Neurology: Baseline blood-brain barrier leakage can predict the microstructure and tissue damage around white matter hyperintensity lesions in cSVD patients

Cerebral small vessel disease (cSVD) is a common age and vascular risk factor related disease, which can cause lacunar stroke and cognitive dysfunction
.

White matter hyperintensity (WMH) is a common radiological marker in cSVD.

Vascular Stroke

Intravoxel incoherent motion (IVIM) imaging (a diffusion-weighted MRI technique) can quantitatively measure parenchymal diffusion without the influence or contribution of intravascular water diffusion
.

Earlier studies showed that the diffusion rate of normal white matter (NAWM) in cSVD patients increased compared with the control group

Recently, Danielle Kerkhofs et al.
, in order to determine the status of the brain parenchymal microstructure, studied the changes in the brain parenchymal diffusion coefficient (a quantitative marker of microstructure tissue status) in patients with cerebral small vessel disease (cSVD) and the risk tissue (ie brain The relationship between the parenchymal diffusion coefficient (a quantitative marker of microstructure and tissue condition) in the white matter surrounding area of ​​hyperintensity (WMH) and the permeability of the blood-brain barrier (BBB) ​​at baseline
.

The findings are published in the journal Neurology

Patients with sporadic cSVD (lacunar stroke or mild vascular cognitive impairment) receive a baseline 3T MRI examination, including dynamic enhanced MRI to quantify the permeability of the blood-brain barrier (ie, the amount of leakage and the rate of leakage) and intra-voxel incoherent motion of the imaging (IVIM), which may provide a substantial diffusion of the D diffusion techniques
.

I did IVIM again after 2 years

Baseline FLAIR image (A), baseline surrounding area (B), baseline permeability (Ki) map (C), baseline parenchymal diffusion map (D) and follow-up (A) of a patient with cerebral small vessel disease (female, 52 years old) E)
.

Baseline FLAIR image (A), baseline surrounding area (B), baseline permeability (Ki) map (C), baseline parenchymal diffusion map (D) and follow-up (A) of a patient with cerebral small vessel disease (female, 52 years old) E)
.

The study analyzed 43 patients (age 68 ± 12 years, 58% were male)
.

In the area around the lesion, ∆D increased by 0.

Longitudinal changes in the amount of leakage, leakage rate, and substantial diffusion rate in the area around the lesion
.

The longitudinal changes of the leakage volume vL (A), the leakage rate Ki (B) and the substantial diffusion coefficient ∆D (C) of the lesion area around WMH

Longitudinal changes in the amount of leakage, leakage rate, and substantial diffusion rate in the area around the lesion

A scatter plot between the substantial diffusivity, the leakage volume, and the longitudinal variation of the leakage rate
.

The scatter plot between the leakage volume vL (%) and the substantial diffusion coefficient ∆D (%) (A) in the area around the lesion around the white matter hyperintensity, the leakage rate Ki (×10 ⁻⁴ min ⁻¹ ) and the substantial diffusion coefficient A scatter plot between ∆D (%) (B) and a corresponding regression line

A scatter plot between the substantial diffusivity, the leakage volume, and the longitudinal variation of the leakage rate
.
The scatter plot between the leakage volume vL (%) and the substantial diffusion coefficient ∆D (%) (A) in the area around the lesion around the white matter hyperintensity, the leakage rate Ki (×10 ⁻⁴ min ⁻¹ ) and the substantial diffusion coefficient A scatter plot between ∆D (%) (B) and a corresponding regression line
.
^{−4 −1}

In 2 years, the closer the brain parenchyma of cSVD patients to WMH, the higher the diffusion coefficient (even higher than that of WMH itself)
.
The baseline blood-brain barrier leakage is related to the changes in the diffusion rate of white matter around the white matter hyperintensity lesions, and therefore also related to tissue integrity
.
This observation supports the hypothesis that blood-brain barrier damage plays an early and critical role in the subsequent microstructural white matter degeneration and the pathophysiological process of cSVD
.
In the future, the measurement of blood-brain barrier leakage may be used to identify patients at risk for the development and progression of tissue degeneration
.
The longitudinal change in the substantial diffusion coefficient measured by IVIM is a promising quantitative biomarker, which may be used in trials to monitor cSVD
.

In 2 years, the closer the brain parenchyma of cSVD patients to WMH, the higher the diffusion coefficient (even higher than that of WMH itself)
.
The baseline blood-brain barrier leakage is related to the change of the white matter diffusion rate around the white matter hyperintensity
lesions, and therefore also related to the tissue integrity.
In 2 years, the closer the cSVD patients to WMH, the higher (or even higher) the diffusion coefficient of the brain parenchyma (In WMH itself) .
Baseline blood-brain barrier leakage is related to the change of white matter diffusion rate around white matter hyperintensity lesions, and therefore also related to tissue integrity.
Blood-brain barrier damage plays an early and critical role in the subsequent microstructural white matter degeneration and the pathophysiological process of cSVD.
The blood-brain barrier injury plays an early and critical role in the subsequent microstructural white matter degeneration and the pathophysiological process of cSVD

Original source

Baseline Blood-Brain Barrier Leakage and Longitudinal Microstructural Tissue Damage in the Periphery of White Matter Hyperintensities.
Danielle Kerkhofs, Sau ay Wong, Eleana Zhang, Julie Staals, Jacobus FA Jansen, Robert J.
van Oostenbrugge, Walter H.
Backes.
Neurology Apr 2021 , 96 (17) e2192-2200; DOI: 10.
1212/WNL.
0000000000011783

Baseline Blood-Brain Barrier Leakage and Longitudinal Microstructural Tissue Damage in the Periphery of White Matter Hyperintensities.
Danielle Kerkhofs, Sau ay Wong, Eleana Zhang, Julie Staals, Jacobus FA Jansen, Robert J.
van Oostenbrugge, Walter H.
Backes.
Neurology Apr 2021 , 96 (17) e2192-2200; DOI : 10.
1212 / WNL.
0000000000011783 in this message