Visuo-motor control of the ipsilateral hand: evidence from right brain-damaged patients

Neuropsychologia 41 (2003) 739–757

Visuo-motor control of the ipsilateral hand: evidencefrom right brain-damaged patients

A. Farnèa,∗, A.C. Roya, Y. Paulignana, G. Rodeb,c,Y. Rossettib,c, D. Boissonb,c, M. Jeanneroda

a Institut des Sciences Cognitives UMR 5015 C.N.R.S., 67 boulevard Pinel, 69675 Bron, Franceb Hospices Civiles de Lyon: Hˆopital Henry Gabrielle, 69565 Saint-Genis-Laval, France

c Espace et Action” I.N.S.E.R.M. Unité 534, 16 avenue du Doyen Lépine, 69676 Bron, France

Received 18 February 2002; received in revised form 9 July 2002; accepted 5 September 2002

Abstract

We investigated the extent to which the right hemisphere is involved in the control of the ipsilateral hand by analysing the kinematicsof right-hand prehension in right brain-damaged (RBD) patients. We required patients to grasp one of five possible objects, equally-sizedand distributed over a 40◦ wide workspace. With the purpose of investigating the right hemisphere contribution to the on-line visuo-motorcontrol, we also assessed patients’ ability to correct their movement “in-flight”, in response to a sudden change of object position. Patients’performance was compared to that of aged-matched controls. A Younger group of healthy subjects, matching the population classicallytested on double-step paradigms, was also evaluated to fully assess whether patients’ kinematics could be partially due to normal ageing. As afurther aim, the possible influence of hemispatial neglect was evaluated by comparing the performances of right brain-damaged patients withand without neglect. In normal subjects, the results confirmed and extended the notion of (a) positional tuning of grip formation, and (b) fastreactions following a change in object position. In addition, subtle effects of ageing on visuo-motor behaviour were shown by less efficientmovement correction in the Elderly group. Patients executing reach-to-grasp actions into the left contralesional hemispace were selectivelyaffected in both temporal and spatial aspects of movements. While their performances were relatively well preserved in the right hemispace,patients did not show positional tuning of grip formation, nor fast corrections of their movements when acting in the left hemispace.Interestingly, similar deficits were found irrespective of the presence of neglect. These results show that the right hemisphere contributesto the processing of visuo-motor information that is necessary for executing actions with the ipsilateral hand in the contralateral space.© 2002 Elsevier Science Ltd. All rights reserved.

Keywords:Visuo-motor control; Reach-to-grasp; Right hemisphere lesion; Ageing; Neglect

1. Introduction

Since the early part of the last century, the differen-tial roles played by the left and right hemisphere in thevisually-guided control of hand movements have been ex-tensively studied through the observation of movementabnormalities following brain lesions[2,7,45,51,82]. Aftera hemispheric lesion, impairments in goal-directed move-ments are manifest in the contralesional, but also in theipsilesional limb. The dominant role of the left hemispherein the control of skilled and complex motor actions has beenrevealed by Liepmann[62,63] following the observation

∗ Corresponding author. Present address: Dipartimento di Psicologia,Universita di Bologna, Viale Berti Pichat 5, 40127 Bologna, Italy.Tel.: +39-51-2091347; fax:+39-51-243086.

E-mail address:[email protected] (A. Farne).

that apraxic deficits shown by left brain-damaged patientsare often present both in the contralesional and ipsile-sional hand. Several studies have confirmed and extendedthis observation[22,87,61,89], by showing that left braindamage produce ipsilesional deficits on a variety of motortasks including single movements[57,58], timing and se-quencing[23–43,47], control of open-loop and alternatingmovements[37,88,94].

By contrast, the degree of severity and type of impair-ment affecting the ipsilateral hand after right brain damageis less clear. Studies of simple motor tasks (e.g. pointing, al-ternating tapping) reported that right brain-damaged (RBD)patients performances, apart from slowness in movementinitiation [29–48], are close to normal controls[29,36–39]implying that the RH plays a limited role in the ipsilateralmotor behaviour. Other investigations, however, found ipsi-lateral motor deficits after RBD even in simple tasks (e.g.

