Affiliations: [a]
Department of Neurology, University Hospital Cologne, Cologne, Germany
| [b]
Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Centre Jülich, Jülich, Germany
| [c]
Department of Psychology, University of Cologne, Cologne, Germany
| [d]
Neurological Rehabilitation Centre Godeshöhe, Bonn, Germany
Correspondence:
[*]
Corresponding author: Claudia Schmidt, Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Centre Jülich, 52425 Jülich, Germany. Tel.: +49 2461 61 2084; Fax: +49 2461 61 1518; E-mail: [email protected].
Abstract: Background and Objective:Apraxia is a deficit of motor cognition leading to difficulties in actual tool use, imitation of gestures, and pantomiming object use. To date, little data exist regarding the recovery from apraxic deficits after stroke, and no statistical lesion mapping study investigated the neural correlate of recovery from apraxia. Accordingly, we here examined recovery from apraxic deficits, differential associations of apraxia task (imitation vs. pantomime) and effector (bucco-facial vs. limb apraxia) with recovery, and the underlying neural correlates. Methods:We assessed apraxia in 39 patients with left hemisphere (LH) stroke both at admission and approximately 11 days later. Furthermore, we collected clinical imaging data to identify brain regions associated with recovery from apraxic deficits using voxel-based lesion-symptom mapping (VLSM). Results:Between the two assessments, a significant recovery from apraxic deficits was observed with a tendency of enhanced recovery of limb compared to bucco-facial apraxia. VLSM analyses revealed that within the lesion pattern initially associated with apraxia, lesions of the left insula were associated with remission of apraxic deficits, whereas lesions to the (inferior) parietal lobe (IPL; supramarginal and angular gyrus) and the superior longitudinal fasciculus (SLF) were associated with persistent apraxic deficits. Conclusions:Data suggest that lesions affecting the core regions (and white matter) of the fronto-parietal praxis network cause more persistent apraxic deficits than lesions affecting other regions (here: the left insula) that also contribute to motor cognition and apraxic deficits.
