Ischemic stroke

Brian Silver MD (

Dr. Silver of the University of Massachusetts Medical School received consulting fees from the Women's Health Initiative as an adjudicator and from Medicolegal Malpractice Review for consulting. He also receives a salary from the Joint Commission for conducting Comprehensive Stroke Center surveys.

)
Steven R Levine MD, editor. (Dr. Levine of the SUNY Health Science Center at Brooklyn has received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.)
Originally released September 11, 1996; last updated April 19, 2018; expires April 19, 2021

This article includes discussion of ischemic stroke, bland infarction, cerebral infarction, cerebrovascular accident, CVA, ischemic infarction, and stroke. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Stroke is the leading cause of serious long-term disability in the United States and the fifth leading cause of death. Nearly 90% of all strokes are ischemic. In this article, the author reviews the history, clinical manifestations, risk factors, and pathology of ischemic stroke. Readers will learn about the important advances made in diagnosis, acute treatment, and prevention of stroke. Readers will also learn about advancements in recovery from stroke.

Key points

 

• Nearly 90% of all strokes are ischemic.

 

• Important stroke risk reduction strategies include: antiplatelets, anticoagulants, arterial revascularization, blood pressure medications, cholesterol medications, cessation of smoking, diet modification, and exercise.

 

• Acute treatment of ischemic stroke includes thrombolytic therapy within 4.5 hours, endovascular treatment within 24 hours, antiplatelet therapy within 48 hours, and stroke unit hospitalization.

 

• Stroke recovery treatments include physical therapy, occupational therapy, speech therapy, and constraint-induced movement therapy.

Historical note and terminology

Around the time of the Babylonian empire (approximately 586 BCE), the following proclamation was made “If I forget thee, O Jerusalem, let my right hand forget its cunning. If I do not remember thee, let my tongue cleave to the roof of my mouth" (Psalms 137:5-6). Although perhaps not fully comprehending the pathogenesis of their observations, the speakers of these words were describing a stroke affecting the left hemisphere.

Over 2000 years ago, stroke was called “apoplexy,” a general term that applied to anyone suddenly struck down with paralysis (Anonymous 2010). Some of the earliest descriptions of stroke are attributed to Hippocrates in 400 BCE. In his aphorisms, he made the following observations: “Persons are most subject to apoplexy between the ages of forty and sixty” (VI:57), and “it is impossible to remove a strong attack of apoplexy, and not easy to remove a weak attack” (II:47) (Aphorisms E-book by Hippocrates 2010). Although these observations might have been true at the time, modern epidemiology has demonstrated that stroke can occur throughout the lifespan. Further, novel treatments have improved the prognosis of patients with acute events.

The first person to investigate the pathology underlying apoplexy was Johann Jacob Wepfer of Switzerland (Anonymous 2010). During the mid-1600s, he identified signs of postmortem bleeding in patients who died of apoplexy. He also learned of the carotid and vertebral arteries while performing autopsies. Wepfer first suggested that apoplexy could be caused by blockage of 1 of the main arteries supplying blood to the brain, besides being caused by bleeding in the brain. Thus, stroke was recognized as a cerebrovascular disease.

Dechambre first used the term “lacunae” in 1838 to describe small cavities that developed during the process of resorption within cerebral softenings (Poirier and Derouesne 1985). In 1901, Pierre Marie described lacunae as small cerebral softenings caused by occlusion of the blood vessels by a "local arteriosclerotic process" (Poirier and Derouesne 1985).

C Miller Fisher made several important contributions to the understanding of stroke pathogenesis. He identified the relationship between obstruction of the internal carotid arteries in the neck and cerebrovascular disease and further suggested that thrombotic debris were responsible for the event (Fisher 1951). He also described the vascular pathology underlying lacunar infarcts (Fisher 1965) and went on to describe many of the lacunar stroke syndromes, including pure motor hemiplegia, pure sensory stroke, homolateral ataxia and crural paresis, dysarthria-clumsy hand syndrome, sensorimotor stroke, and basilar branch syndromes.

Kubik and Adams provided a landmark description of basilar artery occlusion (Kubik and Adams 1946). The clinical characteristics of "top of the basilar" syndrome were described by Caplan (Caplan 1980).

The development of neuroimaging techniques opened a new chapter in the study of stroke. Cerebral angiography was developed by Moniz in 1927 (Ferro 1988). He also gave the first description of internal carotid artery occlusion by angiography in 1937 (Ferro 1988). The first ultrasonic image of the carotid arteries and the bifurcation were recorded by Reid and Spencer in 1972 (Reid and Spencer 1972). Based on previous experiments using computed tomography, Hounsfield introduced CT for commercial use in 1972 (Webb 1992). The first clinical use of head CT was reported by Ambrose (Ambrose 1973). The application of nuclear magnetic resonance to imaging, done independently by Bloch and Purcell, led to magnetic resonance imaging (Andrew 1992). Lauterbur and Damadian developed the first low quality medical images in the early 1970s (Seynaeve and Broos 1995).

The first use of aspirin for vascular prevention is attributed to Craven in 1950 (Craven 1950). McDevitt and colleges described the effectiveness of anticoagulant therapy in 100 patients with cerebral thrombosis or embolism in the 1950s (McDevitt et al 1958).

Eastcott, Rob, and Pickering first reported reconstruction of the internal carotid artery in a patient with intermittent hemiplegia (Eastcott et al 1954). Later, DeBakey and colleagues realized that recanalization of an occluded vessel could lead to intracerebral hemorrhage (Bruetman et al 1963).

Strokes may be either hemorrhagic or ischemic. Eighty-seven percent of all strokes are due to ischemia (Lloyd-Jones et al 2010). On average, every 40 seconds someone in the United States has a stroke.

The classic definition of ischemic stroke, and one still used by the World Health Organization classification, is a sudden, focal neurologic deficit lasting more than 24 hours, confined to an area of the brain or eye perfused by a specific artery, and presumed to be of vascular origin. The classic definition of transient ischemic attack is a sudden, focal neurologic deficit lasting fewer than 24 hours, confined to an area of the brain or eye perfused by a specific artery, and presumed to be of vascular origin (Albers et al 2002). The 24-hour definition distinguishing transient ischemic attacks from ischemic strokes was arbitrarily chosen. Studies using diffusion-weighted magnetic resonance imaging show that about a third of all events classified as transient ischemic attacks are associated with positive scans (Brazzelli et al 2014). The percentage of patients with a diffusion-weighted magnetic resonance imaging lesion increases with increasing total symptom duration (Kidwell et al 1999). A proposed definition of stroke was “a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of acute infarction” (Albers et al 2002). Using such a definition would decrease transient ischemic attack diagnoses by approximately one third and increase stroke diagnoses by less than 10% (Ovbiagele et al 2003). The most current definition of stroke proposed by the American Stroke Association is “CNS infarction is brain, spinal cord, or retinal cell death attributable to ischemia, based on pathological, imaging, or other objective evidence of cerebral, spinal cord, or retinal focal ischemic injury in a defined vascular distribution; or clinical evidence of cerebral, spinal cord, or retinal focal ischemic injury based on symptoms persisting ≥24 hours or until death, and other etiologies excluded” (Sacco et al 2013).

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