Cerebral microinfarcts disruption of remote cortical thickness

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Highlights

  • Cerebral microinfarcts (CMI) are very common small silent brain infarctions.

  • We examined CMIs influence on cortical thickness in remote areas.

  • Follow-up MRI demonstrated reduced cortical thickness in the region of interest.

  • This finding may imply that CMIs have a role in the mechanism of vascular dementia.

Abstract

Introduction

Cerebral microinfarcts (CMI) are common lesions, carrying an important contribution to small-vessel–related cognitive impairment. CMIs were previously found to cause local microstructural damage and disruption of white matter integrity. This study examines CMIs influence on cortical thickness in remote brain areas.

Methods

Six small silent diffuse weighted imaging (DWI) lesions corresponding to subacute CMI were identified among five patients who underwent baseline and follow-up MRI scans from the Tel-Aviv Acute Brain Stroke Cohort (TABASCO). Regions of interest (ROIs) corresponding to the site of the DWI lesions and of the non-lesioned contralateral hemisphere (control ROI) were co-registered. DTI tractography was additionally performed to reconstruct the white matter tracts containing the ROIs. The normalized cortical thickness was calculated for the DWI lesional tract as well as for the contralateral non-lesional tract, and the lesion-to-control cortical thickness ratio (CTR) was calculated.

Results

Post-lesional scans, performed 25.1 ± 1.2 months after CMI detection, demonstrated reduced mean CTR within the ROI from 1.8 to 1.1 (p = 0.032). There was no difference between the CTR of the right hemisphere relative to those on the left hemisphere, or between the CTR change of the cortical and non-cortical CMI.

Discussion

This study demonstrated the prolonged influence of CMI on cortical thickness in remote ROI. The total number of CMIs is difficult to determine, however it has been shown that detecting even a single CMI suggests the existence of hundreds to thousands lesions. Therefore, the cumulative impact of these widely distributed lesions on cerebral cortex may have a significant contribution to the development of vascular cognitive impairment.

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.

References (28)

  • Z. Arvanitakis et al.

    Microinfarct pathology, dementia, and cognitive systems

    Stroke

    (2011)
  • Y.D. Reijmer et al.

    The effect of lacunar infarcts on white matter tract integrity

    Stroke

    (2013)
  • E. Ben Assayag et al.

    Predictors for poststroke outcomes: the Tel Aviv brain acute stroke cohort (TABASCO) study protocol

    Int. J. Stroke

    (2012)
  • Han X, Jovicich J, Salat D, van der Kouwe A, Quinn B, Czanner S, et al. Reliability of MRI-derived measurements of...
  • 1

    D. Kraushar and J. Molad contributed equally to this work.

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