Meyer J S, Muramatsu K, Mortel K F, Obara K, Shirai T
Cerebrovascular Research Laboratories, Department of Veterans Affairs Medical Center, Houston, TX 77030, USA.
Stroke. 1995 May;26(5):735-42. doi: 10.1161/01.str.26.5.735.
Cognitive test performances were correlated prospectively with changes in cerebral CT measurements of atrophy, infarct volume, ventricular enlargement, local tissue density, and local perfusion to contrast annual rates of changes among patients with ischemic vascular dementia (IVD) or dementia of the Alzheimer type (DAT).
The cerebral atrophic index (ATI; ratio of cerebrospinal fluid or infarcted brain to intracranial volume), infarct volume ratio, ventricular volume ratio (VVR; ventricular volume/intracranial volume), cortical and subcortical gray and white matter local perfusion (local cerebral blood flow [LCBF]), and local Hounsfield unit (HU) density were measured concurrently and compared longitudinally with Cognitive Capacity Screening Examinations (CCSE) scores among 24 treated IVD (age, 68.2 +/- 9.7 years; follow-up, 42 +/- 27 months) and 24 DAT patients (age, 74.2 +/- 6.2 years; follow-up, 30 +/- 19 months).
IVD annual changes were as follows: CCSE, +1.2 +/- 5.9; ATI, +2.1%/y; VVR, +3.2%/y; and LCBF in the subcortical basal ganglia, -0.74 mL.100 g-1.min-1.y-1 (-1.8%/y). DAT annual changes were as follows: CCSE, -1.8/y; ATI, +8.1%/y; VVR, +9.6%/y; cortical LCBF, -2.0 mL.100 g-1.min-1.y-1 (-5.2%/y); LCBF in the basal ganglia, -3.0 mL.100 g-1.min-1.y-1 (-6.7%/y); white matter LCBF, -0.75 mL.100 g-1.min-1.y-1 (-4.1%/y); and all cortical tissue densities, -0.83 HU/y (-2.1%/y). In IVD, multiple regression analyses correlated cognitive changes directly with (1) recurrent silent infarctions and (2) bidirectional changes of perfusions within frontal white matter, thalamus, and internal capsules. In DAT, cognitive declines correlated with cerebral atrophy and cortical hypoperfusion related to frontotemporal and parietal cortical polioaraiosis (decreased gray matter tissue densities).
In IVD, recurrent strokes were not observed clinically during risk factor control, and antiplatelet therapy and cognitive impairments improved or stabilized. In DAT, cognitive performance relentlessly declined. Ischemic pathogenesis for vascular dementia is supported by the following: (1) cognitive declines correlate directly with recurrent "silent" strokes, and (2) bidirectional cognitive changes correlate directly with frontal white matter, thalamic, and internal capsular perfusional changes.
