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Article
July 1996

Significant Progression of White Matter Lesions and Small Deep (Lacunar) Infarcts in Patients With Stroke

Author Affiliations

From the Department of Neurology, University Hospital Maastricht (Drs van Zagten, Boiten, and Lodder), and the Department of Epidemiology, University of Limburg (Dr Kessels), Maastricht, the Netherlands.

Arch Neurol. 1996;53(7):650-655. doi:10.1001/archneur.1996.00550070088015
Abstract

Objectives:  To investigate whether the extent of white matter lesions (WMLs) and the number of small deep infarcts and territorial infarcts progress over time in patients with stroke and to test the hypothesis that WMLs are associated with small deep infarcts.

Design:  Computed tomographic follow-up study in a cohort of 107 patients with ischemic stroke (median follow-up, 3.0 years).

Setting:  Primary and referral care center.

Patients:  Sixty-three of 144 registered patients with a first-ever symptomatic lacunar stroke and 44 of 155 with a territorial stroke entered this study. Forty-seven (33%) of the nonparticipating patients with a lacunar stroke and 54 (35%) of those with a territorial stroke died, and 34 (24%) and 57 (37%), respectively, refused computed tomographic follow-up.

Main Outcome Measures:  The extent of the WMLs and the number of small deep and territorial infarcts on computed tomographic scans at study entry and at follow-up.

Results:  Progression of WMLs occurred in 26 patients (26%), and multivariate regression analysis showed that it was associated with symptomatic lacunar stroke at study entry (adjusted odds ratio [aOR], 5.0; 95% confidence interval [CI], 1.2-20.3), silent small deep infarcts at study entry (aOR, 6.0; 95% CI, 1.0-34.6), old age (aOR, 5.5; 95% CI, 1.3-23.1), and longer follow-up (aOR, 12.7; 95% CI, 1.8-89.0). We found progression of small deep infarcts in 41 patients (38%). The progression was associated with symptomatic lacunar stroke at study entry (aOR, 27.7; 95% CI, 6.3-120.9) and longer follow-up (aOR, 7.7; 95% CI, 1.4-41.3). Progression of both WMLs and small deep infarcts, which occurred in 16 patients (16%), was associated with symptomatic lacunar stroke at study entry (aOR, 34.1; 95% CI, 2.5-471.7), silent small deep infarcts at study entry (aOR, 12.5; 95% CI, 1.4-112.0), and longer follow-up (aOR, 29.7; 95% CI, 1.8-501.0). The number of territorial infarcts increased in 14 patients (13%). The increase was associated with symptomatic territorial stroke at study entry (aOR, 7.9; 95% CI, 1.5-40.8) and a history of ischemic heart disease (aOR, 6.6; 95% CI, 1.3-34.8).

Conclusions:  The marked progression of WMLs and small deep infarcts that occurred mainly in patients with lacunar stroke suggests that both WMLs and small deep (lacunar) infarcts are caused by a similar vasculopathy that affects small vessels, which is progressive despite standard stroke treatment.

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