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  • Updated 03.06.2018
  • Released 09.18.1995
  • Expires For CME 03.06.2021

Cerebral embolism

Introduction

This article includes discussion of cerebral embolism, atheroembolic stroke, and cardioembolic stroke. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Cardioembolic stroke is one of the more devastating causes of stroke. Significant progress has been made in identifying patients at high risk for cardioembolic stroke. With the aging of the population, an increasing number of patients are at risk for cardioembolism. In this article, the author provides an update on cardioembolic stroke prevention. Data from trials on stroke prevention, including information on novel oral anticoagulants in atrial fibrillation patients, are provided. In addition, studies on closure devices for patent foramen ovale are reviewed. New insights regarding endocarditis and stroke are highlighted. Finally, information is provided regarding antithrombotic therapy for patients with reduced cardiac ejection fraction.

Key points

• Cardioembolic strokes are more severe clinically than other forms of stroke.

• Atrial fibrillation is the leading source of cardioembolic stroke.

• The proportion of cardioembolic strokes will increase with the aging of the population.

• Trials have shown a modest reduction in stroke with patent foramen ovale closure but questions remain on appropriate patient selection.

Historical note and terminology

What is now called "stroke" was referred to as "apoplexy" in the writings of Hippocrates (460 BCE to 370 BCE). Apoplexy was defined as "to be struck down by violence or paralysis." It was probably formed from the Greek words apo ("from"), plesso ("thunderstruck"), and ia ("condition"). The term "apoplexy" was applied to myriad conditions, from illnesses affecting the level of consciousness to disorders causing a change in sensation. Apoplexy was differentiated from other conditions by its sudden onset, resulting in loss of consciousness and paralysis. During the period of the Roman Empire, Aurelius Celsus (25 BCE to 50 AD) differentiated apoplexy from paralysis. He noted that during apoplexy the entire body is paralyzed, including sensation, understanding, and movement, whereas with paralysis the effects are localized (28; 24).

There was little progress in the understanding of stroke during the Middle Ages and Renaissance. During the 18th century, Hermann Boerhaave (1668 to 1738) and his followers returned to a more methodical and analytical approach to medicine. Van Swieten's commentaries on Boerhaave are generally believed to be the first suggestion that cerebral embolism could cause apoplexy:

It has been established by many observations that these polyps occasionally attach themselves as excrescences to the columnae carnae of the heart, and perhaps then separate from it and are propelled, along with the blood, into the pulmonary artery or the aorta, and its branches.... were they thrown into the carotid or vertebral arteries, could disturb—or if they completely blocked all approach of arterial blood to the brain—utterly abolish the functions of the brain (28).

During the 19th century, advances were made in understanding the pathophysiology of cerebral embolism and thrombosis. Julius Cohnhien, trained by Virchow, demonstrated the effects of embolization by producing ischemic and hemorrhagic lesions when wax globules were injected into a frog's tongue arteries (33).

The heart was established as an important source for the development of emboli when Gowers, in 1875, described a case of left middle cerebral artery and retinal artery emboli (33). The auricular appendage associated with mitral stenosis was identified as the likely origin of the emboli.

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