The lipidome has a broad range of biological and signaling functions, including serving as a structural scaffold for membranes and initiating and resolving inflammation. To investigate the biological activity of phospholipids and their bioactive metabolites, precise analytical techniques are necessary to identify specific lipids and quantify their levels. Simultaneous quantification of a set of lipids can be achieved using high sensitivity mass spectrometry (MS) techniques, whose technological advancements have significantly improved over the last decade. This has unlocked the power of metabolomics/lipidomics allowing the dynamic characterization of metabolic systems. Lipidomics is a subset of metabolomics for multianalyte identification and quantification of endogenous lipids and their metabolites. Lipidomics-based technology has the potential to drive novel biomarker discovery and therapeutic development programs; however, appropriate standards have not been established for the field. Standardization would improve lipidomic analyses and accelerate the development of innovative therapies. This review aims to summarize considerations for lipidomic study designs including instrumentation, sample stabilization, data validation, and data analysis. In addition, this review highlights how lipidomics can be applied to biomarker discovery and drug mechanism dissection in various inflammatory diseases including cardiovascular disease, neurodegeneration, lung disease, and autoimmune disease.

Emerging science continues to establish the detrimental effects of malnutrition in acute neurological diseases such as traumatic brain injury, stroke, status epilepticus and anoxic brain injury. The primary pathological pathways responsible for secondary brain injury include neuroinflammation, catabolism, immune suppression and metabolic failure, and these are exacerbated by malnutrition. Given this, there is growing interest in novel nutritional interventions to promote neurological recovery after acute brain injury. In this review, we will describe how malnutrition impacts the biomolecular mechanisms of secondary brain injury in acute neurological disorders, and how nutritional status can be optimized in both pediatric and adult populations. We will further highlight emerging therapeutic approaches, including specialized diets that aim to resolve neuroinflammation, immunodeficiency and metabolic crisis, by providing pre-clinical and clinical evidence that their use promotes neurologic recovery. Using nutrition as a targeted treatment is appealing for several reasons that will be discussed. Given the high mortality and both short- and long-term morbidity associated with acute brain injuries, novel translational and clinical approaches are needed.

MRI is a valuable modality for the etiologic work up in patients with cryptogenic stroke and embolic stroke of undetermined source.

Background: Following aneurysmal subarachnoid hemorrhage, peripherally-drawn lactic acid has been associated with poor outcomes; however, its clinical significance is unknown. We investigated admission factors and patient outcomes associated with serum lactic acid in this population. Methods: This was a retrospective observational study of 105 consecutive patients with serum lactate collected within 24 h of admission. Primary objectives were to determine the incidence of admission lactic acidemia, and factors positively and negatively associated with lactate levels. We also sought to determine if admission lactic acidemia was associated with patient outcomes, including vasospasm, delayed cerebral ischemia, mortality, and discharge disposition. Results: Admission serum lactic acid was elevated in 56 patients (53% of the cohort). Levels were positively associated with Hunt & Hess and modified Fisher grade, glucose, troponin I and white blood cell counts, and negatively associated with GCS and ventilator-free days. Admission lactate was not associated with the development of vasospasm or delayed cerebral ischemia. Patients with elevated lactic acid more often died during hospitalization, and less often were discharged home. After adjusting for other predictors of poor outcome, the adjusted odds of inpatient mortality (OR 0.97, 95% CI 0.79–1.20; p = 0.80) and discharge to home (OR 1.00, 95% CI 0.80–1.26; p = 0.97) was not associated with admission lactic acid. Conclusions: Early serum lactic acid elevation is common following aneurysmal subarachnoid hemorrhage and is associated with the clinical and radiographic grade of hemorrhage. Levels did not independently predict short-term outcomes when adjusted for established predictors of poor outcome. Further study is needed to determine the clinical significance of peripherally-drawn lactic acid in aneurysmal subarachnoid hemorrhage.

Traumatic brain injury (TBI) is a common diagnosis requiring acute hospitalization. Long-term, TBI is a significant source of health and socioeconomic impact in the United States and globally. The goal of clinicians who manage TBI is to prevent secondary brain injury. In this population, post-traumatic cerebral infarction (PTCI) acutely after TBI is an important but under-recognized complication that is associated with negative functional outcomes. In this comprehensive review, we describe the incidence and pathophysiology of PTCI. We then discuss the diagnostic and treatment approaches for the most common etiologies of isolated PTCI, including brain herniation syndromes, cervical artery dissection, venous thrombosis, and post-traumatic vasospasm. In addition to these mechanisms, hypercoagulability and microcirculatory failure can also exacerbate ischemia. We aim to highlight the importance of this condition and future clinical research needs with the goal of improving patient outcomes after TBI.