REDUCTION OF FUNCTIONAL NEURONAL CONNECTIVITY IN LONG-TERM TREATED HYPERTENSION

Citation
Mj. Mentis et al., REDUCTION OF FUNCTIONAL NEURONAL CONNECTIVITY IN LONG-TERM TREATED HYPERTENSION, Stroke, 25(3), 1994, pp. 601-607
Citations number
45
Categorie Soggetti
Neurosciences,"Cardiac & Cardiovascular System
Journal title
StrokeACNP
ISSN journal
00392499
Volume
25
Issue
3
Year of publication
1994
Pages
601 - 607
Database
ISI
SICI code
0039-2499(1994)25:3<601:ROFNCI>2.0.ZU;2-3
Abstract
Background and Purpose Anatomic imaging of patients with chronic well- treated hypertension has demonstrated dilatation of the lateral cerebr al ventricles and left brain atrophy, whereas positron emission tomogr aphy has shown only subtle reductions in regional cerebral metabolic r ates for glucose in some subcortical nuclei. To further explore the im plications of the imaging changes, an analytic technique designed to d etermine functional neuronal connectivity between regions of interest (ROIs) was applied to the data on regional cerebral metabolic rates fo r glucose to determine if and where in the brain reduction of function al neuronal connectivity occurred. Methods Glucose metabolism was meas ured by positron emission tomography in 17 older men (age, 68+/-8 year s) with well-controlled, noncomplicated hypertension of at least 10 ye ars' duration and in 25 age- and sex-matched healthy control subjects. A significant correlation difference analysis was performed to determ ine which ROI pairs had reduced correlation coefficients (reduced func tional neuronal connectivity). The vascular pattern of the reduction w as determined after allocating the ROIs to their appropriate vascular territories. Results Compared with the control subjects, hypertensive patients had reduced correlation coefficients in cortical territories of the internal carotid arteries but not of the vertebrobasilar arteri es. The border zone supplied by the middle and anterior cerebral arter ies was most affected. Conclusions The border zone between the anterio r and middle cerebral arteries is vulnerable to ischemia from carotid pathology, systemic hypotension, or both. We hypothesize that although these hypertensive patients were ''well controlled'' and had normal n europsychological tests, they may have experienced ischemia severe eno ugh to cause border zone reduction of functional neuronal connectivity as a result of carotid pathology, antihypertensive medications, hypot ensive episodes with a right-shifted autoregulation curve, or other fa ctors in isolation or combination.