Background and purpose: The spectrum of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 infection (SARS-CoV-2), includes different neurologic manifestations of the central and peripheral nervous system. Methods: From March through April 2020, in two university hospitals located in western Switzerland, we examined three patients with Guillain-Barr e syndrome (GBS) following SARS-CoV-2. Results: These cases were characterized by a primary demyelinating electrophysiological pattern (Acute inflammatory demyelinating polyneuropathy or AIDP) and a less severe disease course compared to recently published case series. Clinical improvement was observed in all patients at week five. One patient was discharged from hospital after full recovery with persistence of minor neurological signs (areflexia). Two of the three patients remained hospitalized: one was able to walk and the other could stand up with assistance. Conclusions: We report three cases of typical GBS (AIDP) occurring after SARS-CoV-2 infection and presenting with a favourable clinical course. Given the interval between COVID-19-related symptoms and neurological manifestations (mean of 15 days) we postulate a secondary immune-mediated mechanism rather than direct viral damage.

Poor reward sensitivity in stroke patients with damage to the ventral basal ganglia, dorsal thalamus, insula, or prefrontal cortex constitutes a core feature of apathy. These results provide valuable insight into the neural mechanisms and brain substrate underlying apathy.

A 22-year-old male with a typical history of pauci-symptomatic COVID-19 3 weeks earlier, confirmed by positive serology for SARS-CoV-2 (IgG), was admitted to the intensive care unit because of severe myocarditis with refractory cardiogenic shock that required extracorporeal life support. Due to a clinical presentation suggestive of Kawasaki-like disease with coronary aneurysm and severe systemic inflammation, intravenous immunoglobulins were administered in combination with tocilizumab. The initial clinical course was favourable with these treatments. However, the patient subsequently developed a severe mononeuritis multiplex leading to bilateral foot drop, which required intensive immunosuppressive therapy (corticosteroids, cyclophosphamide and rituximab). The clinical presentation meets the criteria for multisystem inflammatory syndrome associated with SARS-CoV-2, but includes very severe organ damages. Early recognition, a multidisciplinary approach and aggressive therapeutic intervention can lead to a favourable outcome.

ObjectiveCoronavirus disease (COVID-19) has been associated with a large variety of neurologic disorders. However, the mechanisms underlying these neurologic complications remain elusive. In this study, we aimed at determining whether neurologic symptoms were caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) direct infection or by either systemic or local proinflammatory mediators.MethodsIn this cross-sectional study, we checked for SARS-CoV-2 RNA by quantitative reverse transcription PCR, SARS-CoV-2–specific antibodies, and 49 cytokines/chemokines/growth factors (by Luminex) in the CSF +/− sera of a cohort of 22 COVID-19 patients with neurologic presentation and 55 neurologic control patients (inflammatory neurologic disorder [IND], noninflammatory neurologic disorder, and MS).ResultsWe detected anti–SARS-CoV-2 immunoglobulin G in patients with severe COVID-19 with signs of intrathecal synthesis for some of them. Of the 4 categories of tested patients, the CSF of IND exhibited the highest level of cytokines, chemokines, and growth factors. By contrast, patients with COVID-19 did not present overall upregulation of inflammatory mediators in the CSF. However, patients with severe COVID-19 (intensive care unit patients) exhibited higher concentrations of CCL2, CXCL8, and vascular endothelium growth factor A (VEGF-A) in the CSF than patients with a milder form of COVID-19. In addition, we could show that intrathecal CXCL8 synthesis was linked to an elevated albumin ratio and correlated with the increase of peripheral inflammation (serum hepatocyte growth factor [HGF] and CXCL10).ConclusionsOur results do not indicate active replication of SARS-CoV-2 in the CSF or signs of massive inflammation in the CSF compartment but highlight a specific impairment of the neurovascular unit linked to intrathecal production of CXCL8.

