Stroke is a leading cause of death and disability affecting 15 million people worldwide. Although rapid recognition and treatment have dropped mortality rates, many are left with permanent disability. Approximately 87% of all strokes result from the occlusion of cerebrovasculature (ischemic strokes). Current research distinguishes between zones of core infarct and areas of metabolically compromised but potentially viable tissue receiving collateral circulation known as penumbra. Research has long focused on how endogenous mechanisms of neuroprotection and neurorepair affect penumbral expansion. Such therapeutic approaches have included antiinflammatory interventions, reactive oxygen species scavengers, and many other targets with the common goal of mitigating the acute and chronic inflammatory responses typically seen in an ischemic stroke. This chapter will discuss acute and chronic molecular mechanisms underlying edema following ischemic stroke.
|Title of host publication||Brain Edema|
|Subtitle of host publication||From Molecular Mechanisms to Clinical Practice|
|Number of pages||15|
|State||Published - Jan 1 2017|
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ASJC Scopus subject areas
- Medicine (all)
- Neuroscience (all)