Book contents
- Frontmatter
- Contents
- Contributors
- Case studies
- Preface to the second edition
- Preface to the first edition
- Abbreviations
- Introduction
- Section 1 Physiological MR techniques
- Section 2 Cerebrovascular disease
- Chapter 13 Cerebrovascular disease
- Chapter 14 Magnetic resonance spectroscopy in stroke
- Chapter 15 Diffusion and perfusion MR in stroke
- Chapter 16 Arterial spin labeling in stroke
- Chapter 17 Magnetic resonance diffusion tensor imaging in stroke
- Chapter 18 Magnetic resonance spectroscopy in severe obstructive carotid artery disease
- Chapter 19 Perfusion and diffusion imaging in chronic carotid disease
- Chapter 20 Susceptibility imaging and stroke
- Section 3 Adult neoplasia
- Section 4 Infection, inflammation and demyelination
- Section 5 Seizure disorders
- Section 6 Psychiatric and neurodegenerative diseases
- Section 7 Trauma
- Section 8 Pediatrics
- Section 9 The spine
- Index
- References
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
- Frontmatter
- Contents
- Contributors
- Case studies
- Preface to the second edition
- Preface to the first edition
- Abbreviations
- Introduction
- Section 1 Physiological MR techniques
- Section 2 Cerebrovascular disease
- Chapter 13 Cerebrovascular disease
- Chapter 14 Magnetic resonance spectroscopy in stroke
- Chapter 15 Diffusion and perfusion MR in stroke
- Chapter 16 Arterial spin labeling in stroke
- Chapter 17 Magnetic resonance diffusion tensor imaging in stroke
- Chapter 18 Magnetic resonance spectroscopy in severe obstructive carotid artery disease
- Chapter 19 Perfusion and diffusion imaging in chronic carotid disease
- Chapter 20 Susceptibility imaging and stroke
- Section 3 Adult neoplasia
- Section 4 Infection, inflammation and demyelination
- Section 5 Seizure disorders
- Section 6 Psychiatric and neurodegenerative diseases
- Section 7 Trauma
- Section 8 Pediatrics
- Section 9 The spine
- Index
- References
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 NeuroimagingPhysiological and Functional Techniques, pp. 248 - 257Publisher: Cambridge University PressPrint publication year: 2009