Clinical and Paraclinical Findings
| Time (d) | Main symptoms/diagnostic tests | Pathogenetic/diagnostic perspectives |
|---|---|---|
| 0 | Systemic and respiratory symptoms; positive swab analysis for SARS-CoV-2 RNA; positive chest CT scan for interstitial pneumonitis | SARS-CoV-2 infection |
| 14–16 | Neurologic features (confusion, agitation); normal MRI; normal cellularity and protein content in CSF | Indirect neurologic effects of systemic disease? |
| 15–16 | Neurologic features (seizures); slow electroencephalogram with epileptiform discharges; CSF reverse-transcriptase polymerase chain reaction negativity for SARS-CoV-2 but positivity for anti-SARS-CoV-2 antibodies | Direct brain involvement? |
| 15 | Negative CSF analysis for neurotropic viruses (herpes simplex-1, herpes simplex-2, human herpes virus-6, varicella-zoster, Epstein-Barr, cytomegalovirus); negative search for antibodies directed against intracellular onconeural (Ma1, Ma2, Hu, Ri, Yo, CV2) or cell surface/synaptic antigens (N-methyl-d-aspartate receptor, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor, γ-aminobutyric acid-A receptor, γ-aminobutyric acid-B receptor, contactin-associated proteinlike 2, leucin-rich glioma inactivated 1) | Exclusion of common infectious or paraneoplastic/autoimmune CNS disorders |
| 38 | Limbic and extralimbic hypermetabolism on 18F-FDG PET | Likely direct brain involvement |
| 82 | Neurologic features (parkinsonism); CSF positivity for anti–basal ganglia antibodies | Direct brain involvement of likely immune-mediated etiology |
| 143 | Post-IVIg normalization of metabolism on 18F-FDG PET | Full recovery after immune-modulatory treatment, further supporting hypothesis of immune-mediated etiology |