Encephalopathy is a neurological complication of COVID-19. The objective of this exploratory study is to investigate the link between systemic inflammation and brain microstructural changes (measured by diffusion-weighted imaging) in patients with COVID-19 encephalopathy. 20 patients with COVID-19 encephalopathy (age: 67.3 $$\pm$$ ± 10.0 years; 90% men) hospitalized in the Geneva University Hospitals for a SARS-CoV-2 infection between March and May 2020 were included in this retrospective cohort study. COVID-19 encephalopathy was diagnosed following a comprehensive neurobiological evaluation, excluding common causes of delirium, such as hypoxemic or metabolic encephalopathy. We investigated the correlation between systemic inflammation (measured by systemic C-reactive protein (CRP)) and brain microstructural changes in radiologically normal white matter (measured by apparent diffusion coefficient (ADC)) in nine spatially widespread regions of the white matter previously associated with delirium. Systemic inflammation (CRP = 60.8 ± 50.0 mg/L) was positively correlated with ADC values in the anterior corona radiata (p = 0.0089), genu of the corpus callosum (p = 0.0064) and external capsule (p = 0.0086) after adjusting for patients’ age. No statistically significant association between CRP and ADC was found in the other six white matter regions. Our findings indicate high risk of white matter abnormalities in COVID-19 encephalopathy patients with high peripheral inflammatory markers, suggesting aggressive imaging monitoring may be warranted in these patients. Future studies should clarify a possible specificity of the spatial patterns of CRP–white matter microstructure association in COVID-19 encephalopathy patients and disentangle the role of individual cytokines on brain inflammatory mechanisms.

Temporary chronic pain reduction related to acute COVID-19 has been observed, providing new knowledge on the possible mechanisms of pain modulation and potential therapeutic options.

Encéphalopathie aiguë et Covid-19 : hypothèses physiopathologiques L'encéphalopathie aiguë est l'une des principales complications neurologiques des patients hospitalisés pour un Covid-19. Si les complications électrolytiques, les différents traitements et l'hypoxémie ont un effet sur l'homéostasie cérébrale entraînant une perturbation de la cognition, les conséquences cérébrales directes ou indirectes du SARS-CoV-2 ne sont pas complètement élucidées. L'implication du virus entraînant une atteinte endothéliale des vaisseaux cérébraux pourrait participer à cette encéphalopathie, via une fragilisation de la barrière hématoencéphalique et un passage facilité des cytokines pro-inflammatoires. L'atteinte virale directe ou la réaction autoimmune secondaire ont également été invoquées. Face aux multiples mécanismes physiopathologiques possibles pouvant expliquer cette encéphalopathie, le débat est ouvert. COVID-19-related acute encephalopathy : physiopathological hypothesisAcute encephalopathy is one of the most frequent neurological complication in patients hospitalized for COVID-19. Electrolyte imbalance, drugs, and hypoxemia can all affect brain homeostasis, leading to acute cognitive dysfunction and direct implications of the SARS-CoV-2 are not completely understood. Neurological complications of SARS-CoV-2 infection are poorly understood : an inflammatory insult to the endothelium affecting the blood-brain barrier may explain the clinical presentation, but other hypotheses including direct viral damage or an immune-mediated reaction are also suggested. Among these various potential mechanisms, often combined, the controversy remains.

Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website.Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre -including this research content -immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

Objective Hippocampal sclerosis (HS) is a prominent biomarker of epilepsy. If acquired later in life, it usually occurs in the context of degenerative or acute inflammatory-infectious disease. Conversely, acute symptomatic seizures (ASS) are considered a risk factor for developing post-stroke epilepsy, but other factors remain unrecognized. Here, we hypothesize that silent hippocampal injury contributes to the development of post-stroke epilepsy. Methods We performed a retrospective observational study of patients hospitalized between 1/2007 and 12/2018 with an acute stroke in the Stroke Center of the Geneva University Hospital. Patients were included if they had a documented normal hippocampal complex at onset and a control MRI at ≥ 2 year interval without new lesion in the meantime. Results 162 patients fulfilled our inclusion criteria. ASS during the first week (p < 0.0001) and epileptiform abnormalities in electroencephalography (EEG; p = 0.02) were more frequently associated with the development of epilepsy. Hemorrhagic stroke was strongly associated to both ASS and future focal epilepsy (p = 0.00097). Three patients (1.8%) developed hippocampal sclerosis ipsilateral to the cerebrovascular event between 2 and 5 years, all with ASS and hemorrhagic stroke. Interpretation ASS and epileptiform EEG abnormalities are strong predictors of post-stroke epilepsy. HS develops in a minority of patients after hemorrhagic lesions, leading to focal epilepsy. Prospective studies are required, including follow-up with EEG and if characterized by epileptiform discharges, with MRI, to determine the true frequency of HS and to better understand predictors of post-stroke epilepsy (AAS, stroke type, and HS), and their impact on stroke recovery.