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The pathological effects of acute ischaemia are well characterised. Acute reduction of blood flow to a focal area of brain will produce infarction, with its attendant pan-necrosis in the circumscribed vascular territory or, with timely revascularisation, the system may escape without injury or lasting neurological dysfunction. In the acute setting, short duration, transient MCA occlusion has also been shown to produce selective neuronal necrosis without pan-necrosis,1 and selective neuronal loss has been inferred by positron emission tomography ligand studies in the acute ischaemic penumbra in humans.2 Much less well understood is the response of brain tissue to intermediate levels or repeated insults of sub-lethal hypoperfusion over an extended period of time. The question of whether chronic ischaemia can produce pathological effects short of frank infarction in humans has been a longstanding question, and difficult to document.
Fierstra et al,3 (see …
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