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John C. M. Brust, MD

Arch Neurol. 1988;45(7):799-801.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

There are different kinds of vascular dementia.¹ Ignoring indirect mechanisms (such as hydrocephalus following subarachnoid hemorrhage²), we might hypothesize a pathophysiologic spectrum. At one end would be circumscribed intellectual impairment from destruction of particular brain areas, for example, memory loss after inferior temporal lobe infarction.³ This type of dementia seldom produces diagnostic (or conceptual) difficulty. At the other end would be more insidiously progressive dementia from diffuse small-vessel pathology (Binswanger's disease).^4-9 This type of dementia is understood by no one, and estimates of its prevalence range from infinitesimal to epidemic. Between these two extremes is cognitive loss from multiple lesions, none of which alone would be expected to cause intellectual impairment (multiinfarct dementia).¹⁰ This type of dementia is overdiagnosed.

Two decades ago Tomlinson et al,¹¹ comparing the brains of 50 old people with dementia with those of control subjects without dementia, diagnosed dementia of . . . [Full Text PDF of this Article]

Author Affiliations
From the Departments of Neurology, Harlem Hospital Center and the Columbia University College of Physicians and Surgeons, New York.

Footnotes
Accepted for publication June 12, 1987.

Reprint requests to Department of Neurology, Harlem Hospital Center, 506 Lenox Ave, New York, NY 10037 (Dr Brust).

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