CLINICAL CHARACTERISTICS OF RAPIDLY PROGRESSIVE LEUKOARAIOSIS

Citation
S. Tarvonenschroder et al., CLINICAL CHARACTERISTICS OF RAPIDLY PROGRESSIVE LEUKOARAIOSIS, Acta neurologica Scandinavica, 91(5), 1995, pp. 399-404
Citations number
16
Categorie Soggetti
Clinical Neurology
ISSN journal
00016314
Volume
91
Issue
5
Year of publication
1995
Pages
399 - 404
Database
ISI
SICI code
0001-6314(1995)91:5<399:CCORPL>2.0.ZU;2-2
Abstract
Introduction - 38 patients found to have either pure leuko-araiosis (L A) or LA combined with infarction(s) on computer tomography (CT) in 19 89 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 clin ically (including 24 hour ambulatory blood pressure measurement), and neuroradiologically (CT) in 1992 for this study. Results - 11 (29%) pa tients were found to have significant (rapid) progression of the exten t of LA on CT during the follow-up. At baseline, there was no signific ant difference in the mean number of brain infarctions between the gro ups 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 significantl y in both groups, but it was mostly because of the increase in cortica l infarctions in the prLA group (p = 0.043) and, conversely, the centr al ones in the nprLA group (p = 0.011). prLA was found to be related t o heart failure (82% vs 37%, p = 0.029) and atrial fibrillation (55% v s 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 infa rction. Other clinical factors, including mean blood pressure and hear t rate, did not clearly differentiate between the groups. Conclusion - The results suggest that there are different subgroups of patients wi th LA associated with various vascular factors. The occurrence of LA i s not related to the distribution of infarctions. The progression of L A is not related to the number of brain infarctions or to the simultan eous increase of infarctions on CT.