srjcmsSRJCMSSRJCMS2788-8851https://doi.org/10.47310/srjcms.2022.v02i01.021SARS-CoV-2 associated Guillain-Barre syndrome occurs globallyJosefFinstererDanielMatovuWe eagerly read the article by Kajita et al. about a 60yo female who developed dysgeusia and hyposmia 6 days after a positive PCR test for SARS-CoV-2 [1]. Ten days after the test she experienced coughing with sputum being treated with appropriate antibiotics [1]. By day 15 after the positive test, she additionally developed numbness of the upper limbs, lower limb weakness, and dyspnoea [1]. By day 24 after the test, she was no longer able to stand and additionally complained about dysphagia, and bifacial palsy [1]. Guillain-Barre syndrome (GBS) was diagnosed and the patient profited from intravenous immunoglobulins (IVIG) [1]. The study is appealing but raises the following comments and concerns. There is a contradiction between the clinical presentation on admission describing bilateral peripheral facial palsy and the clinical neurologic exam on admission revealing “intact cranial nerves” [1]. It should be clarified if there was indeed bilateral facial palsy or not on admission. The second discrepancy refers to dysphagia on admission but unaffected cranial nerves on clinical exam [1]. We should be told if dysphagia was explained by affection of cranial nerves IX and X or by involvement of the brainstem. Did the patient ever undergo central nervous system (CNS) imaging to assess if she had Bickerstaff encephalitis or a supra-tentorial lesion that could explain dysphagia? Another discrepancy refers to the stocking-type sensory disturbances the patient was referred for. Surprisingly, nerve conduction studies (NCSs) of the sural nerves were normal regarding the sensory nerve action potential amplitude and the nerve conduction velocity. Again, it should be excluded that the sensory disturbances were due to a CNS lesion, either on the spinal level or the cerebral level.  Results of NCSs were interpreted as demyelinating [1]. However, compound muscle action potential amplitude of the right median nerve, both tibial nerves, and the sensory nerve action potential amplitude of the right median nerve were reduced suggesting rather an axonal than a demyelinating lesion. We should know if GBS was classified as acute, demyelinating, inflammatory polyneuropathy (AIDP) or as acute, motor and sensory, axonal neuropathy (AMSAN). We do not agree with the statement that the prevalence and incidence of patients with SARS-CoV-2 associated GBS is higher in Europe than anywhere else [1]. No systematic studies about the global prevalence and incidence of SARS-CoV-2 associated GBS (SC2aG) are available. The number of European patients with SC2aG reported in the literatures may be higher than those from other countries, presumably due to the high prevalence of COVID-19 in countries like the UK, Italy, and Spain during the first year of the pandemic [2,3]. This falsely gives the impression that the prevalence of SC2aG is higher than outside Europe. However, SC2aG has been reported from all over the world [4], suggesting that SC2aG occurs globally.       It is not comprehensible why it took 24 days before the patient was seen by a neurologist. Was this prolonged delay between onset of neurological manifestations and the neurological work-up attributable to the patient’s own decision or did the neurological abnormalities remain unrecognised by the treating physicians during this period? Overall, the interesting study has several limitations that should be addressed before drawing definite conclusions. All inconsistencies should be eliminated and all contradictions should be resolved. This will strengthen the results and conclusions and can contribute to the understanding of SC2aG.