Stroke is a complex disease and one of the main causes of morbidity and mortality among the adult population. A huge variety of factors is known to influence patient outcome, including demographic variables, comorbidities or genetics. In this review, we expound what is known about the influence of clinical variables and related genetic risk factors on ischemic stroke outcome, focusing on acute and subacute outcome (within 24 to 48 hours after stroke and until day 10, respectively), as they are the first indicators of stroke damage. We searched the PubMed data base for articles that investigated the interaction between clinical variables or genetic factors and acute or subacute stroke outcome. A total of 61 studies were finally included in this review. Regarding the data collected, the variables consistently associated with acute stroke outcome are: glucose levels, blood pressure, presence of atrial fibrillation, prior statin treatment, stroke severity, type of acute treatment performed, severe neurological complications, leukocyte levels, and genetic risk factors. Further research and international efforts are required in this field, which should include genome-wide association studies.

Background and Purpose— Cerebral edema (CED) develops in the hours to days after stroke; the resulting increase in brain volume may lead to midline shift (MLS) and neurological deterioration. The time course and implications of edema formation are not well characterized across the spectrum of stroke. We analyzed displacement of cerebrospinal fluid (ΔCSF) as a dynamic quantitative imaging biomarker of edema formation. Methods— We selected subjects enrolled in a stroke cohort study who presented within 6 hours of onset and had baseline and ≥1 follow-up brain computed tomography scans available. We applied a neural network-based algorithm to quantify hemispheric CSF volume at each imaging time point and modeled CSF trajectory over time (using a piecewise linear mixed-effects model). We evaluated ΔCSF within the first 24 hours as an early biomarker of CED (defined as developing MLS on computed tomography beyond 24 hours) and poor outcome (modified Rankin Scale score, 3–6). Results— We had serial imaging in 738 subjects with stroke, of whom 91 (13%) developed CED with MLS. Age did not differ (69 versus 70 years), but baseline National Institutes of Health Stroke Scale was higher (16 versus 7) and baseline CSF volume lower (132 versus 161 mL, both P <0.001) in those with CED. ΔCSF was faster in those developing MLS, with the majority seen by 24 hours (36% versus 11% or 2.4 versus 0.8 mL/h; P <0.0001). Risk of CED almost doubled for every 10% ΔCSF within 24 hours (odds ratio, 1.76 [95% CI, 1.46–2.14]), adjusting for age, glucose, and National Institutes of Health Stroke Scale. Risk of neurological deterioration (1.6-point increase in National Institutes of Health Stroke Scale at 24 hours) and poor outcome (adjusted odds ratio, 1.34 [95% CI, 1.15–1.56]) was also greater for every 10% increase in ΔCSF. Conclusions— CSF volumetrics provides quantitative evaluation of early edema formation. ΔCSF from baseline to 24-hour computed tomography is a promising early biomarker for the development of MLS and worse neurological outcome.

Background and Purpose: The genetic relationships between stroke risk, stroke severity, and early neurological changes are complex and not completely understood. Genetic studies have identified 32 all stroke risk loci. Polygenic Risk Scores (PRS) can be used to compare the genetic architecture of related traits. In this study, we compare the genetic architecture of stroke risk, stroke severity, and early neurological changes with that of two stroke risk factors: Type 2 Diabetes Mellitus (T2DM) and Hypertension (HTN). Methods: We assessed the degree of overlap in the genetic architecture of stroke risk, T2DM, HTN, and two acute stroke phenotypes based on the NIH Stroke Scale (NIHSS), which ranges from 0 for no stroke symptoms to 21-42 for a severe stroke: baseline (within 6h after onset) and change in NIHSS (ΔNIHSS=NIHSS at baseline minus NIHSS at 24h). This was done by: 1) SNP by SNP comparison, 2) weighted PRS with sentinel variants and 3) whole genome PRS using multiple p-values thresholds. Results: We found evidence of genetic architecture overlap between stroke risk and T2DM (p=2.53×10 −169), HTN (p=3.93×10 −04) and baseline NIHSS (p=0.03). However, there was no evidence of overlap between ΔNIHSS and stroke risk, T2DM or HTN.

BackgroundSchistosomiasis and soil-transmitted helminthiasis (STHs) are target neglected tropical diseases (NTDs) of preventive chemotherapy, but the control and elimination of these diseases have been impeded due to resource constraints. Few reports have described study protocol to draw on when conducting a nationwide survey. We present a detailed methodological description of the integrated mapping of schistosomiasis and STHs on the basis of our experiences, hoping that this protocol can be applied to future surveys in similar settings. In addition to determining the ecological zones requiring mass drug administration interventions, we aim to provide precise estimates of the prevalence of these diseases.MethodsA school–based cross-sectional design will be applied for the nationwide survey across Sudan. The survey is designed to cover all districts in every state. We have divided each district into 3 different ecological zones depending on proximity to bodies of water. We will employ a probability-proportional-to-size sampling method for schools and systematic sampling for student selection to provide adequate data regarding the prevalence for schistosomiasis and STHs in Sudan at the state level. A total of 108,660 students will be selected from 1811 schools across Sudan. After the survey is completed, 391 ecological zones will be mapped out. To carry out the survey, 655 staff members were recruited. The feces and urine samples are microscopically examined by the Kato-Katz method and the sediment smears for helminth eggs respectively. For quality control, a minimum of 10% of the slides will be rechecked by the federal supervisors in each state and also 5% of the smears are validated again within one day by independent supervisors.DiscussionThis nationwide mapping is expected to generate important epidemiological information and indicators about schistosomiasis and STHs that will be useful for monitoring and evaluating the control program. The mapping data will also be used for overviewing the status and policy formulation and updates to the control strategies. This paper, which describes a feasible and practical study protocol, is to be shared with the global health community, especially those who are planning to perform nationwide mapping of NTDs by feces or urine sampling.Electronic supplementary materialThe online version of this article (10.1186/s12889-017-4719-4) contains supplementary material, which is available to authorized users.

The ability to image the ischemic penumbra during hyper-acute stroke promises to identify patients who may benefit from treatment intervention beyond population-defined therapeutic time windows. MR blood oxygenation level dependent (BOLD) contrast imaging has been explored in ischemic stroke. This review provides an overview of several BOLD-based methods, including susceptibility weighted imaging (SWI), R2, R2*, R2′, R2* under oxygen challenge, MR_OEF and MROMI approaches to assess cerebral oxygen metabolism in ischemic stroke. We will review the underlying pathophysiological basis of the imaging approaches, followed by a brief introduction of BOLD contrast. Finally, we will discuss the applications of the BOLD approaches in patients with ischemic stroke. BOLD-based methods hold promise for imaging tissue oxygenation during acute ischemia. Further technical refinement and validation studies in stroke patients against positron emission tomography (PET) measurements are needed.