Abstract
Although white matter hyperintensities evolve in the course of ageing, few solutions exist to consider the lesion segmentation problem longitudinally. Based on an existing automatic lesion segmentation algorithm, a longitudinal extension is proposed. For evaluation purposes, a longitudinal lesion simulator is created allowing for the comparison between the longitudinal and the cross-sectional version in various situations of lesion load progression. Finally, applied to clinical data, the proposed framework demonstrates an increased robustness compared to available cross-sectional methods and findings are aligned with previously reported clinical patterns.
Highlights
White matter hyperintensities (WMH), known as leukoaraiosis, as observed in FLuid Attenuated Inversion Recovery (FLAIR), T2-weighted (T2) and proton density weighted (PD) magnetic resonance (MR) images are widely observed in the ageing population
Hypotheses related to deleterious changes in the blood supply and in the blood brain barrier (Wardlaw et al, 2013) have been put forward to explain the occurrence of such damage, and cardiovascular risk factors such as hypertension have been shown to be associated to the WMH burden (Abraham et al, 2015; Vuorinen et al, 2011)
Note that the rigid transformation may modify the actual volume of lesion and explains why the ground truth slopes are slightly different from expected in the case of linear transformations
Summary
White matter hyperintensities (WMH), known as leukoaraiosis, as observed in FLuid Attenuated Inversion Recovery (FLAIR), T2-weighted (T2) and proton density weighted (PD) magnetic resonance (MR) images are widely observed in the ageing population. Hypotheses related to deleterious changes in the blood supply and in the blood brain barrier (Wardlaw et al, 2013) have been put forward to explain the occurrence of such damage, and cardiovascular risk factors such as hypertension have been shown to be associated to the WMH burden (Abraham et al, 2015; Vuorinen et al, 2011). Such lesions have been linked with cognitive impairment, in particular with respect to processing speed and executive function (Prins and Scheltens, 2015; Wakefield et al, 2010). Lesion burden at baseline has been associated with faster cognitive decline in Alzheimer’s disease (AD), mild cognitive impairment (MCI) and normal populations (Carmichael et al, 2010)
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