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Chapter 55: Ischemia
Maureen C. Jensen, Michael N. Brant-Zawadzki, and Brian C. Jacobs

• Key Points
• Introduction
• Pathophysiology
• Imaging Strategies
• Clinical Entities Associatied with Cerebral Ischemia
• Summary
• References

The content presented is from Chapter 55 of the upcoming Magnetic Resonance Imaging, Third Edition, text by David D. Stark and William G. Bradley, Jr.

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Introduction

Stroke is the third leading cause of death among adult Americans after ischemic heart disease and all forms of cancer.³² Furthermore, stroke is the major cause of disability in the adult population and has a staggering socioeconomic impact both directly in terms of health care costs and indirectly in lost income.^28,49 Stroke is a vernacular term that denotes the sudden development of a neurological deficit. A stroke may be caused by a diverse spectrum of disorders, such as a vascular occlusion, hypoxia, hypoglycemia, or bleeding into a tumor. However, the overwhelming majority of strokes can be placed into two categories—ischemia (approximately 85%) and hemorrhage (10% to 15%).³² Of ischemic strokes, 85% are thromboembolic in origin, and up to a quarter are cardioembolic.^32-34 Most hemorrhagic strokes are caused by hypertensive arteriopathy, with other less common etiologies including amyloid angiopathy, aneurysms, vascular malformations, and moyamoya disease. The role of the radiologist is to confirm the clinical diagnosis and to more specifically identify the particular insult responsible for the stroke syndrome so that appropriate and timely therapy can be instituted.

Ischemia is a physiological term indicating insufficient blood flow for normal cellular function. Infarction is a pathological term denoting permanent tissue damage caused by ischemia. Transient ischemic attack (TIA), reversible ischemic neurological deficit (RIND), and stroke are terms that describe clinical syndromes. Specifically a neurological event of sudden onset that reflects a vascular distribution and reverses within 24 hours is defined as a TIA. If the symptoms persist for more than a day but less than a week and eventually resolve, the occurrence is defined as an RIND. There is often a dissociation between the events at the cellular level and the clinical status of the patient. For example, even when permanent tissue damage (i.e., infarction) occurs from ischemia, the clinical neurological deficit may be nonexistent, transient, or permanent.^14,66

Magnetic resonance imaging (MRI) offers unique advantages for the evaluation of cerebral ischemia in both the clinical and experimental setting. Ischemia leads to alterations in the brain water content, even in its earliest stages. Because of MRI's inherent sensitivity to depict alterations in tissue-free water content, it can detect ischemic insult to the brain within 1 hour after onset.^22,24 MR angiography (MRA) (see Chapter 56) can depict the major routes of vascular supply to the brain and can be performed simultaneously with evaluation of the parenchyma. The potential of MRI for evaluating ischemia also extends to the field of spectroscopy (see Chapter 72), which offers an in vivo method for investigating fundamental metabolic cellular processes. In addition, as a result of recent advances in MRI scanner hardware and software, the capability to image and measure molecular diffusion and capillary flow or perfusion has emerged, which is likely to significantly alter the future of neuroimaging.

This chapter begins with an overview of the fundamental pathophysiological mechanisms of cerebral ischemia. A review of causative disease entities and their characteristic appearances on MRI follows.

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