0028-3932/02/$ – see front matter © 2002 Elsevier Science Ltd. All rights reserved.PII: S0028-3932(02)00177-X

740 A. Farne et al. / Neuropsychologia 41 (2003) 739–757

alternating tapping), and specifically in the closed-loopphase of the movement prior to target impact[3], where vi-sual feedback-based adjustments are required for accuracy[94].

The right hemisphere is usually thought to be involved inthe global processing required to make visuospatial analysis,such as mapping target and limb positions[12], and in thevisual processing prior to movement[79], independent ofwhether target location is uncertain[29,33,50]or known inadvance[94]. Recent studies, by investigating more complexand natural actions such as prehension, have confirmed andextended the notion that ipsilesional visuo-motor deficits fol-low left as well as right brain damage[48,49]. By analysingthe kinematics of reach-to-grasp movements directed to cen-trally located objects, Hermsdörfer et al.[49] reported thatRBD patients are particularly slow in the last part of themovement, and show stronger variability and imprecision inadjusting their whole-hand grip according to changes in ob-ject size. On the basis of this finding, the authors suggestedthat the RH plays a special role in hand grip formation andrapid on-line visuo-motor transformations[48].

It is difficult to determine a unique explanation for thediscrepancies reported in the literature, mostly because ofcross-study differences in visuo-motor tasks and movementparameters. In addition, the possible influence of associ-ated deficits, such as hemispatial neglect on ipsilesionalvisuo-motor deficits has been rarely taken into account.

Although neglect is usually referred to as a failure to ori-ent, detect and respond to left-sided stimuli, as assessed byvisual perception-based tasks, neglect patients may also beimpaired in acting with the right ipsilesional hand[83,91].In particular, RBD patients with neglect may be slow in initi-ating and/or executing contralesionally directed movements[46,66,68,70]. The spatial trajectory of the transport phaseof the movement of RBD patients with a past history of ne-glect may show an ipsilesional deviation[34–52]that can beexacerbated by the presence of ipsilesional distractors[16].Recent evidence, however, support the opposite conclusion.Spatio-temporal motor performances of RBD patients withflorid neglect can be almost preserved, and comparable tothose of RBD patients with no sign of neglect. Konczak andKarnath[60] found no selective deficits in the execution ofcontralesional pointing movements in neglect patients (i.e.no directional bradykinesia). Rather, neglect and RBD con-trol patients showed a general bradykinesia: movement timewas longer in both groups as compared to healthy controls[59], and the terminal accuracy and hand trajectory wereunaffected by the presence of neglect[54,77]. In case ofprehensile movements, neglect patients are reported to graspobjects skilfully and adapt the opening of the hand to objects’size whichever the side of space (left or right) where the ob-ject appears, similarly to non-neglecting RBD patients[81].

The primary aim of the present study was to examinethe extent to which the right hemisphere is involved in thecontrol of the ipsilateral hand. To this end, we comparedthe kinematics of seven RBD patients while performing

reach-to-grasp movements of objects located both in the leftand right hemispaces. A high level of visuospatial accuracywas stressed by requiring patients to grasp objects betweenthe index and thumb of their ipsilesional right hand, i.e.by using a precision grip. Patients’ ability to rapidly adjustan already prepared movement in a double-step task wasalso evaluated using a classic paradigm of target-positionperturbation[10,41,74]in which patients were required tograsp a central object that, unexpectedly, was virtually dis-placed to the left or to the right. This double-step task hasbeen employed several times in Young subjects and normalkinematic patterns are well known[9,14,32,40,74], allow-ing a reliable comparison of the results of the present studywith those in the literature. Changing object position usu-ally induces fast modifications of the planned movement,as documented by the earlier occurrence of accelerationand velocity peaks in laterally perturbed trials comparedto central unperturbed trials. However, the effect of normalageing on the “in-flight” kinematics of Elderly people hasnever been investigated within our paradigm. For this rea-son, patients’ motor ability in the specific tasks we usedwas directly compared with that obtained by aged-matchedcontrols, but also (indirectly) with that obtained by Younghealthy controls, aged-matched with the population thathas normally been tested in double-step paradigms. Thus,our design was particularly well suited to ascertain whetherany difference with the results previously reported in theliterature depends upon the brain lesion or normal ageing.