Lifelong bilingualism is associated with delayed dementia onset, suggesting a protective effect on the brain. Here, we aim to study the effects of lifelong bilingualism as a dichotomous and continuous phenomenon, on brain metabolism and connectivity in individuals with Alzheimer's dementia. Ninety‐eight patients with Alzheimer's dementia (56 monolinguals; 42 bilinguals) from three centers entered the study. All underwent an [18F]‐fluorodeoxyglucose positron emission tomography (PET) imaging session. A language background questionnaire measured the level of language use for conversation and reading. Severity of brain hypometabolism and strength of connectivity of the major neurocognitive networks was compared across monolingual and bilingual individuals, and tested against the frequency of second language life‐long usage. Age, years of education, and MMSE score were included in all above mentioned analyses as nuisance covariates. Cerebral hypometabolism was more severe in bilingual compared to monolingual patients; severity of hypometabolism positively correlated with the degree of second language use. The metabolic connectivity analyses showed increased connectivity in the executive, language, and anterior default mode networks in bilingual compared to monolingual patients. The change in neuronal connectivity was stronger in subjects with higher second language use. All effects were most pronounced in the left cerebral hemisphere. The neuroprotective effects of lifelong bilingualism act both against neurodegenerative processes and through the modulation of brain networks connectivity. These findings highlight the relevance of lifelong bilingualism in brain reserve and compensation, supporting bilingual education and social interventions aimed at usage, and maintenance of two or more languages, including dialects, especially crucial in the elderly people.

Along with the propagation of COVID-19, emerging evidence reveals significant neurological manifestations in severely infected COVID-19 patients. Among these patients admitted to the intensive care unit (ICU), behavioral unresponsiveness may occur frequently, yet, there are still only a few cases reported and with rare descriptions of their motor behavior after pathological awakening. Several hypotheses regarding central lesions in these patients are conceivable. Here, we describe two acute SARS-CoV-2- infected patients who developed neurological symptoms evoking the condition of clinical cognitive motor dissociation (CMD). This diagnosis could be confirmed first by clinical observation of a dissociation between preserved cognitive abilities and lack of initial motor interaction and second, by performing 18F- FDG PET imaging. Accurate diagnosis led to an appropriate neuro-rehabilitation regimen with long-term neuro-rehabilitation leading to an improved outcome for both patients.

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Objective: Coronavirus disease (COVID-19) has been associated with a large variety of neurological disorders. However the mechanisms underlying these neurological complications remain elusive. In this study we aimed at determining whether neurological symptoms were caused by SARS-CoV-2 direct infection of by pro-inflammatory mediators. Methods: We checked for SARS-CoV-2 RNA by RT-qPCR, SARS-CoV-2-specific antibodies and for 48 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluids (CSF) +/- sera of a cohort of 17 COVID-19 patients with neurological presentation and 55 neurological control patients (inflammatory [IND], non inflammatory [NIND], multiple sclerosis [MS]). Results: We found SARS-CoV-2 RNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (38%). An intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/16 patients. Of the four categories of tested patients, the CSF of IND exhibited the highest level of chemokines (CCL4, CCL5, CXCL8, CXCL10, CXCL12, and CXCL13), followed by the CSF of MS patients (CXCL12, and CXCL13). There was no significant difference between COVID-19 and NIND patients, even if some chemokines (CCL4, CCL5, CXCL8, andCXCL10) tended to be higher in the former. Interestingly, among COVD-19 patients, the CSF of those with a severe disease (encephalitis/encephalopathy) contained higher levels CXCL8 and CXCL10 than those with other neurological presentations. Interpretation: Our results do not show obvious SARS-CoV-2 infection of the central nervous system, but point to a mild inflammatory reaction reflecting an astrocytic reaction. Methods: We checked for SARS-CoV-2 mRNA by qPCR, SARS-CoV-2-specific antibodies and for 49 cytokines/chemokines/growth factors (by Luminex) in the cerebrospinal fluid (CSF) +/- serum of a cohort of 17 COVID-19 patients with neurological presentation and 55 neurological controls (inflammatory, non inflammatory, multiple sclerosis). Results: We found SARS-CoV-2 mRNA and antibodies specific for this virus in the CSF of 0/17 and 8/16 COVID-19 patients, respectively. The presence of SARS-CoV-2 antibodies was explained by a rupture of the blood brain barrier (passive transfer) in 6/16 (37,5%), but an intrathecal synthesis of SARS-CoV2-specific antibodies was present in 2/17.As compared to SARS-CoV-2-negative NIND patients, the CSF of IND patients exhibited the highest level of chemokines (CCL4, CCL5, CXCL8, CXCL10, CXCL12, and CXCL13), followed the CSF of MS patients (CXCL12, and CXCL13). There was no difference between COVID-19 patients with neurological diseases compared to NIND even if some chemokines (CCL4, CCL5, CXCL8, andCXCL10) tended to be higher than NIND. Interestingly, among COVD-19 patients, the CSF of those with a severe disease (encephalitis/encephalopathy) contained higher levels CXCL8 and CXCL10 than those with other neurological presentations. Interpretation: Our results confirm the absence of obvious SARS-CoV-2 infection of the central nervous system and point to a mild inflammatory reaction reflecting an astrocytic reaction.