SARS‐CoV‐2‐related polyradiculitis must be preceded by PCR‐confirmed COVID‐19

Abstract

We read with interest the article by Pourbahtyaran et al. about a prospective study on seven pediatric patients with SARS-CoV-2-associated Guillain Barre syndrome (GBS) recruited between March 2020 and August 2021 in a single Iranian center.1 These patients were compared with 15 GBS patients who were negative for SARS-CoV-2 mRNA as well as antibodies recruited during the same period.1 It was found that the prevalence of GBS did not increase during the pandemic compared with previous years but that the outcome of SARS-CoV-2-related GBS was worse compared with non-COVID-related GBS.1 The study is appealing but carries limitations that raise concerns and should be discussed. The main limitation of the study is that SARS-CoV-2 infection was diagnosed in six patients with SARS-CoV-2-related GBS only by determination of antibodies against SARS-CoV-2.1 It was not communicated whether these antibodies were of the IgG or IgM subtype.1 It was also not discussed that these antibodies can persist for months, why establishing a causal relationship between SARS-CoV-2 infection and GBS is not reliable in these six patients. They should be excluded from the evaluation. Given the fact that the latency between the onset of infection and the onset of neurological manifestations ranged between 2 and 30 days, it is surprising that only one-seventh of patients was PCR-positive for SARS-CoV-2.1 A second limitation of the study is that no information about the cerebrospinal fluid (CSF) findings was provided.1 GBS is usually diagnosed according to the Brighton criteria2 and for level 1 diagnosis of GBS it is mandatory that patients have typical CSF findings. We should be told how many of the seven patients with SARS-CoV-2-related GBS had dissociation-cyto-albuminique and how many did not show this abnormality. Furthermore, CSF can be examined for cytokines, chemokines, glial factors, and 14-3-3, which have been shown elevated in patients with neuro-COVID.3 We disagree with the conclusion that the prevalence of GBS did not increase during the pandemic. First, the number of patients is too small to draw such conclusions. Strictly speaking, only a single patient had SARS-CoV-2-related GBS. In the remaining patients, the acute SARS-CoV-2 infection remained unconfirmed. Second, the pandemic is ongoing and thus lasts more than 3 years. To compare prepandemic prevalences with those during the pandemic patients from the entire pandemic period should be recruited. Third, the pre-COVID period with which COVID patients were compared with is not mentioned. Because GBS prevalences may have undulated in the pre-COVID era, it is crucial to know the exact time of recruitment. Regarding the 15 years old female with lupus erythematosus, we should know about her long-term immunosuppressive treatment. Immuno-suppressed patients are more susceptible to infectious diseases, and since she was SARS-CoV-2 negative, another pathogen is more likely to be the cause. Overall, the interesting study has limitations that call the results and their interpretation into question. SARS-CoV-2-related GBS should only be diagnosed in patients with a PCR-confirmed SARS-CoV-2 infection time linked with the onset of GBS. JF: design, literature search, discussion, first draft, critical comments, final approval. None. No funding was received. The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors. All data are available from the corresponding author.