As a second aim, we investigated whether left visuospa-tial neglect, that was present in four out of the seven RBDpatients, may be responsible for visuo-motor deficits of theipsilesional hand. This is particularly important in light ofthe inconsistency of the results reported in the literature.Predictions were straightforward. First, if the RH plays aspecific role in the visuo-motor control of the ipsilateralhand, then some deficits should be found in the kinematicperformance of RBD patients; otherwise, their performanceshould be comparable to that obtained by healthy controls.Second, if the presence of visuospatial neglect affects somedirectional aspects of movements, then directionally selec-tive deficits should be revealed only in RBD patients withneglect. Alternatively, the motor behaviour of neglect andnon-neglect RBD patients should be comparable.

2. Methods

2.1. Subjects

Two groups of six healthy subjects (Elderly and Young,mean age 55 and 23, respectively) and seven neurologicalpatients with right brain damage participated in this studyafter giving informed consent. All subjects were right handedat the Oldfield’s questionnaire[73].

The RBD group was split into two sub-groups: one of fourpatients with left unilateral visual neglect (RBD+, mean

A. Farne et al. / Neuropsychologia 41 (2003) 739–757 741

Fig. 1. Reconstruction of lesion for RBD patients with (+) and without (−) neglect, according to Damasio and Damasio’s method[21]. The figureillustrates the lesion site and extent (grey shaded areas) on templates of the right hemisphere. Lesion location was coded using regions from templateA18 for patients 2 and 5, and A20 for the remaining patients. Most of patients in both groups suffered from large, cortical and sub-cortical lesionsinvolving the frontal, the parietal and/or temporal lobe (with the exception of patient P5− whose lesion was limited to the sub-cortical white matterinvolving the posterior limb of the internal capsule and the thalamus).

age 52), and one of three patients with no signs of visualneglect (RBD−, mean age 59). All patients manifested lefthemiplegia or hemiparesis. Their lesions, shown inFig. 1,were documented by clinical neuroimaging CT or MRI scans(seeTable 1).

Neglect patients without visual field defects were se-lected from a larger RBD+ group of the inpatient pop-ulation of “Henry Gabrielle” Hospital. The absence ofhemianopia turned out to be a necessary condition, sincethree RBD+ patients with hemianopia we investigated in


Table 1Clinical data on right brain-damaged patients

Patients Sex Age(years)

Etiology Length ofillness (months)

Contralateralmotor deficit

Contralateralsomatos deficit

Neglect Neglect type motorvs. perpectual

Lesion site

P1+ M 59 Isch. 7 ++ ++ ++ Motor F, T, PP2+ M 27 Isch. 2 + ++ + Symmetric F, PP3+ M 60 Isch. 3 + + ++ Perceptual FP4+ M 64 Hem. 2 ++ ++ ++ Perceptual F, BGP5− M 59 Hem. 3 ++ + − – Ic, ThP6− M 61 Isch. 2 ++ + − – F, T, PP7− F 55 Isch. 75 + + − − F, T, P, BG

The ischemic (Isch.) or hemorrhagic (Hem.) nature of the right cerebro-vascular accident, as well as demographic details are reported for neglect (+)and non-neglect (−) RBD patients. The table reports the presence and severity of visuospatial neglect (− absent;+ moderate;++ severe). The presenceand severity of sensori-motor deficits on the left hemi-body, as assessed by neurological examination, is also reported (same conventions). ‘Neglect type’column indicates the relative prevalence of a “motor” or “perceptual” component in neglect patients (symmetric: no prevalence). Lesion site columnindicates the cerebral structures and lobes involved by the lesion. F: frontal; T: temporal; P: parietal; BG: basal ganglia; Ic: internal capsule; Th: thalamus.

a pilot study were unable to perform almost any leftwardmovement, either in the single or double-step task. Patientswere excluded from the study if they were affected by opticataxia or non-neurological motor impairment (e.g. fractures,arthritis).

Visuospatial neglect was assessed with a battery of testsincluding line[1], letter[26] and bell[31] cancellation (dis-played on an A3 sheet of paper), line bisection[42] anddrawing from a model[30] (A4). Diagnosis of neglect de-pended upon the presence of left-sided omissions in thedrawing or cancellation tests (=20%), or rightward dis-placement on the bisection task. Neglect was considered as“moderate” when omissions in cancellation tests were lim-ited to the left-half of the sheet and as “severe” when occur-ring also in the left-sided portion of the right-half of the sheet(seeTable 1). Table 1reports the predominance of percep-tual or motor-directional neglect, as assessed with the epidi-ascope method proposed by Nico[72]. RBD patients wereassigned to the control group when no left-sided elementwas missing in the drawing test, and omissions in cancella-tion tests (=5%) were equally distributed over the display.The performance of RBD patients was nearly errorless.

