A Clinical Trial of Pentoxifylline in Vascular Dementia

Abstract

Damage to the brain from vascular disease is, after Alzheimer’s disease, the second most common cause of the dementia syndrome. Longitudinal studies have demonstrated that approximately 10%-20% of patients with the dementia syndrome have vascular dementia; an approximately equal percentage have “mixed dementia” in which degenerative and vascular causes both contribute to the cognitive impairment [23,33]. The actual incidence of vascular brain damage in demented patients may be even higher. In a study in which serial coronal sections were stained with Weigert’s stain, Brun and Englund [6] found significant vascular damage to white matter in 30 of 48 demented patients who met clinical and neuropathological research criteria for Alzheimer’s disease (63%). The term “multi-infarct dementia” assumes that the pathophysiology in the large majority of cases is multiple, usually small, cerebral infarctions [13]. Such multiple infarcts tend to affect white matter more often than gray, leading to a “lacunar state” [13,21,24]. However, other mechanisms of vascular damage to white matter also occur, including those described originally by Binswanger [4]. Patients with such diffuse white matter damage are clinically heterogeneous; they may develop significant abnormalities of motor function, such as gait disturbances, or may be clinically indistinguishable from patients with Alzheimer’s disease [1,6,7]. Typical pathological findings include thinning of axons, loss of myelin, hyalinzation of smaller vessels, and varying degrees of edema [4].