Stroke and ischaemia

It is a truth generally acknowledged that disruption of the blood flow in the brain causes considerable damage and death of neuronal cells. Generally speaking, the disruption of blood flow can be caused either by blood vessel rupture, which results in haemorrhage, or by a restriction of blood supply to the brain or parts of the brain, commonly referred to as brain ischaemia, due to vascular occlusion

(because of thrombosis or embolism), or to a systemic decrease in blood supply (for example, associated with heart failure). As a consequence, brain ischaemia can be either global, or focal, the latter corresponding to a stroke. Focal ischaemia triggers local cell death, the localization and volume of the damage being determined by anatomical localization of vessel occlusion. Often, the conditions of focal ischaemia are transient as the blood flow can be restored when the vessel blockage is removed; the restored blood flow results in reperfusion of the damaged area; this can be potentially damaging because of the production of reactive oxygen species. The pathogenesis of ischaemia is associated with the limitation of oxygen supply (hypoxia or anoxia), as well as with restrictions in supply of metabolic substrates.

Global ischaemia develops as a consequence of transient heart arrest. This leads to an almost immediate cessation of the cerebral blood flow from a normal ~8 ml/g/min to zero. About 10-15 seconds of global brain ischaemia results in loss of consciousness, while electrical activity of the brain disappears 30-40 seconds after the beginning of circulatory arrest. Global ischaemia lasting for more than 10min at normal temperature is lethal for humans. On a cellular level short periods of global ischaemia trigger delayed selective neuronal death, while, at least initially, astrocytes survive and become activated.

The development of focal ischaemic damage to brain tissue has a much more complicated kinetics. The cessation of, or a considerable decrease in, local cerebral blood flow triggers the onset of infarction. The core (Figure 10.1) of the infarction zone (were the blood flow rates are reduced below 1ml/g/min) is the region of pan-necrosis of all cells including neurones, astrocytes, oligoden-drocytes and ependymal cells. The infarction core is surrounded by a zone of reduced circulation (with rates 2-4 ml/g/min) known as the 'ischaemic penumbra' (Figure 10.1). The penumbra contains viable cells, albeit with compromised metabolism and function. The infarction core is formed very rapidly, within minutes and hours after initiation of the stroke, a much slower process of expansion of the infarction zone follows; this process developing over many hours and even days.

Glial cells are intimately involved in the CNS response to the ischaemia. Astrocytes, in particular, to a very large extent determine the progression and outcome of focal ischaemia. Importantly, astroglial cells have a dual role in the reactions to ischaemia, as they may either reduce or exacerbate neuronal damage, depending on the depth of ischaemia and timing relative to the moment of insult.

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