Presentation
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Neural substrates of the heterogenous evolution of mixed transcortical aphasia
Poster B54 in Poster Session B, Tuesday, October 24, 3:30 - 5:15 pm CEST, Espace Vieux-Port
Diana Lopez-Barroso1,2,3,4, Jose Paredes-Pacheco5,6, María José Torres-Prioris1,2,3,4, Guadalupe Dávila1,2,3,4, Marcelo L. Berthier1,2,3; 1Cognitive Neurology and Aphasia Unit, Centro de Investigaciones Médico‑Sanitarias (CIMES), University of Malaga, Malaga, Spain, 2Research Laboratory on the Neuroscience of Language, Faculty of Psychology and Speech Therapy, University of Malaga, Malaga, Spain, 3Instituto de Investigación Biomédica de Málaga – IBIMA, Malaga, Spain, 4Department of Psychobiology and Methodology of Behavioural Sciences, Faculty of Psychology, University of Malaga, Malaga, Spain, 5Radiology and Psychiatry Department, Faculty of Medicine, Universidade de Santiago de Compostela, Santiago de Compostela, Spain, 6Molecular Imaging Unit, Centro de Investigaciones Médico-Sanitarias (CIMES), General Foundation of the University of Malaga, Malaga, Spain
Mixed transcortical aphasia (MTCA) is a rare aphasia profile characterized by marked deficits in comprehension and production alongside preserved ability for verbal repetition. MCTA may be interpreted within the conceptual framework of the “isolation of the speech-language perisylvian area”, this is a disconnection between the preserved left perisylvian language network (PSLN), responsible for preserved verbal repetition, and the damaged left extrasylvian networks, which contribute to impairments in language production and comprehension. MTCA may progress towards milder variants of aphasia or even to full language recovery. However, despite significant advancements in in vivo neuroimaging, the structural and functional state of the PSLN network in MTCA and its evolution remains unexplored. Thus, the main objective of this study was to examine the functional activity and structural integrity of the PSLN in four cases who developed acute post-stroke MTCA and progressed to different types of aphasia. To accomplish this, a neuroimaging-behavioral study was conducted during the chronic stage. This study relied on different neuroimaging methods, including: (1) functional magnetic resonance imaging (fMRI) during verbal repetition to explore the residual networks sustaining verbal repetition in MTCA; (2) resting state fMRI (rs-fMRI) to study functional connectivity networks related to multi-demand and language-related networks; (3) diffusion tensor imaging (DTI - Tractography) to examine the dorsal and ventral white matter language pathways; and (4) resting 18Fluorodeoxyglucose positron emission tomography (18FDG-PET) to analyze the functional state of the PSLN. Our results revealed that while the behavioral profile of MTCA persisted in one patient, the other three patients progressed to less severe forms of aphasia: anomic aphasia, dynamic aphasia, and latent aphasia with discourse impairment. All patients had two or more lesions affecting frontal and parietal areas, showing partial damage to the PSLN including part of the inferior frontal gyrus, premotor cortex, inferior parietal cortex, and/or superior temporal gyrus. Structural and functional neuroimaging findings indicated that preserved verbal repetition in MTCA does not always depend on the optimal status of the PSLN and its dorsal connections and therefore it cannot be solely explained by the isolation of the speech area mechanism. Instead, the right hemisphere or the left ventral pathway may also contribute to supporting verbal repetition. The variability observed in the clinical evolution of MTCA can be explained by differences in the extent of PSLN damage and individual premorbid neuroanatomical language substrates. This study offers a modern perspective on MTCA in the light of advances in modern neuroscience and provides important insights into the neural basis involved in repetition.
Topic Areas: Disorders: Acquired, Language Production