Cerebral microinfarcts disruption of remote cortical thickness
Introduction
Cerebral microinfarcts (CMI) are the most widespread type of brain infarction [1]. These asymptomatic lesions can be demonstrated by MRI as small hyperintense lesions on diffusion weighted imaging (DWI) only during the acute phase (~10 days), thereby making it difficult to determine the total number of CMIs [1,2]. Previous studies have shown that detecting even a single CMI suggests the presence of hundreds to thousands CMIs [1,3], pointing out their potential important contribution to small-vessel–related cognitive impairment [[4], [5], [6]].
These lesions may cause both local and remote brain structural changes [4,7]. CMIs were previously found to cause local microstructural damage and disruption of white matter integrity [4], but the effect on grey matter has not yet been established. This prospective study examined CMIs long standing influence on cortical thickness in remote areas.
Section snippets
Study population
Five Participants recruited for the Tel-Aviv Brain Acute Stroke Cohort study (TABASCO) [8], were included in the present study. The TABASCO study included men and women aged over 50, admitted to the Tel-Aviv Medical Center from April 2008 to January 2015, due to first ever TIA or mild to moderate acute ischemic stroke (NIH stroke scale [9] (NIHSS) < 17). Out of this cohort, 66 participants had both baseline and follow-up MRI scans. These patients had similar baseline characteristics compared to
Results
Five subjects (Table 1; mean age 71.6 ± 11 years) had a total of 6 DWI lesions; 4 of the 5 had a single DWI lesion, while one (subject A) had 2 lesions on one scan. (See Fig. 1.) The mean time interval between the lesion detecting DWI and the postlesional scans were 25.1 ± 1.2 months. The mean cortical thickness lesion/control ratio within the ROI decreased on the postlesional scans from 1.8 to 1.1 (t = 2.36, p = 0.032) and the median CTR decreased from 2.12 to 1.17 (Z = -1.76, p = 0.039) in
Discussion
In this study we demonstrated that small asymptomatic DWI lesions have prolonged influence on cortical thickness in remote ROI after a mean follow-up interval of 2 years. This finding shows that each CMI cause not only local structural damage, but also persistent remote tissue damage in the cortical grey matter. As the presence of one CMI may reflect the ongoing appearance of numerous lesions [2], the cumulative impact of these widely distributed lesions on cerebral cortex may have an important
Declaration of Competing Interest
None.
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D. Kraushar and J. Molad contributed equally to this work.