Brain Edema in Neurological Diseases

Abstract

In the brain, the transport of water and solute is precisely regulated. This maintains a stable and unique microenvironment that is critical to brain function. Cerebral edema results from the excess of fluid in the brain’s intra- and extracellular spaces. This occurs in response to a wide variety of insults, including cerebral ischemia, hypoxia, infection, brain tumors, and neuroinflammation. Cytotoxic edema leads to intracellular swelling without alterations in vascular permeability. Vasogenic edema is associated with damage to the blood–brain barrier. These types of edema rarely exist in isolation. In most neuropathological conditions, one type of edema predominates, but both coexist. This chapter focuses on the major molecular mechanisms triggering brain edema, including alterations in ion channels and transporters, matrix metalloproteinases, tight junction protein degradation, free radicals, and products of the arachidonic acid metabolism. We review present knowledge of the contribution to brain edema of molecules such as aquaporins, vasopressin, vascular endothelial growth factor, angiopoietins, and bradykinin. We further examine brain imaging modalities that have revolutionized clinical diagnosis of cerebral edema. Finally, we provide a critical evaluation of the current strategies for the treatment of brain edema.