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Mechanisms of Disease: pathophysiological concepts of stroke in hemodynamic risk zones—do hypoperfusion and embolism interact?

Nature Clinical Practice Neurology volume 4, pages 216–225 (2008)Cite this article

Abstract

The pathophysiology of cerebral ischemia in the borderzones between the large cerebral arteries has been the topic of considerable debate since this disease entity was defined in the first half of the twentieth century. Hemodynamic failure and microembolization were two seemingly mutually exclusive pathophysiological concepts that were proposed to explain the phenomenon of borderzone infarction in patients with arterial occlusive disease. Sufficient evidence has now accumulated, however, to indicate that borderzone infarcts are in fact caused by an interaction between hypoperfusion and microembolization. In this Review, we summarize the historical background of borderzone infarction and current knowledge regarding the various possible pathophysiological concepts. We present a representative survey of publications from the 1950s to the present day, starting with early autopsy-based studies, followed by later anatomical and in vitro studies, as well as CT-based and MRI-based investigations. The clinical symptoms of borderzone infarction and the possibility of a clinical distinction between borderzone and territorial infarcts are discussed. In addition, we consider techniques to localize hemodynamic risk zones in patients with arterial occlusive disease, such as perfusion-weighted MRI, and techniques to identify a hemodynamic component of stroke, such as investigation of the cerebrovascular reserve capacity with transcranial Doppler ultrasound.

Key Points

  • First described in the 1950s, borderzone infarcts located at the edges of vascular territories of the large cerebral arteries are a common infarction pattern in patients with occlusive artery disease or hemodynamic failure

  • Borderzone infarcts can be subdivided into cortical and internal borderzone infarcts; the prevalence of cortical borderzone infarcts varies from 4.7 to 7.9% among all cerebral infarcts, whereas the prevalence of internal borderzone infarcts ranges from 4.4–6%, rising to 26–41% in patients with internal carotid artery occlusive disease

  • Two seemingly distinct concepts have been proposed to explain the pathophysiology of borderzone infarcts—hemodynamic failure caused by hypoperfusion in patients with internal carotid artery occlusive disease or acute decrease of blood pressure, and arterio-arterial or cardial microembolization

  • The impaired washout concept combines hemodynamic failure and microembolization, postulating impaired clearance of microemboli as the probable underlying pathophysiology in patients with borderzone infarcts

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Figure 1: Examples of borderzone infarcts on diffusion-weighted MRI.
Figure 2: Computerized registration and overlay of diffusion-weighted MRI lesions on perfusion-weighted MRI images in a patient with a right internal borderzone infarct and right internal carotid artery occlusion.
Figure 3: Brain images from a patient with a right internal borderzone infarct and right internal carotid occlusion.
Figure 4: Schematic illustration of theoretical concepts of stroke in hemodynamic risk zones.
Figure 5: Neurological symptoms in patients with borderzone infarcts.
Figure 6: Impaired cerebral vasomotor reactivity in the right MCA in a patient with high-grade right internal carotid artery stenosis (80%).
Figure 7: Detection of high-intensity transient signals with a multigate transcranial Doppler device in a patient with high-grade internal carotid artery stenosis.

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Authors and Affiliations

  1. and MG Hennerici is Professor of Neurology and Chairman of the Department of Neurology, A Förster is an Intern in Neurology, K Szabo is an Assistant Professor in Neurology and the Senior Physician of the Stroke Unit, at the Universitätsklinikum Mannheim, Mannheim, Germany.,

    Alex Förster, Kristina Szabo & Michael G Hennerici

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  1. Alex Förster
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  2. Kristina Szabo
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  3. Michael G Hennerici
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Correspondence to Michael G Hennerici.

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Förster, A., Szabo, K. & Hennerici, M. Mechanisms of Disease: pathophysiological concepts of stroke in hemodynamic risk zones—do hypoperfusion and embolism interact?. Nat Rev Neurol 4, 216–225 (2008). https://doi.org/10.1038/ncpneuro0752

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