University of Cambridge
Clinical Neurosciences
I am a clinical researcher in the University of Cambridge Department of Clinical Neurosciences where I am currently studying for a PhD under Prof Hugh Markus. My research interests lie in the progression of cerebral small vessel disease and the role of inflammation and blood-brain barrier permeability in its pathophysiology. My work uses a multimodal approach to investigate SVD biomarkers including advanced neuroimaging and immunophenotyping of both peripheral blood and cerebrospinal fluid. I am supported by an Association of British Neurologists Clinical Research Training Fellowship funded by the Guarantors of Brain.

Presenter Of 1 Presentation

REGRESSION OF WHITE MATTER HYPERINTENSITY LESIONS IN CEREBRAL SMALL VESSEL DISEASE

Session Type
Free Communication Session
Date
28.10.2021, Thursday
Session Time
15:45 - 17:15
Room
FREE COMMUNICATIONS A
Lecture Time
16:25 - 16:35

Abstract

Background and Aims

White matter hyperintensities (WMHs) are a radiological hallmark of cerebral small vessel disease (SVD). Previous studies have found that whole brain WMH burden can reduce over time, but the extent of lesion regression and the factors that drive it are not fully understood. We aimed to assess WMH regression in three SVD cohorts.

Methods

Participants were from the SCANS observational study (n=99; MRI at 0/1/2/3 years) and the PRESERVE trial (intensive blood pressure lowering in SVD; standard treatment arm n=42; MRI at 0/1 year) and had symptomatic lacunar infarcts with moderate WMH burden at baseline (Fazekas score>=2). WMHs in SCANS were calculated using a two-step pipeline mapping individual images to a participant average and then warping to a group average space. WMHs in PRESERVE were calculated using a semi-automatic contouring program with pre- and post-treatment FLAIR images marked in parallel (blinded to timepoint). Regression was defined as WMH reduction >0.25cc between scans.

Results

WMH volume at baseline in SCANS was 45.8cc and the mean change between scans was 4.5+/-6.3cc; no subjects showed regression. WMH at baseline in PRESERVE was 31.0cc and the mean change between scans was 5.9+/-6.0cc); 6 subjects showed regression. Compared to non-regressors there were no significant differences in age, sex, baseline WMH volume, lacune number or brain volume.

Conclusions

Few participants showed WMH regression. To test whether this is due to statistical/imaging factors or SVD severity, we will apply the method used to quantify WMHs in PRESERVE to a third cohort with less severe SVD - the RUN-DMC study (n=276).

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