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The role of small diffusion-weighted imaging lesions in cerebral small vessel disease
Kim Wiegertjes1, Annemieke Ter Telgte1, Pedro B Oliveira1
1From the Department of Neurology (K.W., A.t.T., P.B.O., E.M.C.v.L., M.I.B., I.W.M.v.U., H.M.v.d.H., C.J.M.K., A.M.T., F.-E.d.L.) and Center for Cognitive Neuroimaging (D.G.N.), Donders Institute for Brain, Cognition and Behavior, and Diagnostic Image Analysis Group, Department of Radiology and Nuclear Medicine (M.G., B.P.), Radboud University Medical Center; and Institute for Computing and Information Sciences (M.G.), Radboud University, Nijmegen, the Netherlands.
Objective:
To investigate the prevalence of asymptomatic diffusion-weighted imaging-positive (DWI+) lesions in individuals with cerebral small vessel disease (SVD) and identify their role in the origin of SVD markers on MRI.
Methods:
We included 503 individuals with SVD from the Radboud University Nijmegen Diffusion Tensor and Magnetic Resonance Imaging Cohort (RUN DMC) study (mean age 65.6 years [SD 8.8], 56.5% male) with 1.5T MRI in 2006 and, if available, follow-up MRI in 2011 and 2015. We screened DWI scans (n = 1,152) for DWI+ lesions, assessed lesion evolution on follow-up fluid-attenuated inversion recovery, T1 and T2* images, and examined the association between DWI+ lesions and annual SVD progression (white matter hyperintensities [WMH], lacunes, microbleeds).
Results:
We found 50 DWI+ lesions in 39 individuals on 1,152 DWI (3.4%). Individuals with DWI+ lesions were older (p = 0.025), more frequently had a history of hypertension (p = 0.021), and had a larger burden of preexisting SVD MRI markers (WMH, lacunes, microbleeds: all p < 0.001) compared to individuals without DWI+ lesions. Of the 23 DWI+ lesions with available follow-up MRI, 14 (61%) evolved into a WMH, 8 (35%) resulted in a cavity, and 1 (4%) was no longer visible. Presence of DWI+ lesions was significantly associated with annual WMH volume increase and yearly incidence of lacunes and microbleeds (all p < 0.001).
Conclusion:
Over 3% of individuals with SVD have DWI+ lesions. Although DWI+ lesions play a role in the progression of SVD, they may not fully explain progression of SVD markers on MRI, suggesting that other factors than acute ischemia are at play.
Insights
Over 3% of individuals with cerebral small vessel disease (SVD) have asymptomatic diffusion-weighted imaging-positive (DWI+) lesions. These DWI+ lesions contribute to SVD progression but do not fully explain MRI marker changes, indicating other factors are involved.
Area of Science:
- Neurology
- Radiology
- Neuroimaging
Background:
- Cerebral small vessel disease (SVD) is a common condition affecting the brain's small blood vessels.
- Diffusion-weighted imaging (DWI) can detect acute ischemic lesions, but their prevalence and role in SVD progression are not fully understood.
Purpose of the Study:
- To determine the frequency of asymptomatic diffusion-weighted imaging-positive (DWI+) lesions in SVD patients.
- To investigate the association between DWI+ lesions and the development and progression of SVD markers on MRI.
Main Methods:
- Analysis of 1,152 DWI scans from 503 individuals with SVD in the Radboud University Nijmegen Diffusion Tensor and Magnetic Resonance Imaging Cohort (RUN DMC) study.
- Assessment of lesion evolution using follow-up MRI scans (fluid-attenuated inversion recovery, T1, T2*) and examination of associations with SVD progression markers (white matter hyperintensities, lacunes, microbleeds).
Main Results:
- 3.4% of individuals had DWI+ lesions, which were associated with older age, hypertension history, and a higher burden of existing SVD markers.
- Of DWI+ lesions with follow-up, 61% evolved into white matter hyperintensities and 35% into cavities.
- DWI+ lesions significantly correlated with annual increases in white matter hyperintensities and the incidence of lacunes and microbleeds.
Conclusions:
- Asymptomatic DWI+ lesions are present in over 3% of individuals with SVD.
- While DWI+ lesions contribute to SVD progression, they do not entirely account for the observed changes in SVD MRI markers, suggesting additional pathogenic mechanisms beyond acute ischemia.
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