Classically, the relationship between systolic BP (SBP) and clinical outcome was described as U-or J shaped, with both high and low values of BP being independent prognostic factors for poor outcome.2,3 Nonetheless, these studies did not consider the recanalization state of the affected arterial territory, which may directly influence the hemodynamic response.The main objective of this study is to determine the relationship between BP during the first 24 hours after ischemic stroke and clinical outcome in patients submitted to intravenous or intra-arterial recanalization treatments. Methods Study PopulationWe included consecutive patients with acute ischemic stroke from July 2009 to June 2015, treated with intravenous thrombolysis (IVrtPA) or intra-arterial therapies in our tertiary, university hospital in Portugal. The exclusion criteria were as follows: patients who had insufficient BP data (ie, incomplete BP readings in the first 24 hours poststroke due to patient death or early hospital transfer); unavailable information Background and Purpose-Historical stroke cohorts reported a U-or J-shaped relationship between blood pressure (BP) and clinical outcome. However, these studies predated current revascularization strategies, disregarding the recanalization state of the affected arterial territory. We aimed to investigate the relationship between BP in the first 24 hours after ischemic stroke and clinical outcome in patients submitted to intravenous or intra-arterial recanalization treatments. Methods-Consecutive patients with acute stroke treated with intravenous thrombolysis or intra-arterial therapies were enrolled in a retrospective cohort study. BP was measured on regular intervals throughout day and night during the first 24 hours after stroke onset. The mean systolic BP and diastolic BP during the first 24 hours post stroke were calculated.Recanalization was assessed at 6 hours by transcranial color-coded Doppler, angiography, or angio-computed tomography.Functional outcome was assessed at 3 months by modified Rankin Scale. Linear and quadratic multivariate regression models were performed to determine associations between BP and functional outcome for the whole population and recanalyzed and nonrecanalyzed patients. Results-We Conclusions-Systemic

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Our results support the use of PLEX in severe relapses unresponsive to corticosteroids, since it was an effective and relatively safe treatment for most of our patients.

Introduction: Focal cortical dysplasias (FCDs) are a group of malformations of cortical development that constitute a common cause of drug-resistant epilepsy, often subjected to neurosurgery, with a suboptimal long-term outcome. The past few years have witnessed a dramatic leap in our understanding of the molecular basis of FCD. This study aimed to provide an updated review on the genomic and epigenetic advances underlying FCD etiology, to understand a genotype–phenotype correlation and identify priorities to lead future translational research.Methods: A scoping review of the literature was conducted, according to previously described methods. A comprehensive search strategy was applied in PubMed, Embase, and Web of Science from inception to 07 May 2020. References were screened based on title and abstract, and posteriorly full-text articles were assessed for inclusion according to eligibility criteria. Studies with novel gene variants or epigenetic regulatory mechanisms in patients that underwent epilepsy surgery, with histopathological diagnosis of FCD type I or II according to Palmini's or the ILAE classification system, were included. Data were extracted and summarized for an overview of evidence.Results: Of 1,156 candidate papers, 39 met the study criteria and were included in this review. The advent of next-generation sequencing enabled the detection in resected FCD tissue of low-level brain somatic mutations that occurred during embryonic corticogenesis. The mammalian target of rapamycin (mTOR) signaling pathway, involved in neuronal growth and migration, is the key player in the pathogenesis of FCD II. Somatic gain-of-function variants in MTOR and its activators as well as germline, somatic, and second-hit mosaic loss-of-function variants in its related repressors have been reported. However, the genetic background of FCD type I remains elusive, with a pleomorphic repertoire of genes affected. DNA methylation and microRNAs were the two epigenetic mechanisms that proved to have a functional role in FCD and may represent molecular biomarkers.Conclusion: Further research into the possible pathogenic causes of both FCD subtypes is required, incorporating single-cell DNA/RNA sequencing as well as methylome and proteomic analysis. The collected data call for an integrated clinicopathologic and molecular genetic diagnosis in current practice not only to improve diagnostic accuracy but also to guide the development of future targeted treatments.

Background Cerebral edema is frequent in patients with acute ischemic stroke (AIS) who undergo reperfusion therapy and is associated with high mortality. The impact of collateral pial circulation (CPC) status on the development of edema has not yet been determined. Methods We studied consecutive patients with AIS and documented M1-middle cerebral artery (MCA) and/or distal internal carotid artery (ICA) occlusion who underwent reperfusion treatment. Edema was graded on the 24-hour non-contrast computed tomography (NCCT) scan. CPC was evaluated at the acute phase (≤6 hours) by transcranial color-coded Doppler, angiography and/or CT angiography. We performed an ordinal regression model for the effect of CPC on cerebral edema, adjusting for age, baseline National Institutes of Health Stroke Scale, Alberta Stroke Program Early Computed Tomography Score (ASPECTS) on admission, NCCT, parenchymal hemorrhagic transformation at 24 hours and complete recanalization at six hours. Results Among the 108 patients included, 49.1% were male and mean age was 74.2 ± 11.6 years. Multivariable analysis showed a significant association between cerebral edema and CPC status (OR 0.22, 95% CI 0.08-0.59, p = 0.003), initial ASPECTS (OR 0.72, 95% CI 0.57-0.92, p = 0.007) and parenchymal hemorrhagic transformation (OR 23.67, 95% CI 4.56-122.8, p < 0.001). Conclusions Poor CPC is independently associated with greater cerebral edema 24 hours after AIS in patients who undergo reperfusion treatment.

Two elderly men, with previous history of cerebrovascular disease, were admitted to the emergency department due to focal motor status epilepticus with persistent myoclonic jerks of one side of the body. In both cases, the clinical picture evolved into a unilateral and isolated arrhythmic myoclonus of the abdominal muscles with preserved consciousness. These involuntary movements resolved with antiepileptic drugs. Although cerebrovascular disease is one of the most common causes of epilepsia partialis continua, reported cases in the literature with predominant abdominal involvement have a different aetiology. The neuroimaging and electroencephalographic findings showed a wide spectrum of different localizations and aetiologies associated with this particular type of epileptic seizure. Indeed, the pathophysiology of focal motor seizures involving the abdominal muscles is still a matter of discussion. In our second case, we present a patient with epilepsia partialis continua of the abdominal wall with an occipital focus, which, to the best of our knowledge, has not been previously reported. [Published with video sequences]

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Epilepsy should be suspected in patients with Stiff‐person syndrome and new onset paroxysmal episodes. Musicogenic epilepsy may be a manifestation of anti‐GAD‐Ab spectrum, supporting an autoimmune workup in these patients. Appropriate treatment is not well established, and immunotherapy should be considered in patients with only partial response to antiepileptic drugs.