Involvement of Thalamocortical Networks in Patients With Poststroke Thalamic Aphasia.

BACKGROUND AND OBJECTIVE: Theories assume that thalamic stroke may cause aphasia due to dysfunction in connected cortical networks. This takes into account that brain functions are organized in distributed networks and, in turn, localized damage may result in a network disorder such as thalamic aphasia. With this study, we investigate whether the integration of the thalamus into specific thalamo-cortical networks underlies symptoms after thalamic stroke. We hypothesize that thalamic lesions in patients with language impairments are functionally connected to cortical networks for language and cognition.

METHODS: We combined non-parametric lesion mapping methods in a retrospective cohort of patients with acute or subacute first-ever thalamic stroke. Relationship between lesion location and language impairments was assessed using non-parametric voxel-based lesion-symptom mapping. This method reveals regions more frequently damaged in patients with, compared to those without a symptom of interest. To test whether these symptoms are linked to a common thalamo-cortical network, we additionally performed lesion-network-symptom mapping. This method uses normative connectome data from resting-state fMRI of healthy participants (n = 65) for functional connectivity analyses, with lesion sites serving as seeds. Resulting lesion-dependent network connectivity of patients with language impairments was compared to those with motor and sensory deficits as baseline.

RESULTS: 101 patients (mean (SD) age 64.1 (14.6) years, 57 left, 42 right, 2 bilateral lesions) were included in the study. Voxel-based lesion-symptom mapping showed an association of language impairments with damage to left mediodorsal thalamic nucleus lesions. Lesion-network-symptom mapping revealed that language compared to sensory deficits were associated with higher normative lesion-dependent network connectivity to left fronto-temporal language networks and bilateral prefrontal, insulo-opercular, midline cingular and parietal domain-general networks. Lesions related to motor and sensory deficits showed higher lesion-dependent network connectivity within the sensorimotor network spanning prefrontal, pre- and postcentral cortices.

CONCLUSION: Thalamic aphasia relates to lesions in the left mediodorsal thalamic nucleus and to functionally connected left cortical language and bilateral cortical networks for cognitive control. This suggests that dysfunction in thalamo-cortical networks contributes to thalamic aphasia. We propose that inefficient integration between otherwise undamaged domain-general and language networks may cause thalamic aphasia.