In all (n = 72) but four patients [10, 37, 40, 56], GBS manifestations developed after those of COVID-19 [median (IQR): 14 (7–20), min 2–max 33 days]. Differently, COVID-19 symptoms began concurrent in one case [37], 1 day [40] and 8 days [55] after GBS onset in two other cases and never developed in another one [10] (Table 1). Common clinical manifestations at onset included sensory symptoms (72.2%, 52/72) alone or in combination with paraparesis or tetraparesis (65.2%, 47/72, respectively). Cranial nerve involvement (e.g., facial, oculomotor nerves) was less frequently described at onset (16.7%, 12/72). Moreover, all cases but one [26] showed lower limbs or generalized areflexia, whereas in 37.5% (27/72) of the cases, gait ataxia was reported at onset or during the disease course. Even if ascending weakness evolving into flaccid tetraparesis (76.4%, 55/72) and spreading/persistence of sensory symptoms (84.7%, 61/72) represented the most common clinical evolutions, 50.0% (36/72) and 23.6% (17/72) patients showed cranial nerve deficits and dysphagia, respectively, during disease course (Table 1). Moreover, 36.1% (26/72) of the patients developed respiratory symptoms, and some of them evolved to respiratory failure (Table 1). Autonomic disturbances were rarely reported (16.7%, 12/72). In cases with MFS/MFS-GBS overlap, areflexia, oculomotor disturbances, and ataxia were present in 100% (9/9), 66.7% (6/9) and 66.7% (6/9), respectively [8, 19, 23, 30, 32, 33, 43, 44]. The median of time to nadir was calculated in 40 patients with available data and resulted 4 days (IQR 3–9) (Table 1).