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Editorial |

New Insight Into Binswanger Disease

Gustavo C. Román, MD, FRSM
Arch Neurol. 1999;56(9):1061-1062. doi:10.1001/archneur.56.9.1061.
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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 visualized as hyperintensities on magnetic resonance imaging scans,7,8 rendering the name irrelevant. More unfortunately, leukoaraiosis is often used interchangeably with Binswanger disease. The use of this term in this sense should be discouraged, since "leukoaraiosis is neither a disease nor even a specific indicator of white-matter ischemia,"4 and one can hardly study the pathophysiologic characteristics, symptoms, and natural history of a radiologic image.9 It is currently accepted that Binswanger-type leukoencephalopathy is caused by hypoxia-ischemia of distal watershed periventricular territories,9,10 the combined effects of arteriolosclerosis and elongation of medullary arterioles, dilatation of the perivascular spaces (état criblé), and decreased brain perfusion from hypotension or low cardiac output. The most important single risk factor appears to be aging of cerebral arterioles.11,12 In the Cardiovascular Health Study,13 about one third of subjects aged 65 years and older showed Binswanger-type white-matter lesions on magnetic resonance imaging scans. The severity of the lesions increased with age, hypertension, silent lacunar strokes, hypotension, smoking, and low income, the latter risk factor being a probable surrogate for limited access to medical care, inadequate diet, and poor control of hypertension.14 The effects of sustained daytime arterial hypertension, hypertensive crises, and the absence of a normal nocturnal dip in blood pressure (nondipping) are particularly damaging.15,16

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