Cytotoxic brain edema

Brain edema is defined as an abnormal accumulation of fluid associated with volumetric enlargement of the brain (Klatzo, 1967). Excess fluid can accumulate in the intracellular or extracellular spaces. Two types of brain edema have been defined based on the site of damage and where the fluid accumulates. Cytotoxic edema results in intracellular swelling without alterations in vascular permeability. Vasogenic edema is associated with damage to the BBB leading to flow of water and plasma constituents into the brain. These types of edema rarely exist in isolation typically, one type of edema dominates the other, but both co-exist. 

Cerebral tissue acidosis following ischemia or flaumatic brain injury contributes to cytotoxic brain edema formation. In vitro lactacidosis induces swelling of glial cells by intracellular Na" - and Cl accumulation by the Na" /H+-antiporter, Cr/HCOs antiporters, and the Na -K -2C1 cotransport (Staub et al., 1990 Ringel et al., 2006a). 

Sevick, R.J., et al.. Cytotoxic brain edema assessment with diffusion-weighted MR imaging. Radiology, 1992. 185(3) p. 687-90. 

Nervous system Reversible cytotoxic brain edema occurred in a 9-year-old boy with tacrolimus-associated leukoencephalopathy [140 ]. 

Cerebral ischemia causes not only reversible and then irreversible loss of brain function, but also cerebral edema (Symon et al. 1979 Hossman 1983). Ischemic edema is partly cytotoxic and partly vasogenic. Cytotoxic edema starts early, within minutes of stroke onset, and affects the gray more than the white matter, where damaged cell membranes allow intracellular water to accumulate. Vasogenic edema, which starts rather later, within hours of stroke onset, affects the white matter more, where the damaged blood-brain barrier allows plasma constituents to enter the extracellular space. Ischemic cerebral edema reaches its maximum in two to four days and then subsides over a week or two. 

The forces driving water flow to form cytotoxic edema are osmotic, generated in brain injury conditions (ischemia, trauma, hypoxia) by disturbances in ionic homeostasis due to failure of the Na /K+ ATPase and/or dramatic influx of Na" and Ca " via ionotropic glutamate receptors (excitotoxicity) and other ionic channels. These pathological alterations in cellular ionic homeostasis result in Na" " and water flow from the intravascular and extracellular space into the intracellular compartment. 

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