text:  sup 18 sup F FDG brain PET hypometabolism in post SARS CoV 2 infection substrate for persistent delayed disorders 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 Review of clinical examination and whole brain voxel based analysis of sup 18 sup F FDG PET metabolism in comparison with healthy subjects p voxel 0 001 p cluster 0 05 uncorrected of two patients with confirmed diagnosis of SARS CoV 2 explored at the post viral stage of the disease Hypometabolism of the olfactory rectus gyrus was found on the two patients especially one with 4 week prolonged anosmia Additional hypometabolisms were found within amygdala hippocampus parahippocampus cingulate cortex pre post central gyrus thalamus hypothalamus cerebellum pons and medulla in the other patient who complained of delayed onset of a painful syndrome These preliminary findings reinforce the hypotheses of SARS CoV 2 neurotropism through the olfactory bulb and the possible extension of this impairment to other brain structures sup 18 sup F FDG PET hypometabolism could constitute a cerebral quantitative biomarker of this involvement Post viral cohort studies are required to specify the exact relationship between such hypometabolisms and the possible persistent disorders especially involving cognitive or emotion disturbances residual respiratory symptoms or painful complaints 