Neurosciences Critical Care Division, Departments of Neurology, Anesthesiology-Critical Care Medicine and Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21287, USA.
Neurotherapeutics. 2019 Oct;16(4):1133-1148. doi: 10.1007/s13311-019-00779-4.
Cerebral edema is commonly associated with cerebral pathology, and the clinical manifestation is largely related to the underlying lesioned tissue. Brain edema usually amplifies the dysfunction of the lesioned tissue and the burden of cerebral edema correlates with increased morbidity and mortality across diseases. Our modern-day approach to the medical management of cerebral edema has largely revolved around, an increasingly artificial distinction between cytotoxic and vasogenic cerebral edema. These nontargeted interventions such as hyperosmolar agents and sedation have been the mainstay in clinical practice and offer noneloquent solutions to a dire problem. Our current understanding of the underlying molecular mechanisms driving cerebral edema is becoming much more advanced, with differences being identified across diseases and populations. As our understanding of the underlying molecular mechanisms in neuronal injury continues to expand, so too is the list of targeted therapies in the pipeline. Here we present a brief review of the molecular mechanisms driving cerebral edema and a current overview of our understanding of the molecular targets being investigated.
脑水肿通常与脑病理学有关,其临床表现在很大程度上与基础损伤组织有关。脑水肿通常会放大损伤组织的功能障碍,脑水肿的负担与疾病的发病率和死亡率增加相关。我们目前对脑水肿的医学治疗方法主要围绕着,细胞毒性和血管源性脑水肿之间日益人为的区分。这些非靶向干预措施,如高渗剂和镇静剂,一直是临床实践的基础,为严重问题提供了非明智的解决方案。我们对导致脑水肿的潜在分子机制的理解正在变得更加先进,不同疾病和人群之间存在差异。随着我们对神经元损伤的潜在分子机制的理解不断扩展,处于研发管道中的靶向治疗方法的清单也在不断增加。在这里,我们简要回顾了导致脑水肿的分子机制,并概述了我们对正在研究的分子靶点的理解。