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.

Background Status epilepticus (SE) persisting despite two anti‐seizures medications (ASM) and anesthetics is labeled super refractory (SRSE), correlating with important morbidity and mortality. Its treatment relies on expert opinions. Due to its pharmacological properties, ketamine (KET) has received increasing attention, but data are essentially retrospective. Aims To describe an unselected cohort of adults receiving KET for SRSE. Methods Analysis of a prospective registry of consecutive SE episodes, identifying SRSE patients receiving ketamine (KET). Comparison with recent adult series including more than 10 patients. Results Eleven patients received KET after a median of 4 days (range: 2–20); median dose was 5 mg/kg/h (range: 2.5–15). KET provided permanent SE control in three (27%). Previous series, using KET administration delays and doses similar to our cohort, report KET efficacy in 28–96% of cases. Conclusions We found a lower SE control rate than existing literature, whose data are, however, often retrospective, potentially selecting patients with less severe SE forms or responding to KET. This might explain outcome differences, as KET administration modalities were comparable with our cohort. Since randomized controlled studies are lacking on this subject, the analysis of this prospective, unselected cohort, if confirmed, suggests a current overestimation of KET efficacy in SRSE.

We report the case of a 34-year-old female patient complaining of headaches one day after childbirth, initially interpreted as post-dural puncture headache (PDPH) and treated successfully with an epidural blood patch. Five days later, she presented an acute proportional right sensorimotor hemisyndrome and a new onset left-sided headache, attributed to a venous stroke from left-sided cerebral sinus venous thrombosis (CSVT). Simultaneously, we found radiological signs of reversible cerebral vasoconstriction syndrome (RCVS), considered as asymptomatic. We started the patient on anticoagulant therapy and she showed full motor recovery at the 3-month clinical follow-up.PDPH, CSVT and RCVS are well-known neurological complications of the peripartum period. All three conditions present with headaches and headache features may overlap, masking co-occurrence and making accurate diagnosis (differentiation) of these diseases difficult. Each disease can potentially lead to disabling deficits, but all respond to specific treatment.Knowledge of the causes of headaches in the peripartum period, their specific clinical characteristics and potential complications helps to prioritize and interpret diagnostic tests to offer appropriate therapy.