Object Naming After Thalamic Damage: Evidence from a Large-Scale, Chronic-Phase Study of Left Hemisphere Stroke Survivors

Abstract Functional imaging and clinical cases implicate the left thalamus in object naming, yet the prevalence of naming impairment after focal thalamic damage is low with variable impact and often rapid resolution. This suggests that compensatory mechanisms, within or beyond the thalamus, may support recovery. We hypothesized that thalamic damage would (i) not cause chronic anomia if other naming-related regions remain intact, but (ii) exacerbate anomia when co-occurring with damage to non-thalamic naming regions. To test these hypotheses, we retrospectively assessed naming ability in 550 left-hemisphere chronic stroke survivors (52% with anomia). Lesion sites included focal thalamic lesions (n = 14), combined thalamic and non-thalamic lesions (n = 271), and lesions sparing the thalamus (n = 265). Whole-brain lesion-symptom mapping (LSM), using multivariate support vector regression, identified brain regions where damage was significantly related to naming ability. Contributions of different thalamic subregions to naming were assessed using ridge regression. Focal thalamic lesions were not associated with chronic anomia. LSM identified two naming-related clusters, a temporo-parietal region of interest (ROI-TP) and a subcortical-insular region (ROI-SC) including the lateral thalamus. However, lesion load in the lateral thalamus did not independently contribute to naming performance when controlling for damage to other parts of ROI-SC. Nor did any thalamic nuclei show additive effects beyond ROI-TP and non-thalamic ROI-SC. These findings suggest that thalamic damage in the dominant hemisphere does not cause long-term anomia in chronic stroke. Future research therefore needs longitudinal designs to track the trajectory of transient thalamic effects from the acute to chronic phases, and to investigate whether naming impairments after thalamic lesions are: (i) lesion-specific but context-dependent, emerging under increased cognitive load, or (ii) attributable to non-lesion-site-dependent post-stroke factors such as fatigue.