Poster B54, Tuesday, August 20, 2019, 3:15 – 5:00 pm, Restaurant Hall
Neural architecture of discourse-derived fluency in post-stroke chronic aphasia
Brielle Stark1, Barbara Marebwa2, Alexandra Basilakos3, Lorelei Philip3, Helga Thors3, Grigori Yourganov3, Chris Rorden3, Leonardo Bonilha2, Julius Fridriksson3;1Indiana University, 2Medical University of South Carolina, 3University of South Carolina
Fluency, as a construct, involves both speed and quality of verbal output. Fluency has often quantified by verbal fluency tasks (e.g. phonological fluency, “list words that start with /s/”). Of particular interest is connected speech fluency; for example, mean length of utterance in words (MLU). In addition to enhanced ecological validity, measuring mean length of utterance in words has the added benefit of accounting for word-finding difficulty and pauses, in addition to efficiency of verbal output1. Research evaluating MLU performance in primary progressive aphasia (PPA) suggests that reduction in cortical thickness in dorsal stream structures, including bilateral posterior middle frontal gyrus and left inferior frontal sulcus, impair fluency (Rogalski et al., 2011). Complementary work evaluating MLU in PPA suggests importance of the left frontal aslant tract for fluency (Catani et al., 2013). A recent study evaluated fluency derived from a phonological verbal fluency task in stroke, where fluency was negatively associated with lesion damage to the left frontal aslant tract and positively associated with fractional anisotropy of the tract (Li et a., 2017). Therefore, the purpose of the current study was to evaluate neural architecture associated with discourse-extracted fluency in post-stroke aphasia, effectively elaborating on prior research in stroke using non-discourse fluency and prior research conducted in PPA using discourse-derived fluency. In 49 people with chronic aphasia as a result of left hemisphere stroke (14 F; moderate aphasia [WAB-R aphasia quotient M=64.99±17.71]; age at assessment, M=60.71±10.15 years; months post-stroke at assessment, M=40.06±37.39), we acquired structural and diffusion-weighted MRI scans and a sample of spoken discourse (the Cinderella story). Discourse was transcribed and analyzed with CHAT/CLAN software (MacWhinney et al., 2000), allowing us to extract MLU, which we z-scored. To analyze lesion damage associated with fluency, we performed voxel-wise lesion-symptom mapping (5000 permutations; p<.05) with cluster correction (z>2.33), regressing lesion volume. To analyze structural disconnection associated with fluency, we performed connectome lesion-symptom mapping between gray matter parcels for left language (Lang) and domain-general (DG) networks. These analyses were done using NiiStat. Finally, to analyze network organization associated with fluency, we computed the modularity statistic (Q) for the left hemisphere Lang and DG networks from which partial correlations with lesion volume and fluency were computed. Fluency was associated with a cluster of lesion damage involving left anterior dorsal stream structures, including inferior frontal gyrus (IFG) (peak z: opercularis, z=-2.33; triangularis, z=-2.33; orbitalis, z=-2.51). Reduced fluency was also associated with damage to connections between left middle frontal gyrus (MFG) and precentral gyrus (z=2.91) (DG), superior frontal gyrus posterior segment and supramarginal gyrus (z=3.09) (DG) and MFG posterior segment and IFG pars opercularis (z=3.15) (Lang), suggesting disruption to frontal aslant tract and anterior superior longitudinal fasciculus / arcuate fasciculus. Finally, Lang network modularity was positively correlated with fluency when controlled for total lesion volume (r=.45, p=.0001). Our result extrapolates on prior work, suggesting that fluency, derived from discourse, is modulated by left anterior dorsal stream structures and connections between structures, as well as preserved modularity of the left language network.
Themes: Language Production, Disorders: Acquired
Method: White Matter Imaging (dMRI, DSI, DKI)