000851757 001__ 851757 000851757 005__ 20220930130157.0 000851757 0247_ $$2doi$$a10.3233/RNN-180815 000851757 0247_ $$2Handle$$a2128/20231 000851757 0247_ $$2pmid$$apmid:30282379 000851757 0247_ $$2WOS$$aWOS:000451336100001 000851757 037__ $$aFZJ-2018-05281 000851757 082__ $$a610 000851757 1001_ $$0P:(DE-Juel1)165846$$aKusch, M.$$b0 000851757 245__ $$aRecovery from apraxic deficits and its neural correlate 000851757 260__ $$aAmsterdam$$bIOS Press$$c2018 000851757 3367_ $$2DRIVER$$aarticle 000851757 3367_ $$2DataCite$$aOutput Types/Journal article 000851757 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1543494353_22948 000851757 3367_ $$2BibTeX$$aARTICLE 000851757 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000851757 3367_ $$00$$2EndNote$$aJournal Article 000851757 520__ $$aBackground and Objective: Apraxia is a deficit of motor cognition leading to difficulties in actual tool use, imitation of gestures, and pantomiming object use. To date, little data exist regarding the recovery from apraxic deficits after stroke, and no statistical lesion mapping study investigated the neural correlate of recovery from apraxia. Accordingly, we here examined recovery from apraxic deficits, differential associations of apraxia task (imitation vs. pantomime) and effector (bucco-facial vs. limb apraxia) with recovery, and the underlying neural correlates. Methods: We assessed apraxia in 39 patients with left hemisphere (LH) stroke both at admission and approximately 11 days later. Furthermore, we collected clinical imaging data to identify brain regions associated with recovery from apraxic deficits using voxel-based lesion-symptom mapping (VLSM). Results:Between the two assessments, a significant recovery from apraxic deficits was observed with a tendency of enhanced recovery of limb compared to bucco-facial apraxia. VLSM analyses revealed that within the lesion pattern initially associated with apraxia, lesions of the left insula were associated with remission of apraxic deficits, whereas lesions to the (inferior) parietal lobe (IPL; supramarginal and angular gyrus) and the superior longitudinal fasciculus (SLF) were associated with persistent apraxic deficits. Conclusions: Data suggest that lesions affecting the core regions (and white matter) of the fronto-parietal network cause more persistent apraxic deficits than lesions affecting other regions (here: the left insula) that also contribute to motor cognition and apraxic deficits. 000851757 536__ $$0G:(DE-HGF)POF3-572$$a572 - (Dys-)function and Plasticity (POF3-572)$$cPOF3-572$$fPOF III$$x0 000851757 588__ $$aDataset connected to CrossRef 000851757 7001_ $$0P:(DE-Juel1)169625$$aSchmidt, Claudia$$b1$$eCorresponding author 000851757 7001_ $$0P:(DE-HGF)0$$aGöden, L.$$b2 000851757 7001_ $$0P:(DE-Juel1)171739$$aTscherpel, C.$$b3 000851757 7001_ $$0P:(DE-HGF)0$$aStahl, J.$$b4 000851757 7001_ $$0P:(DE-HGF)0$$aSaliger, J.$$b5 000851757 7001_ $$0P:(DE-HGF)0$$aKarbe, H.$$b6 000851757 7001_ $$0P:(DE-Juel1)131720$$aFink, G. R.$$b7 000851757 7001_ $$0P:(DE-HGF)0$$aWeiss, P. 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