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Slide Slam A2

Secondary damage of the thalamus in post-stroke aphasia: a new player in language recovery outcome

Slide Slam Session A, Tuesday, October 5, 2021, 12:30 - 3:00 pm PDT Log In to set Timezone

Melody Courson1,2,3, Karine Marcotte2,4, Christophe Bedetti1,3, Bérengère Houzé1,3, Gabriel Devenyi5,6, Alex Desautels2,7,8, Mallar Chakravarty5,6,9, Simona Brambati1,2,3; 1Centre de recherche de l’Institut universitaire de gériatrie de Montréal, Montréal, Canada, 2Centre de recherche du Centre intégré universitaire de santé et de services sociaux du Nord-de-l’Île-de-Montréal, Montréal, Canada, 3Département de psychologie, Université de Montréal, Montréal, Canada, 4École d'orthophonie et d'audiologie, Université de Montréal, Montréal, Canada, 5Cerebral Imaging Center, Douglas Mental Health University Institute, Montreal, Canada, 6Department of Psychiatry, McGill University, Montreal, Canada, 7Département de neurosciences, Université de Montréal, Montréal, Canada, 8Centre d'études avancées en médecine du sommeil, Hôpital du Sacré-Coeur de Montréal, Montréal, Canada, 9Department of Biomedical Engineering, McGill University, Montreal, Canada

Background. Secondary damage refers to the damage of a non-lesioned cerebral area following the primary lesion of another remote but connected cerebral area. Secondary damage of the thalamus was reported between three and twelve months post-stroke [1,2]. However, whether it is present in post-stroke aphasia (PSA) and whether it impacts language recovery is still unknown. Research on thalamic deep brain stimulation [3] and thalamic stroke [4] has shown that the thalamus and thalamic nuclei (i.e. pulvinar, ventral anterior nucleus and ventral lateral nucleus) are involved in lexical access but not repetition. We thus hypothesized that PSA patients with a volume reduction in thalamus and thalamic nuclei of interest would show lower lexical access but not repetition skills. Methods. 15 PSA patients following an ischemic stroke in the territory of the left middle cerebral artery (7 women, 71 12 years) and 18 healthy controls (10 women, 64  16 years) were recruited. The volumes of the left thalamus and the three left thalamic nuclei of interest were measured at the subacute (10 days post-stroke) and chronic (6 months post-stroke) stages for PSA patients and at two timepoints, 6 months apart, for controls. Volume change was computed for each region of interest (i.e. Vreduction = Vsubacute – Vchronic), as well as scores for lexical access (i.e. orthographic fluency) and word repetition. Analyses of variance were used to compare the volume change in thalamus and thalamic nuclei between patients and controls. Then, a set of independent samples analyses was conducted to investigate the relationship between thalamic volume reduction and language performance in PSA patients. Analyses were corrected for multiple comparisons using a first discovery rate. Results. The volume of the thalamus significantly decreased in patients between the subacute and chronic stages compared to controls (F(1,30) = 15.307, p = .004, partial 2 = .338). It was also the case for the pulvinar (F(1,30) = .14,336 p = .001, partial 2 = .323), ventral anterior nucleus (F(1,30) = 15.978, p = .002, partial 2 = .348) and ventral lateral nucleus (F(1,30) = 19.462, p = .001, partial 2 = .393). Patients were then divided into two subgroups: patients who showed a thalamic volume reduction and those who did not. Congruent with our hypothesis, patients with a thalamic volume reduction performed more poorly on the orthographic fluency task (U = 52, p = .032) but not on the repetition task (U = 26, p = .867). Conclusion. This is the first report of secondary damage to the thalamus in patients with PSA. Furthermore, results show that this thalamic secondary damage is specifically linked to the outcome of lexical access at the chronic stage of the disease. These findings bring to light the role of the thalamus in the neurobiological mechanisms influencing language recovery outcome in PSA. [1] Baudat et al. (2020) Neuroradiology. [2] Haque et al. (2019) Front Neurol. [3] Hebb et al. (2013) Brain Lang. [4] de Witte et al. (2011) Cortex.

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