiatric and neurodegenerative diseases of neuroinflammatory origin. A propagation mechanism has been proposed across the cribriform plate of the ethmoid bone, from the nose to the olfactory epithelium, and possibly afterward to other limbic structures, and deeper parts of the brain including the brainstem. Methods Review of clinical examination, and whole-brain voxel-based analysis of 18 F-FDG PET metabolism in comparison with healthy subjects ( p voxel
ISSN:	1619-7070 1619-7089
DOI:	10.1007/s00259-020-04973-x