Fronto-thalamic networks and the left ventral thalamic nuclei play a key role in aphasia after thalamic stroke.

Thalamic aphasia results from focal thalamic lesions that cause dysfunction of remote but functionally connected cortical areas due to language network perturbation. However, specific local and network-level neural substrates of thalamic aphasia remain incompletely understood. Using lesion symptom mapping, we demonstrate that lesions in the left ventrolateral and ventral anterior thalamic nucleus are most strongly associated with aphasia in general and with impaired semantic and phonemic fluency and complex comprehension in particular. Lesion network mapping (using a normative connectome based on fMRI data from 1000 healthy individuals) reveals a Thalamic aphasia network encompassing widespread left-hemispheric cerebral connections, with Broca's area showing the strongest associations, followed by the superior and middle frontal gyri, precentral and paracingulate gyri, and globus pallidus. Our results imply the critical involvement of the left ventrolateral and left ventral anterior thalamic nuclei in engaging left frontal cortical areas, especially Broca's area, during language processing.

"Thalamic aphasia" after stroke is associated with left anterior lesion location.

BACKGROUND: Aphasic symptoms are typically associated with lesions of the left fronto-temporal cortex. Interestingly, aphasic symptoms have also been described in patients with thalamic strokes in anterior, paramedian or posterolateral location. So far, systematic analyses are missing. METHODS: We conducted a retrospective analysis of consecutive patients admitted to our tertiary stroke care center between January 2016 and July 2017 with image-based (MRI) proven ischemic stroke. We evaluated stroke lesion location, using 3-T MRI, and presence of aphasic symptoms. RESULTS: Out of 1064 patients, 104 (9.8%) presented with a thalamic stroke, 52 of which (4.9%) had an isolated lesion in the thalamus (ILT). In patients with ILT, 6/52 had aphasic symptoms. Aphasic symptoms after ILT were only present in patients with left anterior lesion location (n = 6, 100% left anterior vs. 0% other thalamic location, p < 0.001). CONCLUSIONS: Aphasic symptoms in thalamic stroke are strongly associated with left anterior lesion location. In thalamo-cortical language networks, specifically the nuclei in the left anterior thalamus could play an important role in integration of left cortical information with disconnection leading to aphasic symptoms.