SARS‐CoV‐2–associated Guillain‐Barre syndrome in 62 patients

Abstract

We read with interest 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. The number of patients experiencing GBS in the context of COVID-19 is much higher than reported by De Sanctis et al. Currently (12 August 2020), at least 62 COVID-19 patients with polyradiculitis have been reported in 48 articles (Table 1). Ages ranged from 11 to 94 years (Table 1). Twenty patients were female and 36 were male (Table 1). In 58 patients, GBS began after onset of clinical manifestations of COVID-19. Latency between onset of COVID-19 and GBS ranged from 3 to 33 days. Forty-two patients were diagnosed with AIDP, six with acute motor axonal neuropathy, five with Miller-Fisher syndrome and three with acute motor sensory axonal neuropathy. In six patients, the subtype was not specified (Table 1). SARS-CoV-2 in the cerebrospinal fluid (CSF) was detected in none of the patients (Table 1). Fifty patients received intravenous immunoglobulin and eight plasmapheresis (Table 1). Two patients received steroids exclusively (Table 1). Eighteen patients required artificial ventilation (Table 1). Twenty-four patients recovered completely and 23 partially. Only two patients died. The authors regard SARS-CoV-2 as causative for GBS in the 18 included patients. However, proof for this speculation was not provided. They reported that the CSF was negative for the virus in all included cases. Immunological parameters (cytokines, lymphocyte counts and specification) were provided only in one article [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 with GBS in COVID-19 patients. Whether hypogeusia/hyposmia, frequently observed in COVID-19 patients, is due to radiculitis of the seventh, ninth, and tenth cranial nerve remains speculative. Considering hypogeusia/hyposmia as a manifestation of a radiculitis, the prevalence of GBS would dramatically increase, as 5.1% to 85% of the COVID-19 patients reported hypogeusia/hyposmia [4]. Prolonged latency and reduced compound muscle action potentials on nerve conduction studies of the facial nerve argues in favour of polyradiculitis [5]. Overall, this interesting review lacks inclusion 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-CoV-2 triggers the development of GBS requires further investigations. The authors declare no financial or other conflicts of interest.

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