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New Insight Into Binswanger Disease
Arch Neurol. 1999;56:1061-1062.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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BINSWANGER DISEASE is a well-established clinical pathological entity1 characterized by an ischemic periventricular leukoencephalopathy that typically spares the arcuate subcortical U fibers and is manifested clinically by subcortical frontal executive dysfunction, parkinsonian gait disturbances, urinary incontinence, mood changes, and pseudobulbar palsy.2 Binswanger disease is one of the most common forms of vascular dementia in the elderly.3 However, intense controversy still surrounds its clinical manifestations, pathophysiology, and prevalence.4 Unfortunately, as noted by Caplan,2 "dispute over the name of the condition has diverted attention away from more important issues." In addition to the descriptive but cumbersome periventricular leukoencephalopathy, a dozen other synonyms have been proposed to name Binswanger-type white-matter lesions.5 Currently, the concise term leukoaraiosis (Greek for white rarefaction) is widely used. Proposed initially as a noncommittal, purely descriptive radiological term, leukoaraiosis is used to describe the white-matter hypodensities seen on brain computed tomographic scans.5-6 Nonetheless, these lesions are usually . . . [Full Text of this Article]
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