2.2. Materials and procedure

Five translucent plastic cylinders (10 cm high, 1.5 cm ofdiameter) were placed upright, above an embedded LED,on a horizontal table at which the subject was comfortablyseated, in a dimly illuminated room. Homogeneous red illu-mination of each cylinder was obtained by switching on theembedded LED. Objects were located concentrically to thesubject’s body axis (seeFig. 2A), from the left (−20 and−10◦) to the right (+20 and+10◦), with a central position(0◦). The thumb and index fingertips, forming a pinch grip,were positioned on a micro-switch located 25 cm from thesubject’s body along the sagittal axis. The subject’s ulnaredge of the right hand rested on the table immediately to theright of that axis. The distance between targets and the rightwrist, as measured by an infrared-emitting diode (IRED),were 39.9, 35.2, 31.3, 28.4 and 27 cm from left to right.

Subjects were required to gaze a fixation point that wasilluminated just in front of the central dowel. After a randomdelay (ranging between 500 and 2000 ms), the fixation pointwas turned off and no further constraint was imposed onhead or eye movements. Two conditions were possible (seeFig. 2B). In the “fixed” condition, the random illuminationof one of the five dowels provided the subject with the GOsignal for grasping it. Subjects were instructed to grasp andlift the target object rapidly and accurately between thumband index fingertips. Fifty trials were obtained, 10 for eachposition. For the “perturbed” condition (180 trials), in 78%of trials the central dowel was the illuminated target. In theremaining 22% of trials, the central dowel was first illu-minated, but as the subject began to move (i.e. when themicro-switch was released), the central dowel was switchedoff and a lateral dowel was randomly illuminated, either onthe right (+10 or +20◦) or left (−10 or −20◦) hemispace.Ten perturbed movements were thus obtained for each po-sition, interleaved with 140 non-perturbed movements thatserved as control. Subjects were instructed to rapidly andaccurately grasp the last illuminated target. In both condi-tions, run in separate blocks, target illumination lasted untilthe object was lifted up. Data acquisition continued for 2 safter the GO signal for healthy participants and up to 6 s forRBD patients. Practice trials were provided at the start ofeach block to familiarise the subject with testing conditions.

2.3. Movement recording

Movements of the right arm were recorded by means ofan Optotrak 3020 system (Northern Digital Inc.). The spa-tial position of active markers was sampled at 200 Hz bya camera, composed of three linear infrared sensors, whichwas located 2.5 m above the working space (Fig. 2C). Twomarkers were stuck on the nails of the index finger and thethumb, respectively. One was placed at wrist level on thestyloid process of the radius. These markers were used formeasuring the two main components of prehension, namelythe grasping component (the change over time of the dis-tance between the index and the thumb markers) and the


Fig. 2. Schematic view of the experimental set-up and conditions. (A): Spatial arrangement of objects relative to the patient, viewed from above; (B):graphic representation of the sequence of events in the two experimental conditions (fixed: single-step task; perturbed: double-step task). FP: fixationpoint (red ON, grey OFF); SP: hand starting position. The target object for the subject’s action was flagged by its lightening (red ON, grey OFF); (C):spatial location of the movement tracking system.

transport component (the change over time of the position ofthe wrist marker). Static and dynamic precision was 0.1 mm.

2.4. Data processing

Data were filtered off-line with a second-order low-passButterworth filter with a forward and reverse pass (10 Hzcut-off frequency). Movement onset was defined as thefirst increasing value of an 11 points sequence on the timecourse of thumb position. Movement endpoint was similarlydetermined as the point where both the inter-finger distanceand the wrist velocity stopped decreasing. These pointswere computed semi-automatically: they were visually con-trolled for each individual movement after computer-baseddetection. Kinematic parameters were measured on markertrajectories using specially designed software (OptodispCopyright UCBL-CNRS). For the transport component,the time and amplitude of tangential acceleration and ve-locity of the wrist marker were measured. The time andamplitude of the maximum inter-finger distance, minus theindividual thumb-index distance at movement beginningwere measured for the grasping component.

