Browsing by Author "Ezzes, Zoe"
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Publication Assessing processing speed and its neural correlates in the three variants of primary progressive aphasia with a non-verbal tablet-based task(2024) Gajardo-Vidal, Andrea; Maxime Montembeault, Maxime; Lorca-Puls, Diego L.; Licata, Abigail E.; Bogley, Rian; Erlhoff, Sabrina; Ratnasiri, Buddhika; Ezzes, Zoe; Battistella, Giovanni; Tsoy, Elena; Watson Pereira, Christa; DeLeon, Jessica; Lead Tee , Boon; Henry, Maya L.; Miller, Zachary A.; Rankin, Katherine P.; Mandelli, Maria Luisa; Katherine L. Possin, Katherine; Gorno-Tempini, Maria LuisaPrior research has revealed distinctive patterns of impaired language abilities across the three variants of Primary Progressive Aphasia (PPA): nonfluent/agrammatic (nfvPPA), logopenic (lvPPA) and semantic (svPPA). However, little is known about whether, and to what extent, non-verbal cognitive abilities, such as processing speed, are impacted in PPA patients. This is because neuropsychological tests typically contain linguistic stimuli and require spoken output, being therefore sensitive to verbal deficits in aphasic patients. The aim of this study is to investigate potential differences in processing speed between PPA patients and healthy controls, and among the three PPA variants, using a brief non-verbal tablet-based task (Match) modeled after the WAIS-III digit symbol coding test, and to determine its neural correlates. Here, we compared performance on the Match task between PPA patients (n = 61) and healthy controls (n = 59) and across the three PPA variants. We correlated performance on Match with voxelwise gray and white matter volumes. We found that lvPPA and nfvPPA patients performed significantly worse on Match than healthy controls and svPPA patients. Worse performance on Match across PPA patients was associated with reduced gray matter volume in specific parts of the left middle frontal gyrus, superior parietal lobule, and precuneus, and reduced white matter volume in the left parietal lobe. To conclude, our behavioral findings reveal that processing speed is differentially impacted across the three PPA variants and provide support for the potential clinical utility of a tabled-based task (Match) to assess non-verbal cognition. In addition, our neuroimaging findings confirm the importance of a set of fronto-parietal regions that previous research has associated with processing speed and executive control. Finally, our behavioral and neuroimaging findings combined indicate that differences in processing speed are largely explained by the unequal distribution of atrophy in these fronto-parietal regions across the three PPA variants.Publication Neural basis of speech and grammar symptoms in non-fluent variant primary progressive aphasia spectrum(2024) Lorca-Puls, Diego L.; Gajardo-Vidal, Andrea; Mandelli, Maria Luisa; Illán-Gala, Ignacio; Ezzes, Zoe; Wauters, Lisa D.; Battistella, Giovanni; Bogley, Rian; Ratnasiri, Buddhika; Licata, Abigail E.; Battista, Petronilla; García, Adolfo M.; Lead Tee, Boon; Lukic, Sladjana; Boxer, Adam L.; Rosen, Howard J.; Seeley, William W.; Grinberg, Lea T.; Spina, Salvatore; Miller, Bruce L.; Henry, Maya L.; Dronkers, Nina F.; Gorno-Tempini, Maria LuisaThe nonfluent/agrammatic variant of primary progressive aphasia (nfvPPA) is a neurodegenerative syndrome primarily defined by the presence of apraxia of speech (AoS) and/or expressive agrammatism. In addition, many patients exhibit dysarthria and/or receptive agrammatism. This leads to substantial phenotypic variation within the speech-language domain across individuals and time, in terms of both the specific combination of symptoms as well as their severity. How to resolve such phenotypic heterogeneity in nfvPPA is a matter of debate. “Splitting” views propose separate clinical entities: “primary progressive apraxia of speech” (PPAOS) when AoS occurs in the absence of expressive agrammatism, “progressive agrammatic aphasia” (PAA) in the opposite case, and “AOS + PAA” when mixed motor speech and language symptoms are clearly present. While therapeutic interventions typically vary depending on the predominant symptom (e.g., AoS vs expressive agrammatism), the existence of behavioral, anatomical, and pathological overlap across these phenotypes argues against drawing such clear-cut boundaries. In the current study, we contribute to this debate by mapping behavior to brain in a large, prospective cohort of well characterized patients with nfvPPA (n = 104). We sought to advance scientific understanding of nfvPPA and the neural basis of speech-language by uncovering where in the brain the degree of MRI-based atrophy is associated with inter-patient variability in the presence and severity of AoS, dysarthria, expressive agrammatism, or receptive agrammatism. Our cross-sectional examination of brain-behavior relationships revealed three main observations. First, we found that the neural correlates of AoS and expressive agrammatism in nfvPPA lie side by side in the left posterior inferior frontal lobe, explaining their behavioral dissociation/association in previous reports. Second, we identified a “left-right” and “ventral-dorsal” neuroanatomical distinction between AoS versus dysarthria, highlighting (i) that dysarthria, but not AoS, is significantly influenced by tissue loss in right-hemisphere motor-speech regions and (ii) that, within the left hemisphere, dysarthria and AoS map onto dorsally versus ventrally located motor-speech regions, respectively. Third, we confirmed that, within the large-scale grammar network, left frontal tissue loss is preferentially involved in expressive agrammatism and left temporal tissue loss in receptive agrammatism. Our findings thus contribute to define the function and location of the epicenters within the large-scale neural networks vulnerable to neurodegenerative changes in nfvPPA. We propose that nfvPPA be redefined as an umbrella term subsuming a spectrum of speech and/or language phenotypes that are closely linked by the underlying neuroanatomy and neuropathology.