Pathophysiological aspects of brain edema

Abstract

Two mayor types of brain edema, related to two different pathomechanisms, can be recognized: 1) cytotoxic type-where the main feature is the swelling of cellular elements of brain parenchyma and 2) vasogenic type-where an increased vascular permeability leading to accumulation of edema fluid in the extracellular spaces plays the principal role. In this type of edema, there is a close interrelationship between extravasation of serum proteins and retention of water in the brain tissue. In the ischemic brain edema both cytotoxic and vasogenic mechanisms are involved. A biphasic opening of the blood-brain barrier, associated with vasogenic edema, is observed following release of major cerebral artery occlusion. The first opening of the barrier is related to a reactive hyperemia which follows promptly recirculation. The second opening, recognizable after a delay, is associated with a severe ischemic brain tissue injury.

Mechanisms of Astrocyte-Mediated Cerebral Edema

“…Historically, edema was classified into physiological categories with no molecular or cellular underpinnings [51]. More recently, improved understanding of the molecular mediators of edema formation prompted a reevaluation and reinterpretation of classical subtypes of cerebral edema [52].…”

“…Notably, in these studies, the type of edema was termed “cytotoxic” edema, reflecting the older edema classification scheme developed by Igor Klatzo, in which true cytotoxic (purely cellular) edema, as the term is currently used, was combined with ionic edema [51]. The aforementioned studies did not directly measure astrocyte swelling, but instead showed that AQP4 knockout or inhibition reduced post-injury increases in brain volume and brain water content, consistent with the formation of ionic edema, as defined in the current scheme [54–57].…”

Selective vasopressin-1a receptor antagonist prevents brain edema, reduces astrocytic cell swelling and GFAP, V1aR and AQP4 expression after focal traumatic brain injury

“…et al, 2006b, 2013, Marmarou et al, 2006, Okuno et al, 2008, Taya et al, 2008, 2010). Astrocytic swelling following TBI was initially described by Klatzo as cytotoxic edema (Klatzo, 1987). Astrocytes are key players in cerebral water homeostasis and respond to injury with molecular and morphological changes described as astrogliosis.…”

Brain Turgor (Kb): Intrinsic Property of the Brain to Resist Distortion

“…When the fluid is intracellular, it is trapped there and must await cell death or repair to be removed. When the fluid is extracellular, such as normal brain ECF or vasogenic edema, clearance of the water is via bulk flow into the ventricle and absorption with the remainder of CSF [5,14], It is therefore reasonable to assume that the same volumetric increase in water will lead to a greater increase in Kb when that increase is intracellular than when it is extracellular.…”