With interest we read the article by Scheidl et al. about a 54 years-old female with non-symptomatic COVID-19 who experienced Guillain Barre syndrome (GBS), subtype acute, inflammatory, demyelinating neuropathy (AIDP) three weeks after having been tested positive for SARS-CoV-2 and two weeks after onset of typical manifestations of the viral infection [1]. The cerebrospinal fluid (CSF) was negative for SARS-CoV-2 and the patient significantly improved upon administration of intravenous immunoglobulins (IVIG) [1] We have the following comments and concerns.

We do not agree with the notion that CVOID-19 associated GBS is rare [1]. In a recent review 62 patients as per 12^th of August with SARS-CoV-2 associated GBS have been described [2]. As per the end of December 2020 >160 patients with SARS-CoV- associated GBS have been published, suggesting that SARS-CoV-2 associated GBS is not so infrequent as stated in the review.

We do not agree with the statement the SARS-CoV-2 enters the central nervus system (CNS) only via the nose and the olfactory nerve [1]. There is evidence that SARS-CoV-2 can disrupt the blood brain barrier (BBB) and thus enters the brain via the hematogenic pathway [3i]. Whether there are additional routes via which the virus reaches the CNS remains speculative. 

Though we agree that the majority of patients with SARS-CoV-2 associated GBS develops the AIDP subtype, an increasing number of patients with the axonal subtype (acute, motor, axonal neuropathy (AMAN)) has been published [2,4]. There are also a number of patients who developed Miller-Fisher syndrome or isolated mononeuropathy of the oculomotor, trochlear, facial or glossopharyngeal cranial nerves [5].

We do not agree that SARS-CoV-2 associated GBS develops 5-10 days after onset of the viral infection [1]. The range is much broader and there are even cases, in which GBS preceded the onset of the viral infection [2]. Even the patient described by Scheidl et al. developed with a latency of 14d after the first COVID-19 symptoms (loss of smell and taste). In case GBS develops prior to the onset of COVID-19 it is quite likely that patients were only subclinically infected and that GBS was the initial clinical manifestation.

There is a discrepancy between the description of the patient with paraparesis, reduced tendon reflexes and numbness and tingling of all four extremities and the description that “the general physical examination was normal” [1]. We should know if there were progressive muscle weakness and sensory disturbances or not.   

In conclusion, the case of a patient with SARS-CoV-2 associated GBS described by Scheidl et al. is quite usual. Contrary to what is stated in the review, the frequency of SARS-CoV-2 associated GBS is higher than anticipated, the virus enters the CNS via the hematogenic route, the latency between onset of COVID-19 and onset of GBS is highly variable and several subtypes of GBS are increasingly acknowledged. Missing is the investigation for virus-RNA in the CSF but there are indications that in most of the cases of SARS-CoV-2 associated GBS the CSF is free of virus RNA, suggesting that SARS-CoV-2 associated GBS is indeed due to the immune reaction against the virus but not due to a direct viral attack.