2.5. Statistics

Due to the rare occurrence of errors in movement execu-tion, less than 3% of trials were excluded from analysis fornormal subjects. Errors are here defined as the lack of a sta-ble grasp when subjects slipped the cylinder in the attemptto lift it up. In this case, errors were equally distributed

between hemispaces and trials were excluded from analysis.A small proportion of left-sided targets were omitted in bothconditions by RBD patients with neglect (see below). Pa-tients without neglect (RBD) made no left-sided omissions,and less than 3% of trials was lacking as for normal subjects.

A direct comparison between patients and aged-matchedcontrols was performed using a repeated measures ANOVAwith one between-subject factor (group: RBD, Elderly)and one within-subject factor (position:−20, −10, 0,+10,+20◦) on the mean value of each parameter for the experi-mental conditions (fixed, perturbed). Preliminary inspectionof this analysis, however, revealed that Elderly controls didnot show significant effects of movement correction in theperturbed condition, despite the fact that this finding hasbeen replicated several times in previously published studieson Young normal subjects. In order to clearly disambiguate,the effects induced on patients’ kinematics by normal age-ing and the brain lesion, an additional repeated measuresANOVA with Age (Young, Elderly) as between-subjectfactor, and the same within-subject factor position, wasconducted on the mean value of each parameter for normalsubjects.

To evaluate the influence of visual neglect on patients’motor behaviour, a similar repeated measures ANOVA withNeglect (RBD+, RBD−) as between-subject factor and thesame within-subject factor position was conducted on themean value of each parameter for the two sub-groups ofpatients. Newman–Keuls post-hoc test was used. Whenevermain effects were explained by significant interactions, onlythese latter are described.


3. Results

Description of the results will proceed in three steps. First,we will consider the comparison of movement parametersbetween RBD patients and aged-matched controls (Elderlygroup). Second, results will be presented relative to the com-parison between RBD patients with and without neglect and,third, between Young and Elderly healthy subjects.

3.1. A comparison between RBD patients and agematched controls

3.1.1. Fixed conditionBoth controls and RBD subjects (with and without ne-

glect) reached and grasped the target object accurately. Theynever bumped into non-illuminated cylinders, showing aprecise performance (seeFig. 3A–C). Neglect patients omit-ted on average 13 and 8% of leftward trials (−20 and−10◦,

Fig. 3. Spatial path of prehension movements directed to the five object positions in a representative healthy subject from the Elderly group (upper row)as a function of condition ((A): fixed, (B): perturbed). Spatial path of a representative RBD patient with neglect are also reported (lower row) as afunction of condition ((C): fixed, (D): perturbed). Single spatial paths are illustrated for wrist (blue), thumb (red) and index finger (green).

respectively), omissions being considered as the absenceof movement or the execution of leftward movements thatstarted too late to be entirely recorded. Thus, the presenceof left visuospatial neglect did not severely hamper patients’ability to respond to left-sided visual targets. Indeed, a red,10 cm high 3D object suddenly appearing in a dimly illu-minated room is a much more salient stimulus than a small2D shape intermingled with several distractors. Therefore,the small proportion of left-sided targets omitted by neglectpatients, otherwise showing a rather severe deficit, is not sur-prising. Nonetheless, neglect severity was reflected in the in-dividual rate of omissions, the smallest amount of omissions(10 and 0% for−20 and−10◦, respectively) being observedin the patient with moderate neglect (P2+, seeTable 1).

3.1.1.1. Reaction and movement times.Patients showedlonger RT than controls (647 ms versus 260 ms) [F(1, 11) =14.67; P < 0.003], as well as longer MT (1066 ms versus


581 ms) [F(1, 11) = 28.53; P < 0.0003]. In both groups,MT was longer in −20◦ position (900 ms), which in-volved the longest distances between the wrist and theobject, than for the remaining positions (P < 0.02 for allcomparisons).

