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(Stroke. 2006;37:1348.)
© 2006 American Heart Association, Inc.

Editorials

Leukoaraiosis and Ischemia

Beyond the Myth

David G. Munoz, MD, FRCPC

From the University of Toronto, Department of Laboratory Medicine & Pathobiology, Toronto, ON, Canada.

Correspondence to David G. Munoz, University of Toronto, Department of Laboratory Medicine & Pathobiology, Room # 2-097 Cardinal Carter, St Michael’s Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada. E-mail dave_munoz@yahoo.com

Key Words: etiology • ischemia • leukoaraiosis

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

See related article, pages 1391–1398

Although Alois Alzheimer had described in 1902 a baffling extensive and severe degeneration of the cerebral white matter (misnamed Binswanger disease), over half a century of regular examination of brains by histological techniques failed to recognize the common occurrence of bilateral, patchy or confluent, white matter lesions revealed first as hypodense areas by computed tomography and later with much improved definition as hyperintensities in T2 and FLAIR sequences in magnetic resonance.¹ Even in retrospect, it is hard to identify on histological sections the exact location of lesions so brightly demonstrated on magnetic resonance images. The name leukoaraiosis will be used in this editorial to designate these white matter lesions, as opposed to others related to demyelinating, infectious, toxic, or metabolic processes.²

Having named the finding we were left with an existentialist lesion in search of significance. As a marker, leukoaraiosis is a prognostic factor for stroke and myocardial infarction.^3,4 Its consequences, even in samples restricted to nondisabled elderly, include impaired cognitive function,^5,6 mediated by deterioration in information processing speed and executive functions,⁷ as well as reduced motor function,⁸ and possibly late onset-depression.⁹

But how are the lesions produced? Epidemiological studies suggest association with aging and vascular risk factors such as hypertension and diabetes,^10,11 whereas histological studies indicate association with arteriolosclerosis of small blood vessels in the brain, consisting of replacement of mural smooth muscle by fibrohyaline material which eventually results in thickening of the wall and sometimes narrowing of the lumen.^12,13 Several mechanisms are . . . [Full Text of this Article]

Related Article:

White Matter Lesions in an Unselected Cohort of the Elderly: Molecular Pathology Suggests Origin From Chronic Hypoperfusion Injury • Annex – Supplemental Online-Only Content

Malee S. Fernando, Julie E. Simpson, Fiona Matthews, Carol Brayne, Claire E. Lewis, Robert Barber, Raj N. Kalaria, Gill Forster, Filomena Esteves, Stephen B. Wharton, Pamela J. Shaw, John T. O’Brien, Paul G. Ince on behalf of the MRC Cognitive Function and Ageing Neuropathology Study Group
Stroke 2006 37: 1391-1398. [Abstract] [Full Text] [PDF]

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