iarjcrIARJCRIARJCR2789-6064https://doi.org/10.47310/iarjcr.2022.v01i01.008Is the Outcome of Sars-Cov-2 Associated Guillain-Barre Syndrome at Variance Between Rich and Poor?JosefFinstererNeurology and Neurophysiology Center, Vienna, AustriaWe read with interest the article by Nigatu et al. about a 70 years old male who developed quadruparesis and respiratory failure requiring intubation and mechanical ventilation one week after onset of mild COVID-19 [1]. The patient was tested positive for SARS-CoV-2 and diagnosed with Guillain-Barre syndrome (GBS) based upon the clinical presentation, nerve conduction studies (NCSs) and cerebrospinal fluid (CSF) investigations [1]. The patient was treated with glucocorticoids and achieved an incomplete recovery at the last follow-up three weeks after admission [1]. It was concluded that early identification and management of SARS-CoV-2 associated GBS (SC2aG) can improve the clinical outcome and that screening for SARS-CoV-2 in patients presenting with GBS is warranted. The study is appealing but raises concerns that need to be discussed. We disagree with the notion that since the outbreak of the SARS-CoV-2 pandemic “some case reports of COVID-19 associated GBS” have been published [1]. As per the end of December 2020, at least 220 patients with SARS-CoV-2 associated GBS (SC2aG) have been reported [2]. As per the end of 2021 at least 400 patients with SC2aG have been published (Finsterer, submitted). The patient was diagnosed with GBS subtype acute, motor and sensory, axonal neuropathy (AMSAN) [1]. However, distal latencies were prolonged, nerve conduction velocities reduced, particularly in the lower limbs, and F-wave latencies were prolonged, suggesting demyelination. We should be told why the patient was diagnosed with AMSAN and not with acute, inflammatory, demyelinating, polyneuropathy (AIDP) or mixed axonal and demyelinating polyneuropathy.  Since AMSAN can be associated with autonomic dysfunction due to affection of the peripheral autonomic nervous system (ANS), we should know if the index patient manifested with involvement of the ANS. Even AMSAN patients with severe pulmonary hypertension have been reported [3]. The patient had elevated liver transaminases, which were attributed involvement of the liver in COVID-19 [1]. However, the patient also had received antibiotics [1]. We should be told when liver function parameters normalised again and if transaminases normalised with discontinuation of the antibiotics. Since COVID-19 can be complicated by autoimmune hepatitis [4], we should know how immune hepatitis was excluded as the cause of liver transaminases.