3.1.1.2. Transport component.Patients’ time to peak ac-celeration (TPA) was slower for left-sided positions (−20◦:229 ms;−10◦: 213 ms) than for right-sided positions (+20◦:190 ms,P < 0.002; +10◦: 182 ms,P < 0.02). The TPAin controls did not differ among object positions. Peak ac-celeration (PA) was lower in patients (4419 mm/s2) thancontrols (8348 mm/s2, P < 0.0003) and, in both groups,PA was lower for left-sided positions (−20◦: 5958 mm/s2;−10◦: 5711 mm/s2) compared to right-sided positions(+20◦: 7463 mm/s2, P < 0.0002; +10◦: 6673 mm/s2,P < 0.005).

While patients showed a later time to peak velocity (TPV)than controls (345 mm/s versus 227 mm/s) [F(1, 11) =30.67; P < 0.0002], TPV was similarly affected by objectposition in both groups, being longer for left-sided (−20◦:329 ms;−10◦: 308 ms) than right-sided positions (+20◦:262 ms;+10◦: 254 ms, bothP < 0.0002). Although peakvelocity (PV) was lower in patients than controls (635 mm/sversus 964 mm/s) [F(1, 11) = 21.37; P < 0.0007], it washigher in both groups in left-sided (−20◦: 903 mm/s;−10◦:831 mm/s) than right-sided positions (+20◦: 781 mm/s;+10◦: 712 mm/s, bothP < 0.0003).

3.1.1.3. Grasp component.The time to maximum grip-aperture (TGA) was longer in patients than controls (656 msversus 366 ms) [F(1, 11) = 35.63; P < 0.0001]. Inboth groups, TGA was longer for movements directed toleft-sided (−20◦: 598 ms;−10◦: 529 ms) than right-sidedpositions (+20◦: 486 ms;+10◦: 463 ms, bothP < 0.006).The maximum grip-aperture (MGA) was smaller for left-ward (−20◦: 46.9 mm; −10◦: 47.9 mm) with respect torightward positions (+20◦: 57.5 mm;+10◦: 51.7 mm, bothP < 0.0005). The nearly significant interaction Group XPosition [F(4, 44) = 2.56; P = 0.051] suggested thatMGA pattern tended to differ between groups. While MGAin controls progressively increased from left- to right-sidedpositions (49.3, 51.2, 54.6, 55.5, 61.4 mm), patients’ MGAappeared to increase only from the central to right-sidedpositions (44.5, 44.7, 44.4, 47.9, 53.6 mm).

3.1.2. Perturbed conditionOn perturbed trials subjects grasped the target object in

its novel position. Perturbed movements were composedof two sub-movements (Fig. 3B–D), the first one directedat the location of the initial 0◦ target and the second oneat the new target location. The second sub-movement dis-played a secondary velocity peak and, in most cases, asecondary peak in grip-aperture. Neglect patients omit-ted on average 25 and 13% of perturbed trials (−20◦ and−10◦, respectively). The absence of movement’s redirection

(i.e. grasping of the non-illuminated central cylinder), orredirection of movement after contact with the centralobject were both considered as omissions. In case of redi-rected movements, patients never misreached the targetobject.

3.1.2.1. Reaction and movement times.Patients showedlonger RT (901 ms versus 242 ms) [F(1, 11) = 9.8;P < 0.01] and MT than controls (1597 ms versus 817 ms)[F(1, 11) = 8.02; P < 0.02]. Duration of left- andright-sided perturbed movements was increased in bothgroups with respect to centrally directed control move-ments (P < 0.006 in all comparisons). In RBD patients,movements perturbed to the leftmost position took longerto be executed than those directed to the rightmost position(1982 ms versus 1768 ms,P < 0.03), this difference beingabsent in controls.

3.1.2.2. Transport component.The TPA was longer inpatients than controls (190 ms versus 117 ms) [F(1, 11) =14.76; P < 0.003] and PA was of lower amplitude[F(1, 11) = 23.46; P < 0.0006]. In RBD patients, thewrist acceleration peak occurred later for leftward (−20◦:214 ms; −10◦: 197 ms) than rightward positions (+20◦:179 ms;+10◦: 165 ms, bothP < 0.03). Moreover, the PAfor +10◦ (165 ms) position occurred earlier compared tothe control central position (0◦: 197 ms,P < 0.04). Nodifferences were found between perturbed and unperturbedtrials in control subjects.

