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Glutamate stimulates AMPA receptors and Ca ++-permeable NMDA receptors, which leads to even more calcium influx into cells.Intracellular calcium levels become too high and trigger the release of the excitatory amino acid neurotransmitter glutamate.ATP-reliant ion transport pumps fail, causing the cell membrane to become depolarized leading to a large influx of ions, including calcium (Ca ++), and an efflux of potassium.Lactic acid is an irritant, which has the potential to destroy cells by disruption of the normal acid-base balance in the brain.Cells in the affected area switch to anaerobic metabolism, which leads to a lesser production of ATP but releases a by-product called lactic acid.Without adequate blood supply and thus lack of oxygen, brain cells lose their ability to produce energy - particularly adenosine triphosphate (ATP).(Source: ) Important steps of the ischaemic cascade The goal of acute stroke therapy is to normalise perfusion and intervene in the cascade of biochemical dysfunction to salvage the penumbra as much and as early as possible.Īlthough it is called a cascade, events are not always linear (figure 2).

#Thebrain forums series#

This is a series of biochemical reactions in the brain and other aerobic tissues, which usually goes on for two to three hours, but can last for days, even after normal blood flow returns.

Figure 1: Ischaemic penumbra – Potential to reverse neurologic impairment with post-stroke therapyĪfter seconds to minutes of cerebral ischaemia, the ischaemic cascade is initiated. They may undergo apoptosis after several hours or days but if blood flow and oxygen delivery is restored shortly after the onset of stroke, they are potentially recoverable (figure 1). Cells in this area are endangered but not yet irreversibly damaged. This region is rendered functionally silent by reduced blood flow but remains metabolically active. The tissue in the region bordering the infarct core, known as the ischaemic penumbra, is less severely affected. In the core area of a stroke, blood flow is so drastically reduced that cells usually cannot recover and subsequently undergo cellular death.

Stroke of undetermined aetiology – after exclusion of all of the above.

Stroke of determined aetiology – such as inherited diseases, metabolic disorders, and coagulopathies.

Embolic stroke – the most common cause of an embolic stroke is atrial fibrillation.

Small vessel disease – changes due to chronic disease, such as diabetes, hypertension, hyperlipidaemia, and smoking, that lead decreased compliance of the arterial walls and/or narrowing and occlusion of the lumen of smaller vessels.

Large artery disease – atherosclerosis of large vessels, including the internal carotid artery, vertebral artery, basilar artery, and other major branches of the Circle of Willis.

In an embolic stroke, blood clots or debris from elsewhere in the body, typically the heart valves, travel through the circulatory system and block narrower blood vessels.īased on the aetiology of ischaemic stroke, a more accurate sub-classification is generally used: As the plaques grow in size, the blood vessel becomes narrowed and the blood flow to the area beyond is reduced.ĭamaged areas of an atherosclerotic plaque can cause a blood clot to form, which blocks the blood vessel – a thrombotic stroke.

Narrowing is commonly the result of atherosclerosis – the occurrence of fatty plaques lining the blood vessels. Ischaemic strokes can be broadly subdivided into thrombotic and embolic strokes. The common pathway of ischaemic stroke is lack of sufficient blood flow to perfuse cerebral tissue, due to narrowed or blocked arteries leading to or within the brain. The two major categories of stroke are ischaemic (lack of blood and hence oxygen to an area of the brain) and haemorrhagic (bleeding from a burst or leaking blood vessel in the brain) stroke. A stroke occurs when the blood flow to an area of the brain is interrupted, resulting in some degree of permanent neurological damage.