key: cord-0822223-fafi0iut
authors: Finsterer, J.; Scorza, FA.; Fiorini, AC.
title: SARS‐CoV‐2 associated Guillain‐Barre syndrome in 62 patients
date: 2020-09-25
journal: Eur J Neurol
DOI: 10.1111/ene.14544
sha: 436334687b4287638ebea23eb875fe3fcddf6b15
doc_id: 822223
cord_uid: fafi0iut

With interest we read the review article by De Sanctis et al. about 18 patients with Guillain‐Barre syndrome (GBS) associated with the SARS‐CoV‐2 infection (COVID‐19) [1]. Acute, inflammatory, demyelinating polyneuropathy (AIDP) was the most frequent subtype of GBS. We have the following comments and concerns.

. Acute, inflammatory, demyelinating polyneuropathy (AIDP) was the most frequent subtype of GBS. We have the following comments and concerns. Only 2 patients died.

The authors regard SARS-CoV-2 as causative for GBS in the 18 included patients. However, a proof for this speculation was not provided. They

This article is protected by copyright. All rights reserved reported that the cerebro-spinal fluid (CSF) was negative for the virus in all included cases. Immunological parameters (cytokines, lymphocyte counts and specification) were provided only in one paper [2] .

A further argument against a causal relation between the virus and GBS is that in four cases clinical manifestations of GBS started before clinical manifestations of the viral infection (table 1) . However, it cannot be excluded that in these cases the viral infection remained subclinical for several days prior to onset of clinical manifestations.

A further argument against a causal relation between SARS-CoV-2 and GBS is that the overall prevalence of GBS did not increase since the outbreak of the pandemic, as was the case with Zika. During the Zika endemic the prevalence of GBS dramatically increased [3] . Thus, other triggering factors for GBS in COVID-19 patients should be considered.

Frequently, it is not easy to differentiate between concomitant disease and a dominating other disease as may be the case in COVID-19 patients.

Whether hypogeusia/hyposmia, frequently observed in COVID-19 patients, is due to radiculitis of the 7 th , 9 th , and 10 th cranial nerve, remains speculative. Considering hypogeusia/hyposmia as a manifestation of a radiculitis, the prevalence of GBS would dramatically increase, as 5.1-85% of the COVID-19 patients report hypogeusia/hyposmia [4] .

Prolonged latency and reduced compound muscle action potential on nerve conduction studies of the facial nerve argues in favour of polyradiculitis [5] .

Overall, the interesting review lacks inclusions of a number of SARS-CoV-infected patients with GBS. Furthermore, a causal relation between SARS-CoV-2 and GBS remains unproven. Whether the immune-reaction against SARS-CioV-2 triggers the development of GBS requires further investigations. 

Guillain Barré Syndrome associated with SARS-CoV-2 infection. A Systematic Review

COVID-19 polyradiculitis in 24 patients without SARS-CoV-2 in the cerebro-spinal fluid

Prevalence of Guillain-Barré syndrome among Zika virus infected cases: a systematic review and meta-analysis

Anosmia and ageusia associated with coronavirus infection (COVID-19) -what is known

Clinical neurophysiology and cerebrospinal liquor analysis to detect Guillain-Barré syndrome and polyneuritis cranialis in COVID-19 patients: A case series

Accepted Article