Poster D16, Wednesday, August 21, 2019, 5:15 – 7:00 pm, Restaurant Hall
Longitudinal atrophy of the left inferior frontal gyrus following post-stroke aphasia
Natalia Egorova1,2, Mohamed Khlif2, Emilio Werden2, Laura Bird2, Amy Brodtmann2;1The University of Melbourne, 2The Florey Institute of Neuroscience and Mental Health, Melbourne
Previous studies of post-stroke aphasia focused on functional and structural brain reorganisation that signals recovery. However, the hallmark of stroke is accelerated neurodegeneration. The aim of this study was to understand 1) whether post-stroke aphasia is associated with long-term brain atrophy, extending beyond the lesion, and 2) whether post-stroke neurodegeneration related to language deficits is global or specific to the language neural network. We used FreeSurfer to longitudinally quantify structural brain volume changes in a control group (N=29), as well as in stroke participants with (N=32) and without (N=59) aphasia, assessed using the 16 item Token Test at 3 months after the insult. The two stroke groups were significantly different on the Boston Naming Test Scores, as well as the COWAT Animal and FAS Scores. We extracted percent volume change from 3 to 12 months from 82 regions of interest (ROI) covering the whole brain. For each ROI, we performed ANCOVAs controlling for age, sex, stroke severity, level of education, and total intracranial volume, and correcting for multiple comparisons at Bonferroni p<0.0006 level. Stroke participants with aphasia symptoms at 3 months showed significant atrophy (>2%, p=0.0001) of the orbital part of the left inferior frontal gyrus (left IFG-po) over just 9 months, compared to average yearly brain loss of 0.2-0.5% in healthy aging. This brain volume reduction was not observed in either the control or non-aphasic stroke participants (p=0.0003). None of the participants in the aphasic stroke group had lesions that overlapped with left IFG-po. Furthermore, there were no group differences in the rate of language decline, suggesting that the atrophy in the language network was not a marker of aggravated language deficit in the aphasic group but was triggered by the mere presence of aphasia early after stroke. We conclude that post-stroke language deficits are associated with accelerated structural decline beyond the lesion location but within the language brain network. Thus, aphasia affects the course of post-stroke neurodegeneration, specifically targeting the language network.
Themes: Disorders: Acquired, Language Production
Method: Other