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Published Online
on June 4, 2009

Stroke. 2009
Published online before print June 4, 2009, doi: 10.1161/STROKEAHA.109.549378
A more recent version of this article appeared on July 1, 2009
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Right arrow Embolic stroke
Right arrow Doppler ultrasound, Transcranial Doppler etc.

Submitted on February 3, 2009
Revised on March 10, 2009
Accepted on April 14, 2009

Simultaneous Occurrence and Interaction of Hypoperfusion and Embolism in a Patient With Severe Middle Cerebral Artery Stenosis

Stefanie Schreiber MD*; Mine Serdaroglu; Frank Schreiber; Martin Skalej MD; Hans-Jochen Heinze MD; and Michael Goertler MD

From the Department of Neurology (S.S., M.S., H.-J.H., M.G.) and the Institute of Neuroradiology (M.S.), University of Magdeburg, Magdeburg, Germany; and the Institute of Control Engineering (F.S.), University of Braunschweig, Braunschweig, Germany.

* To whom correspondence should be addressed. E-mail: stefanie.schreiber{at}med.ovgu.de.

Background and Purpose—The coincidence of hemodynamic and embolic findings in patients with stroke from large artery stenosis has suggested an interaction of both pathologies. This has emerged into the hypothesis of an impaired washout of emboli in the presence of hypoperfusion. We propose an additional link between both pathologies.

Summary of Case—A 48-year-old woman presented with a recurrent symptomatic severe left middle cerebral artery stenosis. MRI depicted left hemispheric ischemic infarcts in the deep and subcortical white matter and in the cortical border zone. One-hour transcranial Doppler monitoring detected 64 microembolic signals distal to the arterial stenosis. Monitoring also revealed recurrent thrombus formation at the stenotic plaque with decline of poststenotic flow velocity followed by embolism with abrupt excessive flow velocity increase and subsequent normalization at the initial baseline level. Cerebrovascular reserve in the distribution territory of the stenosed artery as assessed by transcranial Doppler after carbon dioxide stimulation revealed a normal reserve capacity in periods with baseline poststenotic flow velocity and an exhausted reserve capacity when flow velocity was decreased due to stenotic thrombus formation.

Conclusion—In our patient, adherent thrombus formation resulted in an increasing severity of the stenosis with subsequent vasodilatation and diminution of flow resistance in the depending vascular distribution territory. MRI suggested that adherent thrombi were predominantly washed into terminal supply and border zone brain regions, ie, into regions with supposed maximum vasodilatation and least flow resistance immediately before thrombus avulsion. Preferred wash-in of emboli into regions with low blood flow resistance might be an additional mechanism besides impaired washout in patients with severe large artery disease.


Key words: embolism • hypoperfusion • middle cerebral artery stenosis • transcranial Doppler sonography