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Inflammatory activity within atherosclerotic lesions is associated with plaque rupture and embolic events,1 and can be detected non-invasively with 18F-Fluorodeoxyglucose positron emission tomography (FDG-PET).2
A 70-year-old hypertensive man presented with sudden mild right hemiparesis and dysarthria. A CT scan of the head was normal. There was no cardiac source of embolism, and ultrasound and catheter angiography revealed ∼75% stenosis of the left carotid bifurcation. Imaging with FDG-PET and MRI to clarify the embolic source2 (fig 1) suggested that the “culprit” lesion was inflamed aortic atheromata rather than the presumed symptomatic tight carotid stenosis. This novel pathophysiological approach can add to the aetiological work-up of stroke and has potential in guiding management.
Acknowledgments
This article has been adapted from Moustafa R R, Izquierdo D, Weissberg P L, Baron J-C, Warburton E A. Identifying aortic plaque inflammation as a potential cause of stroke Journal of Neurology, Neurosurgery and Psychiatry 2008;79:236
Footnotes
Competing interests: None.