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Imaging in stroke and vascular disease—part 1: ischaemic stroke
  1. Shelley Renowden
  1. Correspondence to Dr Shelley Renowden, Department of Neuroradiology, Frenchay Hospital, NHS Trust, Bristol, UK; Shelley.Renowden{at}

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Stroke is the third leading cause of death in Europe, the USA, Canada and Japan and is the primary cause of adult disability in these countries. Over 80% are ischaemic (cardiogenic, atherosclerotic, lacunar, haemodynamic and cryptogenic). The remainder are haemorrhagic (largely parenchymal and subarachnoid) and are considered in a separate article. Some pathologies may cause infarction and haemorrhage, for example, hypertensive vascular disease, moyamoya, vasculitis, reversible vasoconstriction syndrome, arterial dissection and venous occlusive disease.

Cranial CT is the most useful initial imaging modality to differentiate between ischaemia and haemorrhage and to exclude stroke mimics.

Hyperacute ischaemic stroke

Following arterial occlusion, a core of brain tissue dies. Surrounding this is hypoperfused, viable brain, surviving because of collaterals, at risk but potentially salvageable—the ischaemic penumbra. Brain parenchyma compensates for hypoperfusion by increasing oxygen extraction when the cerebral blood flow (CBF) falls to 20–23 mL/100 g/min. Below this level, neuronal function is impaired but remains viable, although can recover unless CBF is below 10–15 mL/100/min. Membrane channel failure then results in a net uncontrolled shift of extracellular water into the intracellular compartment. Cytotoxic oedema and irreversible damage (infarct core) depend upon the extent and severity of the blood flow reduction. The rate of change in size of the core and penumbra is a dynamic process, depending on whether or not cerebral reperfusion occurs. Without revascularisation, the infarct core enlarges and progressively replaces the penumbra. If there is recanalisation, the penumbra may be salvaged.

The volume of salvageable brain depends upon occlusion duration, collaterals, site and extent of occlusion—there may be viable parenchyma from between up to 3 h to more than 48 h, and 75–80% of hyperacute ischaemic stroke (HIS) patients have viable tissue after 6 h. The probability of a good outcome falls with increasing time to recanalisation. Thus, time and collaterals are brain.

The current standard of care in the …

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