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Clinical characteristics of rapidly progressive leuko‐araiosis
Author(s) -
TarvonenSchröder S.,
Räihä I.,
Kurki T.,
Rajala T.,
Sourander L.
Publication year - 1995
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1995.tb07028.x
Subject(s) - medicine , psychology
Introduction – 38 patients found to have either pure leuko‐araiosis (LA) or LA combined with infarction(s) on computer tomography (CT) in 1989 were re‐examined in 1992 in order to evaluate the progression of LA. The follow‐up period averaged 3.2 years. Material and methods ‐ The clinical and radiological data on patients in 1989 were collected from hospital records and re‐evaluated. The patients were re‐examined clinically (including 24 hour ambulatory blood pressure measurement), and neuroradiologically (CT) in 1992 for this study. Results – 11 (29%) patients were found to have significant (rapid) progression of the extent of LA on CT during the follow‐up. At baseline, there was no significant difference in the mean number of brain infarctions between the groups with progressing (prLA) and non‐progressing LA (nprLA) or between the number of cortical and central infarctions within these groups. At follow‐up, the total number of infarctions had increased significantly in both groups, but it was mostly because of the increase in cortical infarctions in the prLA group (p = 0.043) and, conversely, the central ones in the nprLA group (p = 0.011). prLA was found to be related to heart failure (82% vs 37%, p = 0.029) and atrial fibrillation (55% vs 19%, p = 0.047), whereas nprLA was strongly associated with a sudden onset of symptoms (78% vs prLA 18%, p = 0.001) like a‐true brain infarction. Other clinical factors, including mean blood pressure and heart rate, did not clearly differentiate between the groups. Conclusion ‐ The results suggest that there are different subgroups of patients with LA associated with various vascular factors. The occurrence of LA is not related to the distribution of infarctions. The progression of LA is not related to the number of brain infarctions or to the simultaneous increase of infarctions on CT.

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