In our population, most common clinical manifestations and distribution of clinical variants resemble those of classic GBS confirming the predominance of the sensorimotor syndrome compared to MFS and other rare variants [57–59, 66]. Similarly, the results of CSF analysis reflected typical neurochemical findings in non-COVID-19 GBS. In the latter, elevated CSF proteins and pleocytosis were described in about 50–80% [57, 78] and 11–15% cases, respectively [58, 79, 80], largely overlapping with the percentages in our cohort. In this regard, the mostly normal cell count, together with the absence of SARS-CoV-2 RNA in all tested CSF samples [6–9, 12–14, 16, 21–24, 31, 33, 36, 42, 44, 52, 55], makes the possibility of a direct invasion from SARS-CoV-2 into the nerve roots with intrathecal viral replication less probable. However, a possible bias might rely on the lack of systematic data concerning the latency between symptom onset and CSF sampling in COVID-19 GBS cases. On another issue, in a further case of MFS associated withCOVID-19, who came to our attention, we observed the absence of intrathecal synthesis of SARS-CoV-2 antibodies together with a massive increase of CSF phosphorylated neurofilament heavy chain (pNfH) and serum neurofilament light chain (NfL) proteins, supporting the role of neurochemical markers as easily implementable tools for the detection of nervous system affection in COVID-19-related diseases [81, 82].