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Chapter 18 - Magnetic resonance spectroscopy in severe obstructive carotid artery disease

from Section 2 - Cerebrovascular disease

Published online by Cambridge University Press:  05 March 2013

By
Jeroen van der Grond  and
Dirk R. Rutgers
Edited by
Jonathan H. Gillard ,
Adam D. Waldman  and
Peter B. Barker
Jonathan H. Gillard
Affiliation:
University of Cambridge
Adam D. Waldman
Affiliation:
Imperial College London
Peter B. Barker
Affiliation:
The Johns Hopkins University School of Medicine
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Summary

Hemodynamic changes in severe obstructive carotid artery disease

Severe stenosis or occlusion of the internal carotid artery (ICA) causes a reduction in arterial pressure distal to the stenosis or occlusion. This activates several regulatory mechanisms in the brain to maintain cellular function. The primary physiological changes are recruitment of collateral channels: that is, collateral flow via the circle of Willis, the ophthalmic artery, or the leptomeningeal vessels. The recruitment of blood flow through these alternative channels is stimulated by a reduction in the peripheral resistance as a result of vasodilatation of the peripheral brain arteries. Under normal circumstances, this mechanism is adequate and a small decrease in the cerebral perfusion pressure has little effect on the cerebral blood flow (CBF). However when the cerebral perfusion pressure continues to fall, this mechanism may be insufficient to maintain a normal CBF. Three stages of hemodynamic failure have been identified.[1–3] Stage 1, hemodynamic compensation, is identified as an increase in cerebral blood volume (CBV) in the hemisphere distal to the occlusive lesion, with normal CBF, oxygen extraction fraction (OEF), and the cerebral metabolic rate of oxygen metabolism (CMRO2) (Fig. 18.1). When the mechanisms for collateral flow are limited, for example poor collateral flow in the circle of Willis or poorly developed leptomeningeal vessels, or when the capacity for compensatory vasodilatation has been exceeded, autoregulation fails and a decrease in the cerebral perfusion pressure results in a decreased CBF.[4–6] To preserve cellular integrity (CMRO2), the OEF increases.[7] This situation is known as stage 2 of hemodynamic failure. In addition, it has been recognized that CBF, CBV, OEF, and CMRO2 are all likely to decrease when the arterial pressure continues to fall (stage 3 of hemodynamic failure).[2] In patients with chronic cerebral hemodynamic compromise, it has been suggested that stage 3 is important in the pathophysiology of so-called low-flow infarctions.[2] These low-flow infarctions, or border-zone infarctions, are located in the most distal part of the perfusion territory of the main cerebral arteries and are the first areas to suffer ischemic damage when blood flow decreases.[8–10] The entire concept of hemodynamical staging is based on position emission tomography (PET) techniques in patients with severe atherosclerotic carotid artery stenosis or occlusion and have been widely applied in the study of human cerebrovascular disease.[5,11]

Type
Chapter
Information
Clinical MR Neuroimaging
Physiological and Functional Techniques
 , pp. 248 - 257
Publisher: Cambridge University Press
Print publication year: 2009

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