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(Stroke. 2003;34:1916.)
© 2003 American Heart Association, Inc.

Original Contributions

Editorial Comment—The Progression of Leukoaraiosis

Department of Neurology, Royal Free Hospital, London, England

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Leukoaraiosis (LA), the presence of rarefaction of the white matter originally described on CT¹ but now more commonly recognized on MRI, was originally largely ignored as an inconsequential finding seen in association with cerebrovascular disease. More recently, it has become clear that LA impairs cognition.² When LA is sufficiently prominent to be seen on CT, its associated cognitive impairment is readily detected. When seen only on MRI, a more sensitive technique, more sensitive cognitive tools are needed.³ At least as important is the effect of one cognitive disorder to accelerate another, and LA may causally accelerate the progression of Alzheimer disease, for example.⁴ LA is therefore not the unimportant phenomenon it was once considered.

LA encompasses a wide range of histological changes ranging from local edema⁵ to demyelination, loss of axons and oligodendroglia, and mild reactive gliosis without cavitation but does not include frank infarction. The mechanism is not considered to be chronic low perfusion as cerebral blood flow in affected areas lies within normal limits at rest or is modestly decreased in proportion to tissue loss. There is, however, clear evidence of diminished perfusion reserve,^6,7 and it is hypothesized that episodic mild ischemia occurs as a result of intermittent changes in cerebral perfusion pressure. The process has been termed "incomplete infarction."⁸ That extensive areas of LA may be seen without local evidence of completed ischemic events has led to the suggestion that part of the mechanism may be increased blood-brain barrier permeability leading to leakage of serum proteins, which . . . [Full Text of this Article]

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