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

Volumetric 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.

Retrospective structural MRI scans from 104 S survivors with at least 2 observations (k = 301 observations; mean time between scans = 31 months) were included. Lesion demarcation was performed using an automated lesion segmentation software and lesion volumes at each timepoint were subsequently calculated. A linear mixed effects model was conducted to investigate the effect of days between scan on lesion expansion. 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.

Most participants (81 %) showed evidence of lesion expansion. The mixed effects model revealed lesion volumes significantly increase, on average, by 0.02 cc each day (7.3 cc per year) following a scan (p < 0.0001). Change on 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 10 cc increase in lesion size, language performance decreases by 0.9 points, and for every 10-year increase in age at stroke, language performance decreases by 1.9 points.

The 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.