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Poster D49, Friday, August 17, 4:45 – 6:30 pm, Room 2000AB

Dissociable thalamo-cortical network disruption explains language, motor and sensory deficits after stroke

Anika Stockert1, Sophia Hormig1, Max Wawrzyniak1, Mandy Pirlich1, Stefan Schob1, Dorothee Saur1;1University Clinic of Leipzig, Germany

Background: Besides motor and sensory symptoms thalamic stroke can cause deficits in several cognitive domains including aphasia that resembles cortical stroke. Based on structural (pre-) frontal and parietal connectivity motor and sensory functions have been linked to the ventral lateral/anterior (VL/VA) and the ventral-posterior lateral/medial (VPL/VPM) thalamic nucleii respectively (Behrens et al. 2003, Lambert et al. 2017). Similarly, thalamic nuclei that connect to the left frontal, parietal and temporal cortex, namely VL/VA nucleus, pulvinar (PUL), medial geniculate (MG) and lateral posterior (LP) nucleus have been associated with language (Barbas et al. 2013, Hackett et al. 1998). Aim: To date, no systematic analysis has been conducted to explore the functional specificity of particular thalamic nuclei in causing clinical stroke symptoms. Alternativly to a non-overlapping, dissociable lesion-symptom association with thalamic nuclei, overlapping thalamic regions may play a multifunctional role in processing motor, sensory as well as language information. Therefore lesion-functional network associations with cortical motor, sensory or language networks could give a more comprehensive view on how thalamic stroke causes different stroke symptoms. Method: In 74 patients with thalamic stroke we combined a voxel-based lesion-symptom mapping (VLSM) and lesion-network symptom mapping (LNSM) approach (Boes et al. 2015, Wawrzyniak et al. 2018). Information on the presence of motor, sensory or language symptoms was taken from the patients’ records. Firstly, non-parametric voxel-wise analysis was performed to examine the relationship between lesion location and motor, sensory or language symptoms. Secondly, lesion-dependent network connectivity (LNC) was identified based on normative functional connectome data (NKI Rockland Sample) to study the association between thalamo-cortical networks affected by a thalamic lesion and these symptoms. Results: The analyses revealed that (i) lesion affecting the right VL led to left motor symptoms, (ii) lesions in the right VPL/VPM resulted in left sensory symptoms and (iii) overlapping lesion in the left VPL/VPM were concomitantly linked with right motor and sensory symptoms, while (iv) lesion in left VL and PUL were significantly associated with aphasic symptoms. LNSM revealed that language symptoms were associated with higher normative LNC to left superior temporal and fusiform gyrus. In contrast right sensory symptoms were linked to lesions that showed higher LNC to left parietal cortex and right motor symptoms were associated with higher prefrontal LNC. Conclusions: These findings suggest specificity of thalamic nuclei and associated functional thalamo-(sub-)cortical networks for language as compared to sensory and motor networks.

Topic Area: Language Disorders