srjcmsSRJCMSSRJCMS2788-8851https://doi.org/10.47310/srjcms.2022.v02i01.024Before SARS-Cov-2 Is Held Responsible For a Guillain-Barre Syndrome, Alternative Causes Must Be Ruled OutJosefFinstererWe read with interest the article by Taguchi et al. about a 70 years-old female who developed Guillain-Barre syndrome (GBS) two months after onset of a mild SARS-CoV-2 infection [1]. Her history was conspicuous for left carotid endarterectomy, infliximab-treated rheumatoid arthritis, thyroid carcinoma, and apixaban-treated atrial fibrillation [1]. After the second cycle of intravenous immunoglobulins (IVIGs) the patient’s mental status deteriorated and she developed unilateral facial palsy [1]. She partially recovered only after plasmapheresis therapy [1]. It was concluded that SARS-CoV-2 can trigger GBS even two months after onset of the viral infection [1]. The study is appealing but raises concerns that need to be discussed. We disagree that there is a causal relationship between the COVID-19 infection and GBS. In a study of 220 patients with SARS-CoV-2 associated GBS the latency period between viral infection and the onset of GBS was <5 weeks in the vast majority of cases [2]. Furthermore, no increased cytokines (interleukin (IL)-6, IL-8, IL-1a, TNF-alpha) were detected in the cerebrospinal fluid (CSF), as previously shown in patients with SARS-CoV-2 associated GBS [3]. We do not agree that the patient had posterior reversible encephalopathy syndrome (PRES) [1]. PRES is usually associated with arterial hypertension and visual disturbances [4] and only rarely with GBS. However, the patient was not diagnosed with high blood pressure [1]. Another argument against PRES is the disappearance of the cerebral lesion with plasmaphereses. PRES usually resolves after blood pressure values have returned to normal. The beneficial effect of plasmapheresis suggests an immunological rather than a non-immunological cause of the lesions. Another argument against PRES is that the combination of PRES and GBS has rarely been reported.  The patient received the last infliximab injection one month before the onset of her COVID-19 infection [1]. It should be discussed to what extent immunosuppression with infliximab favoured the development of the SARS-CoV-2 infection, since infliximab can attenuate the anti-SARS-CoV-2 antibody response [5].  The altered mental state of the patient is not adequately explained. The patient obviously had hypothyroidism [1]. It should be discussed whether the cerebral lesion is due to hypothyroid (Hashimoto) encephalopathy as previously reported. Since IVIGs do not usually cause encephalopathy, hypothyroidism should be considered as the cause of the psychological change.  In order to diagnose AMSAN it is crucial to detect the axon loss not only in motor but also in sensory fibers. It should be reported in which sensory nerves the amplitude of the sensory nerve action potentials was reduced. Since SARS-CoV-2 infections can be complicated by ischemic stroke, we should be informed about the presentation of the lesion on diffusion weighted imaging (DWI) and apparent diffusion coefficient (ADC) sequences in cerebral MRI.  A sufficient explanation of the elevated creatine-kinase (CK) is lacking. CK elevation could also be due to muscle toxic drugs the patient was taking for COVID-19, such as chloroquine. To   that end, it is important to know what medication she was currently taking in order to be able to assess whether one of the medications she was taking regularly or used during her hospital stay was causative. CK elevation could also be due to rheumatoid arthritis if accompanied by polymyositis, rhabdomyolysis, or due to ischemic stroke. Overall, the interesting study has limitations that call into question the results and their interpretation. The long latency between COVID-19 and GBS argues against a causal relationship. Alternative causes could be a delayed side effect of infliximab, another subclinical infection, or a vaccination.