Localizing apraxia in corticobasal syndrome: a morphometric MRI study

Author:

Constantinides Vasilios C12ORCID,Paraskevas George P1234,Velonakis Georgios56,Stefanis Leonidas12,Kapaki Elisabeth34

Affiliation:

1. First Department of Neurology , School of Medicine, , 72 Vas. Sofias Avenue, Athens, P.C. 11528 , Greece

2. National and Kapodistrian University of Athens, Eginition Hospital , School of Medicine, , 72 Vas. Sofias Avenue, Athens, P.C. 11528 , Greece

3. Second Department of Neurology , School of Medicine, , 1 Rimini Street, Athens, P.C. 12462 , Greece

4. National and Kapodistrian University of Athens, Attikon Hospital , School of Medicine, , 1 Rimini Street, Athens, P.C. 12462 , Greece

5. Second Department of Radiology , School of Medicine, , Attikon Hospital, 1 Rimini Street, Athens, P.C. 12462 , Greece

6. National and Kapodistrian University of Athens , School of Medicine, , Attikon Hospital, 1 Rimini Street, Athens, P.C. 12462 , Greece

Abstract

Abstract Apraxia localization has relied on voxel-based, lesion-symptom mapping studies in left hemisphere stroke patients. Studies on the neural substrates of different manifestations of apraxia in neurodegenerative disorders are scarce. The primary aim of this study was to look into the neural substrates of different manifestations of apraxia in a cohort of corticobasal syndrome patients (CBS) by use of cortical thickness. Twenty-six CBS patients were included in this cross-sectional study. The Goldenberg apraxia test (GAT) was applied. 3D-T1-weighted images were analyzed via the automated recon-all Freesurfer version 6.0 pipeline. Vertex-based multivariate General Linear Model analysis was applied to correlate GAT scores with cortical thickness. Deficits in imitation of meaningless gestures correlated with bilateral superior parietal atrophy, extending to the angular and supramarginal gyri, particularly on the left. Finger imitation relied predominantly on superior parietal lobes, whereas the left angular and supramarginal gyri, in addition to superior parietal lobes, were critical for hand imitation. The widespread bilateral clusters of atrophy in CBS related to apraxia indicate different pathophysiological mechanisms mediating praxis in neurodegenerative disorders compared to vascular lesions, with implications both for our understanding of praxis and for the rehabilitation approaches of patients with apraxia.

Publisher

Oxford University Press (OUP)

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