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Published 16 February 2009
Cite this as: BMJ Case Reports 2009 [doi:10.1136/bcr.2007.123232]
Copyright © 2009 by the BMJ Publishing Group Ltd.

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Identifying aortic plaque inflammation as a potential cause of stroke

R R Moustafa1, D Izquierdo2, P L Weissberg3, J-C Baron1, E A Warburton1

1 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
2 Wolfson Brain Imaging Centre, University of Cambridge, Cambridge, UK
3 Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK

Correspondence to:
rrmm2{at}cam.ac.uk

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.


 

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

Competing interests: None.

REFERENCES

  1. Ross, R. Atherosclerosis—an inflammatory disease. N Engl J Med 1999;340:115–26.[Free Full Text]
  2. Davies, JR, Rudd, JH, Fryer, TD, et al. Identification of culprit lesions after transient ischemic attack by combined 18F fluorodeoxyglucose positron-emission tomography and high-resolution magnetic resonance imaging. Stroke 2005;36:2642–7.[Abstract/Free Full Text]

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