T Imaging of Ischaemic Stroke14

T. Popolizio, A. Simeone, G. M. Giannatempo, A. Stranieri, M. Armillotta, T. Scarabino

Ischaemic stroke accounts for 70 % of all acute cerebral vasculopathies and is among the leading causes of death and disability in the Western world. It is most often due to brain vessel atherosclerosis and less commonly to infectious arteritis, emboli from the carotid artery or cardiac pump deficits, resulting in systemic hypoperfusion. A significantly reduced blood flow in the vascular territory supplying the affected vessels induces a metabolic tissue imbalance (hypoxia and hy-poglycaemia) that gives rise to variably reversible anatomical injury. Four grades of clinical severity can be distinguished on the basis of the duration of symptoms, which are mainly characterized by a focal neurological deficit:

1 TIA (transient ischaemic attack): a sudden-onset, focal, non-convulsive condition that usually resolves within a few minutes and always within 24 h

2 RIND (reversible ischaemic neurological deficit): symptoms last no more than 48 h and normal conditions are restored within 3 weeks

3 Progressive stroke: progressive onset of clinical symptoms worsening over the first 24-48 h and leaving a persistent functional deficit

4 Completed stroke: a stable clinical condition since onset that may improve in time

This classification is not only useful from a clinical point of view, but also from the neuroradiological standpoint, because the duration of parenchymal hypo-perfusion, which causes a more or less persistent symptomatology, is related to pathological anatomical characteristics that correspond with distinctive neuroradio-logical findings. Transient ischaemia damages nerve cells, the elements most sensitive to hypoxia, but not the parenchyma, neither microscopically nor, consequently, „radiologically". In these patients standard imaging, including high-field MRI, is unable to depict the small hypoperfused area. The cell distress alone can be detected, using functional techniques such as MR diffusion (DWI) and spectroscopic techniques. In ischaemia of longer duration, the glial and mesodermal elements also undergo necrosis and morphostructural changes that can be visualized on standard imaging. In practice, functional DWI, perfusion (PWI) and spectroscopic techniques can identify the affected area in the hours immediately following the stroke, whereas conventional techniques enable evaluation of the later phases.

The recent introduction of fibrinolytic therapies [1] capable of inducing the recanalization of occluded vessels before the tissue damage becomes established has made the early identification of the ischaemic focus extremely important. In the hyperacute phase, besides differentiating ischaemia from haemorrhage, the irreversibly injured tissue must be distinguished from that susceptible to functional recovery

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