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

Area of Science:

• Neuroscience
• Infectious Diseases
• Medical Imaging

Background:

• SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection has been linked to various neurological complications.
• Speculation exists regarding the virus's neurotropism and its potential to trigger delayed neuroinflammatory and neurodegenerative conditions.
• A proposed mechanism involves viral entry via the olfactory pathway, potentially spreading to deeper brain structures.

Observation:

• This study examined two patients diagnosed with SARS-CoV-2 at the post-viral stage using clinical evaluation and whole-brain 18F-FDG PET metabolism analysis.
• Compared to healthy subjects, both patients exhibited hypometabolism in specific brain regions.

Findings:

• One patient with prolonged anosmia showed hypometabolism in the olfactory/rectus gyrus.
• The second patient, experiencing a delayed painful syndrome, displayed additional hypometabolism in the amygdala, hippocampus, cingulate cortex, thalamus, cerebellum, pons, and medulla.
• These findings support the hypothesis of SARS-CoV-2 neurotropism via the olfactory bulb and subsequent spread to other brain areas.

Implications:

• 18F-FDG PET hypometabolism may serve as a quantitative biomarker for SARS-CoV-2-related brain involvement.
• Further cohort studies are necessary to elucidate the precise relationship between these metabolic changes and persistent post-viral disorders, including cognitive, emotional, or pain-related symptoms.