Patients showed longer TPV than controls [F(1, 11) =10.04; P < 0.002] and their PV was also of lower am-plitude (552 mm/s versus 997 mm/s) [F(1, 11) = 25.25;P < 0.0004]. Patients TPV was longer in leftward (−20◦:354 ms; −10◦: 336 ms) than rightward perturbed trials(+20◦: 304 ms;+10◦: 298 ms, bothP < 0.02), and bothrightward perturbations showed shorter TPV than centralcontrol trials (0◦: 356 ms, bothP < 0.002). Again, per-turbed and unperturbed trials did not differ in controls.

3.1.2.3. Grasp component.In both groups, a double-peakpattern of grip-aperture characterised most of perturbed tri-als. In RBD patients, the first TGA was longer in leftward(−20◦: 689 ms;−10◦: 629 ms) than rightward perturbed tri-als (+20◦: 575 ms;+10◦: 533 ms, bothP < 0.002) that, inturn, displayed shorter TGA compared to central control tri-als (0◦: 639 ms, bothP < 0.05). No differences were foundin the control group. The first MGA was smaller in patientsthan controls (38.4 mm versus 51.3 mm) [F(1, 11) = 6.71;P < 0.03] and, in both groups, it was smaller in leftward(−20◦: 44.7 mm;−10◦: 45.2 mm) and rightward perturbedpositions (+20◦: 43.4 mm;+10◦: 43.1 mm) with respect tothe central control position (0◦: 47.7 mm, allP < 0.05),without differing among perturbed positions.

While in control subjects the second TGA (TGA2) didnot differ among perturbed positions, in RBD patients it waslonger for leftward (−20◦: 1587 ms;−10◦: 1417 ms) than


rightward perturbations (+20◦: 1292 ms;+10◦: 1073 ms,both P < 0.02). The significant Group X Position interac-tion [F(4, 44) = 3.11; P < 0.03] revealed that the secondMGA (MGA2) increased from left- to right-sided locationsonly in control subjects (42.5, 45, 52.1, 49, 55.1 mm). Inparticular, MGA2 for−20 and−10◦ positions was smallerthan for the central 0◦ position (P < 0.0007 andP < 0.006,respectively), and for the+20◦ position (P < 0.0002 andP < 0.0003, respectively). By contrast, patients’ MGA2 in-creased only from the central to right-sided positions (43.8,42.3, 43.3, 46.6, 52.3 mm). In particular, MGA2 was com-parable among−20,−10 and 0◦ control positions (allP =0.8), while MGA2 for the+20◦ position was larger than forthe+10 and 0◦ control positions (P < 0.04 andP < 0.001,respectively).

3.1.3. DiscussionIn the fixed condition, patients were slower than con-

trols in initiating and executing reach-to-grasp movements,as well as in achieving maximum acceleration, velocityand grip-aperture. The amplitude of PA and PV were alsoreduced compared to controls. However, object positionsimilarly influenced movement kinematics in both groups.Relative to rightward movements, leftward movements (im-plying longer objects-wrist distance) were characterised bylonger MT, later TPV and TGA, lower PA and higher PV.Compared to control subjects, the general slowing of RBDpatients’ temporal parameters, and the reduction of PA andPV were present also in the perturbed condition. Only pa-tients, tough, showed longer MT, and later TPA, TPV andTGA in leftward than rightward perturbations. Comparedto control trials, their rightward perturbed movements werecharacterised by shorter TPA (+10◦), TPV and TGA (+10and+20◦), while these difference were not present in controlsubjects.

Subjects’ grip-aperture was also affected by the suddenchange of the object’s position. The first MGA was smallerin perturbed than control trials, without differing betweenleft- and right-sided perturbed locations, in agreement withthe fact that it was originally planned for grasping the cen-tral object. The second MGA was not similarly modulatedby object position between groups. Instead of starting toincrease from leftward positions as in controls, patients’MGA2 was undifferentiated among leftward locations, onlyincreasing from the central to the right-most location. Thisasymmetric pattern was clearly present in the perturbed con-dition, where the crucial Group X Position interaction wassignificant, while a similar tendency was present in the fixedcondition, where the crucial interaction only verged on sig-nificance. Thus, the direct comparison of RBD patients andaged-matched controls revealed hemispatial asymmetries inpatients’ performance, both in the temporal and spatial as-pects of perturbed movements. The lack of significant ef-fects of the lateral perturbation on the performance of thecontrol group was quite an unexpected result, which will beaddressed inSection 3.3.

