We eagerly read the article by Poisson et al. about a SARS-CoV-2 positive 8yo female, who was diagnosed with cerebral vasculitis upon two brain biopsies [1]. Since IgM antibodies against SARS-CoV-2 were positive in the cerebro-spinal fluid (CSF), vasculitis was attributed to COVID-19 [1]. The study is appealing but raises concerns which require discussion. The condition presented in the case report could be also interpreted as acute, haemorrhagic, necrotising encephalitis (AHNE). This condition has been recently described in an adult patient with tuberculosis and COVID-19 [2]. Thus, it is crucial that cerebral tuberculosis had been excluded by culture, immune-histology, and PCR in the CSF and the brain tissue at autopsy. Cerebral tuberculosis is accompanied by cerebral vasculitis in a quarter of the cases [3]. Unfortunately, only serum antibodies against mycobacterium tuberculosis had been determined in the index patient. Missing are the results of conventional digital subtraction angiography (DSA), computed tomography angiography (CTA), or magnetic resonance angiography (MRA) to confirm the histological diagnosis. Vascular imaging may not only help to confirm the histological diagnosis but also to delineate between vasculitis of large, medium-sized, or small arteries. 

We do not agree with the notion that neuro-COVID only includes stroke, venous sinus thrombosis (VST), seizures, meningitis, encephalitis, ADEM, acute fulminant cerebral edema, posterior reversible encephalopathy syndrome (PRES), headache, myelitis, Guillain-Barre syndrome (GBS), cranial neuropathies, and myositis. The spectrum of neuro-COVID is much broader and additionally includes reversible cerebral vasoconstriction syndrome (RCVS), acute, haemorrhagic, necrotising encephalitis (AHNE), hypophysitis, cerebellitis, myoclonus syndrome, immune encephalitis, multiple sclerosis, neuromyelitis optica spectrum disorder, ventriculitis, pontine myelinolysis, subarachnoid bleeding, Wernicke encephalopathy, insomnia, psychosis, myasthenia, and myasthenic syndrome.

Overall, the elegant study has limitations which challenge the results and their interpretation. Cerebral tuberculosis should be excluded by appropriate means. 

We read with interest the article by Murawska-Baptista et al. about a 71 years old male who developed respiratory distress due to severe COVID-19 requiring a high-flow nasal canula (HFNC) [1]. His past medical history was positive for arterial hypertension, hyperlipidemia, atrial fibrillation, ablation therapy, obstructive sleep apnea, and Guillain-Barre Syndrome (GBS) following an influenza vaccination, from which he recovered completely [1]. The patient recovered from COVID-19 under remdesivir and steroids [1]. The study is appealing but raises concerns that require discussion. Whether patients with a previous history of GBS are prone to experience a relapse of GBS during a SARS-CoV-2 infection is unknown but there are indications that patients with a previous history of demyelinating neuropathy have an increased risk to experience neuro-immunologic complications. The risk of experiencing a SARS-CoV-2 infection associated GBS may be particularly increased among those with clinical recovery but electrophysioloic evidence of persisting neuropathy. 

The patient presented with progressing respiratory failure despite treatment with remdesivir and steroids but it is unclear if worsening of respiratory insufficiency was due to COVID-19 pneumonia or due to exacerbation of GBS predominantly affecting the respiratory muscles. We should be told if the patient was seen by a neurologist and if there were any indications for relapse of the GBS. GBS is a well-known neurological complication of SARS-CoV-2 infection and has been reported in >400 patients as per the end of June 2021 [2, Finsterer, submitted]. 

We disagree with the statement that GBS following a SARS-CoV-2 vaccination is a rare complication of SARS-CoV-2 vaccinations [1]. Looking at table 1 of the index study it clearly indicated that >500 patients with post-SARS-CoV-2 vaccination GBS have been reported as per the end of December 2021 [1]. Assuming that most cases of SARS-CoV-2 vaccination associated GBS are never published or reported to a database, it is conceivable that the real-world prevalence of SARS-CoV-2 vaccination associated GBS is much higher than anticipated. 

We do not agree with the classification of the vaccine in the patient with SARS-CoV-2 vaccination associated GBS reported by Finsterer as “unknown” [3]. The patient developed GBS eight days after the first dose of a vector-based vaccine (Astra-Zeneca vaccine (AZV)) [1]. 

Overall, the interesting study has some limitations which challenge the results and their interpretation. Addressing these limitations may upvalue the conclusions. Patients with a previous history of GBS should not undergo vaccination for SARS-CoV-2 if there was only clinical but not electrophysiological recovery.