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This suggests that compensatory mechanisms, within or beyond the thalamus, may support recovery. We hypothesized that thalamic damage would (a) not cause chronic anomia if other naming-related regions remain intact but (b) 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\u2013symptom 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 temporoparietal region of interest (ROI-TP) and a subcortical\u2013insular region of interest (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 the ROI-SC, nor did any thalamic nuclei show additive effects beyond the ROI-TP and the 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 (a) lesion specific but context dependent, emerging under increased cognitive load, or (b) attributable to non-lesion-site-dependent post-stroke factors such as fatigue.<\/jats:p>","DOI":"10.1162\/nol.a.231","type":"journal-article","created":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T13:33:47Z","timestamp":1765287227000},"update-policy":"https:\/\/doi.org\/10.1162\/mitpressjournals.corrections.policy","source":"Crossref","is-referenced-by-count":1,"title":["Object Naming After Thalamic Damage: Evidence From a Large-Scale, Chronic-Phase Study of Left Hemisphere Stroke Survivors"],"prefix":"10.1162","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1397-5224","authenticated-orcid":true,"given":"Jie","family":"Zhang","sequence":"first","affiliation":[{"name":"Center for Rehabilitation Medicine, Rehabilitation & Sports Medicine Research Institute of Zhejiang Province, Department of Rehabilitation Medicine, Zhejiang Provincial People\u2019s Hospital, Affiliated People\u2019s Hospital, Hangzhou Medical College, Hangzhou, China"},{"name":"Department of Imaging Neuroscience, Queen Square Institute of Neurology, University College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas","family":"Neville","sequence":"additional","affiliation":[{"name":"Department of Imaging Neuroscience, Queen Square Institute of Neurology, University College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Storm","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Imaging Neuroscience, Queen Square Institute of Neurology, University College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophie M.","family":"Roberts","sequence":"additional","affiliation":[{"name":"Department of Imaging Neuroscience, Queen Square Institute of Neurology, University College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas M. 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