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.

Differential Effects of Parietal and Cerebellar Stroke in Response to Object Location Perturbation

“…Movement onset was delayed for both groups. In accordance with previous research in heterogeneous and parietal stroke (Michaelsen et al, 2004 ; Thielmann et al, 2004 ; Lang et al, 2005 ; vanVliet and Sheridan, 2007 ) and cerebellar lesions (Haggard et al, 1994 ; Bastian and Thach, 1995 ; Rand et al, 2000 ; Zackowski et al, 2002 ; Brandauer et al, 2008 ; Konczak et al, 2010 ; Kuper et al, 2011 ), MD was longer and PV was reduced for parietal and cerebellar participants.…”

“…Although correlations between key events were present and have been previously found in cerebellar patients with lesions in the posterior and superior cerebellar artery territory (Kuper et al, 2011 ), correlational analyses were present in a smaller number of the cerebellar group for all three coupled events compared to other groups, and there was a trend toward a weaker correlation between PD and the time of MA, compared to the parietal and control groups. This echoes previous findings where increased variability of time to MA was noted in cerebellar participants with MA occurring both before and after PD (MA is usually after PD in healthy people) (Zackowski et al, 2002 ) and higher variability of timing of MA and PV in cerebellar subjects compared to controls (Rand et al, 2000 ).…”

Digit somatotopy in the human cerebellum: A 7T fMRI study

“…A functional difference between lobule V and VIII has been proposed (Glickstein et al, 2011) where the lobule V of the anterior cerebellum, SMA and the prefrontal cortex form a preparatory loop, with activity preceding the action and lobule VIII as part of an executive network, together with the motor cortex and thalamus. Cerebellar lesions in either lobule V or VIII also result in slightly different impairments in hand movements (Kuper et al, 2011a).…”

Age-specific CT and MRI templates for spatial normalization

“…However, we also feel there is a clear rationale for creating symmetrical templates for analyzing brain injury. First of all, many studies of brain injury intentionally flip lesions to collapse across lesion side (Donchin et al, 2012; Zeller et al, 2011; Küper et al, 2011). Asymmetrical templates will pose challenges if the flipping is done after normalization, and can lead to differential biases if flipping occurs prior to normalization (e.g.…”