LAUSR

We read with interest the article by El Mezzeoui et al. about a previously healthy three years-old female who developed progressive sensory disturbances followed by muscle weakness initially of the lower limbs which progressively ascended to the upper limbs two weeks after an upper respiratory tract infection [1]. Muscle weakness did not include the respiratory muscles but was associated with dysphagia [1]. Guillain-Barre syndrome (GBS) was diagnosed after exclusion of differentials by means of a cerebral MRI and intravenous immunoglobulins (IVIG) were started with a beneficial effect, resulting in complete recovery within four weeks of hospitalisation [1]. The study is appealing but raises concerns that need to be discussed. We do not agree that only few studies investigated the relation between SARS-CoV-2 infections and neurological manifestations in the paediatric population [1]. Several retrospective, observational studies about the type, degree, treatment, and outcome of neurological compromise in children are meanwhile available [2,3]. We do not agree that GBS in the index patient was due to SARS-CoV-2 as pretended [1]. The patient was never tested positive for the virus by means of a PCR Furthermore, various differentials of SARS-CoV-2 as the cause of GBS, such as infections with campylobacter jejunii, influenza-A hemophilus influenza, mycoplasma pneumoniae, cytomegaly virus, Zika, and Epstein-Barr virus were not appropriately excluded. GBS is usually diagnosed according to the Brighton, Besta, Ashford, or Hadden criteria [4]. Application of any of these diagnostic criteria includes the implementation of nerve conduction studies (NCSs) and investigations of the cerebro-spinal fluid (CSF). NCSs allow the classification of GBS into a demyelinating (acute, inflammatory demyelinating polyneuropathy (AIDP)) and axonal subtype (acute, motor, axonal neuropathy (AMAN), acute, motor and sensory, axonal neuropathy (AMSAN)). Differentiating between AIDP and AMAN respectively AMSAN is crucial as the treatment and outcome may vary between these two subtypes. CSF investigations are essential not only for demonstrating a dissociation between normal cell count and elevated CSF protein but also to exclude various differentials, such as encephalitis, immune encephalitis, acute, disseminated encephalomyelitis (ADEM), or other demyelinating disorders. CFS studies in patients with SARS-CoV-2 associated GBS have shown that cytokines, chemokines, or glial factors can be elevated in the CSF [5]. Upregulation of interleukin (IL)-6, IL-8, OL-1b, or tumour necrosis factor (TNF) alpha suggest an infection with SARS-CoV-2 as the cause of the neurological abnormalities. The CSF can be also investigated for the presence or absence of SARS-CoV-2 virus RNA. We should know the results of CSF investigations for virus-RNA and IL levels. Missing is an explanation of dysphagia. Missing are the reference limits. Overall, the interesting study has several limitations which challenge the results and their interpretation. The diagnostic criteria upon which GBS was diagnosed were not mentioned and the patient did not undergo NCS. Various differential causes of GBS were not appropriately excluded. A causal relation between SARS-CoV-2 and GBS remained unproven.