Progressive lesion necrosis is related to increasing aphasia severity in chronic stroke

Abstract

AbstractBackgroundVolumetric investigations of cortical damage resulting from stroke indicate that lesion size and shape continue to change even in the chronic stage of recovery. However, the potential clinical relevance of continued lesion growth has yet to be examined. In the present study, we investigated the prevalence of lesion expansion and the relationship between expansion and changes in aphasia severity in a large sample of individuals in the chronic stage of aphasia recovery.MethodsRetrospective structural MRI scans from 104 stroke survivors with at least 2 observations more than 6 months apart (k=301 observations) were included. Lesion demarcation was performed using an automated lesion segmentation software and lesion volumes at each timepoint were subsequently calculated. A paired-sample t-test between initial and final scans was conducted to determine if chronic lesion volumes change over time. Finally, we investigated the association between lesion expansion and changes on the Western Aphasia Battery (WAB) in a group of participants assessed and scanned at 2 timepoints (N=54) using a GLM.ResultsMost participants (81%) showed evidence of lesion expansion. A t-test revealed lesion volumes at follow-up scans were significantly larger than initial scans (p<0.0001).Change on the language performance was significantly associated with change in lesion volume (p=0.025) and age at stroke (p=0.031). The results suggest that with every 100cm3increase in lesion size, language performance decreases by 8.8 points, and for every 10-year increase in age at stroke, language performance decreases by 1.9 points.ConclusionsThe present study confirms and extends prior reports that lesion expansion occurs well into the chronic stage of stroke. For the first time, we present evidence that expansion is predictive of longitudinal changes in language performance in individuals with aphasia. Future research should focus on the potential mechanisms that may lead to necrosis in areas surrounding the chronic stroke lesion.