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Clinical, radiological and pathological correlates of leukoaraiosis

Authors


Eitan Auriel, Department of Neurology, Tel Aviv Medical Center, 6 Weitzman st,Tel Aviv, Israel 64239
Tel.: 972-52-4262721
Fax: 972-3-6973146
e-mail: eitanman1@gmail.com

Abstract

Auriel E, Bornstein NM, Berenyi E, Varkonyi I, Gabor M, Majtenyi K, Szepesi R, Goldberg I, Lampe R, Csiba L. Clinical, radiological and pathological correlates of leukoaraiosis.
Acta Neurol Scand: 2011: 123: 41–47.
© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard.

Introduction - Leukoaraiosis is characterized by an abnormal appearance of the brain white matter on imaging. Its pathogenesis is still a matter of investigation. The purpose of this study was to investigate the radiological, clinical and pathological correlates of leukoaraiosis. Methods - The study population consisted of 93 deceased patients. The pre-mortem T2W magnetic resonance images were evaluated for the presence and grading of leukoaraiosis. The clinical and pathological characteristics based on the clinical charts and autopsy reports were evaluated. Tissue specimens of the blocks of 19 brains that demonstrated severe leukoaraiosis and those of five control brains were excised and stained. Results - The variables found to be significantly associated with leukoaraiosis were age and a clinical history of Parkinson’s disease. Other risk factors and pathological markers of atherosclerosis were not significantly correlated with leukoaraiosis. No significant difference was found between the scoring of the myelin integrity, glial fibrillary acidic protein, cluster of differentiation 68 and smooth muscle actin. There was a significant difference with respect to thickening of vessels walls. Conclusions - Our pathological results indicate that structural vascular abnormalities characterized by vessel wall thickening are associated with leukoaraiosis, supporting the assertion that vascular changes and ischemia generate leukoaraiosis. The relations between parkinsonism and leukoaraiosis may be explicable through vascular effects on the circuitry of the basal ganglia.

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