title: Impaired prehension is associated with lesions of the superior and inferior hand representation within the human cerebellum.
abstract: Impairment of patients with cerebellar disease in prehension is well recognized. So far specific localizations within the human cerebellum associated with the impairment have rarely been assessed. To address this question we performed voxel-based lesion symptom mapping (VLSM) in patients with chronic focal cerebellar lesions in relation to specific deficits in prehensile movements. Patients with stroke within the posterior inferior cerebellar artery territory (n = 13) or the superior cerebellar artery (SCA) territory (n = 7) and corresponding control subjects were included in the study. Participants reached out, grasped, and lifted an object with either the left or right hand and with fast or normal movement speed. Both kinematic and grip-force parameters were recorded. Magnetic resonance imaging anatomical scans of the cerebellum were acquired, and lesions were marked as regions of interest. For VLSM analysis, a nonparametric test (Brunner-Munzel) was applied. Cerebellar patients showed clear abnormalities in hand transport (impaired movement speed and straightness) and, to a lesser degree, in hand shaping (increased finger touch latencies) while grip function was preserved. Deficits were most prominent in patients with SCA lesions and for ipsilesional, fast movements. Disorders in hand transport may be more difficult to compensate than deficits in hand shaping and grip-force control in chronic focal lesions of the cerebellum because of higher demands on predictive control of interaction torques. Lesions of the superior cerebellar cortex (lobules IV, V, VI) were associated with slower hand transport, whereas lesions of both superior (lobules VI, V, VI) and inferior cerebellar cortex (lobules VII, VIII) were associated with impaired movement straightness. These findings show that both the superior and inferior hand representations within the cerebellum contribute to hand transport during prehensile movements; however, they may have a different functional role.
authors.affiliation: Department of Neurology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany. Michael.Kueper@uni-due.de
authors.forename: Michael
authors.initials: M
authors.lastname: Küper
authors.forename: Barbara
authors.initials: B
authors.lastname: Brandauer
authors.forename: Markus
authors.initials: M
authors.lastname: Thürling
authors.forename: Beate
authors.initials: B
authors.lastname: Schoch
authors.forename: Elke R
authors.initials: ER
authors.lastname: Gizewski
authors.forename: Dagmar
authors.initials: D
authors.lastname: Timmann
authors.forename: Joachim
authors.initials: J
authors.lastname: Hermsdörfer
mesh_terms: D000328:Adult; D000368:Aged; D001931:Brain Mapping / Q000379:methods; D002525:Cerebellar Cortex / Q000473:pathology* / Q000502:physiology*; D002526:Cerebellar Diseases / Q000209:etiology / Q000473:pathology*; D002531:Cerebellum / Q000473:pathology / Q000502:physiology; D005260:Female; D006225:Hand / Q000502:physiology*; D018737:Hand Strength / Q000502:physiology*; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D009068:Movement / Q000502:physiology; D020521:Stroke / Q000150:complications / Q000473:pathology