Cytotoxic brain oedema

Homeostatic regulation of brain volume and water content is of paramount importance for its function. Brain size is limited by the skull, and therefore even minute increases in brain volume lead to an increase in intracranial pressure and compression damage of neural tissue. Water redistribution between brain compartments compromises the extracellular space with similarly grave consequences. Brain oedema is in essence a collapse of brain volume/water regulation, which exists in two forms - vascular and cellular (also known as cytotoxic); vascular oedema is a consequence of disruption of the blood-brain barrier, which triggers water flow into the tissue, whereas cellular oedema is a redistribution of water into cellular compartments, which does not necessarily affect total volume of the brain parenchyma.

Physiologically, astrocytes are capable of rapidly responding to changes in extracellular osmotic pressure by an initial swelling and consequent regulatory volume decrease; this response is regulated by ion and water movements (Chapter 7.9). In pathology, these mechanisms are compromised, which hampers the ability of astrocytes to maintain their volume and water content.

Cellular oedema is primarily astroglial pathology, as astrocytes are capable of large volume changes due to water fluxes. Indeed many brain insults, such as ischaemia or acute trauma, result in rapid swelling of astrocytes, which is

Figure 10.6 Pathological potential of astroglial swelling. Astroglial swelling decreases extracellular volume, hence increasing concentration of neurotransmitters and damage signals in the interstitium and compresses brain capillaries, further compromising circulation in the damaged area

Swelling The Brain

Figure 10.6 Pathological potential of astroglial swelling. Astroglial swelling decreases extracellular volume, hence increasing concentration of neurotransmitters and damage signals in the interstitium and compresses brain capillaries, further compromising circulation in the damaged area

Swollen perisynaptic process

Decrease in ex trasynaptic volume, increase of glutamate and PC concentration, opening of volume-sensitive channels and further release of glutamate

Swollen perisynaptic process accompanied by a significant increase in astroglial surface area. Astroglial swelling can trigger numerous secondary effects, which exacerbate the brain damage (Figure 10.6). In particular, swelling of perivascular astrocytes and astrocyte endfeet may compress brain vessels and limit circulation. This compression, for example, accounts for noncomplete filling of brain vessels during reperfusion following focal ischaemia; this is known as the no-reflow phenomenon. Swelling of astrocytes can result in opening of volume-regulated ion channels, permeable to glutamate and other excitatory amino acids; release of the latter can induce or exacerbate excitotoxic cell death. Prominent swelling of astrocytes can severely reduce the extracellular space volume with obvious consequences of increased concentration of extracellular glutamate and K+ ions. In fact, a several fold reduction in extracellular space can increase the concentration of the latter to excitotoxic levels.

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