Abstract
Background and Objectives: Apraxia is commonly attributed to left hemisphere lesions of the cortical fronto-temporo-parietal praxis networks or white matter lesions causing disconnections between cortical nodes. In contrast, the contribution of lesions to the subcortical gray matter, i.e., basal ganglia or thalamus, to apraxic deficits remains controversial. Here, we investigate whether damage to these subcortical gray matter structures (i.e., caudate nucleus, putamen, globus pallidus, thalamus) or the adjacent white matter tracts was associated with apraxic deficits.
Methods: We identified patients with distinct subcortical lesions with and without apraxia from a large retrospective sample of sub-acute left hemisphere ischemic stroke patients (n = 194). To test which subcortical structures (caudate nucleus, putamen, globus pallidus, thalamus, and adjacent white matter tracts), when lesioned, contributed to apraxic deficits, we statistically compared the proportion of lesioned voxels within subcortical gray and white matter structures between the apraxic and non-apraxic patients.
Results: Of the 194 stroke patients screened, 39 (median age = 65 years, range 30−82 years; median time post-stroke at the apraxia assessment = 7 days, range 1−44 days) had lesions confined to subcortical regions (gray and white matter). Eleven patients showed apraxic deficits when imitating gestures or pantomiming object use. Region-wise statistical lesion comparison (controlled for lesion size) revealed a more significant proportion of damage (‘lesion load’) in the caudate nucleus in apraxic stroke patients (mean difference = 6.9%, 95% confidence interval [CI] 0.4–13.3, P = 0.038, ηp2 = 0.11). In contrast, apraxic patients had lower lesion load in the globus pallidus (mean difference = 9.9%, 95% CI 0.1–19.8, P = 0.048, ηp2 = 0.10), while the lesion load in other subcortical structures (putamen, thalamus, adjacent white matter tracts) did not differ significantly between the apraxic and non-apraxic patients.
Discussion: These findings provide new insights into the subcortical anatomy of apraxia following left hemisphere stroke, suggesting a specific contribution of caudate nucleus lesions to apraxic deficits.
- Received November 26, 2022.
- Accepted in final form May 15, 2023.
- © 2023 American Academy of Neurology
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