3.2. A comparison between neglect and non-neglectRBD patients

This section examines whether neglect affected patients’performance. This possibility was verified by an ANOVAcomparing neglect (RBD+) and non-neglect (RBD−)patients’ kinematics. Individual analysis was also performedto control for consistency of the results, and is reportedonly when differing from the group pattern. Mean values ofthe kinematic parameters of both groups are fully detailedin Tables 2 and 3(fixed and perturbed condition).

Besides replicating the previous results for the fixed con-dition, this analysis showed that neglect did not significantlyinfluence any of the parameters considered. RBD+ patientstended to react more slowly to left- than right-sided posi-tions, but this effect was not significant (P = 0.2). TheMGA of leftward positions were comparable to that of thecentral position, which was smaller than those of rightwardpositions (bothP < 0.04). Smaller MGA was obtained for+10◦ than+20◦ position (P < 0.0003). Noteworthy, thisasymmetric pattern was not due to a floor effect, being ob-served in each patient irrespective of the individual perfor-mance on grip-aperture (seeFig. 4C).

Perturbed movements took longer than control trials (allP < 0.002), with homologous perturbed positions not diffe-ring across hemispaces. The TPA of−20◦ position (211 ms)was longer than+10◦ position (167 ms,P < 0.04), but TPAof right-sided perturbations was not shorter than control tri-als. This pattern was homogeneous among patients, exceptfor patient P5 in the RBD− group (seeTable 1), who showedthe opposite tendency. Although not significant, the individ-ual analysis showed shorter TPA for leftward (−20◦: 224 ms,−10◦: 209 ms) than control (0◦: 251 ms) and rightwardperturbed movements (+20◦: 283 ms,+10◦: 259 ms). Theamplitude of the acceleration peak was significantly affectedby Neglect [F(1, 5) = 10.9; P < 0.03], the PA being lowerin RBD+ (2939 mm/s2) than RBD− patients (4750 mm/s2).

Similarly to the first analysis, the TPV of rightward per-turbed movements (+20, +10◦) largely led that of controlmovements (0◦, bothP < 0.02) which, in contrast, did notdiffer from TPV of leftward perturbed movements. Again,this finding was consistent among all patients but P5, whoseperformance was rather symmetrical (seeFig. 5C) showinga significant shortening of TPV for both−10◦ (293 ms) and+10◦ (304 ms) perturbed positions with respect to 0◦ controlposition (385 ms, bothP < 0.004). More eccentrically per-turbed positions showed a similar tendency (−20◦: 339 ms,+20◦: 363 ms). The left-sided performance obtained by thispatient on TPA and TPV explains the apparent differencebetween RBD+ and RBD− mean values (Table 3). The in-teraction Group X Position was not significant.

In the first sub-movement, TGA was longer in RBD+ thanRBD− patients (714 ms versus 478 ms,P < 0.03). In bothgroups, the MGA occurred later for left- (−20◦: 666 ms,−10◦: 610 ms) than right-perturbed movements (+20◦:559 ms,+10◦: 521 ms, bothP < 0.02). The TGA2 was

A.

Farne

et

al./N

eu

rop

sycho

logia

41

(20

03

)7

39

–7

57

747

Table 2Kinematic parameters of reach-to-grasp movements in the fixed condition: RBD patients

RBD− (position) RBD+ (position)

−20◦ −10◦ 0◦ +10◦ +20◦ −20◦ −10◦ 0◦ +10◦ +20◦

RT (ms) 478 (41) 476 (49) 497 (122) 476 (98) 474 (75) 1008 (522) 765 (220) 698 (192) 664 (133) 724 (241)MT (ms) 980 (277) 960 (241) 916 (176) 917 (133) 976 (183) 1318 (249) 1156 (193) 1078 (190) 1031 (103) 1190 (128)

TransportTPA (ms) 227 (33) 234 (25) 185 (30) 216 (37) 217 (30) 231 (69) 197 (47) 165 (32) 157 (48) 169 (61)PA (mm/s2) 4336 (575) 4286 (178) 4280 (567) 5167 (776) 5780 (928) 3691 (1399) 3804 (919) 3822 (1286) 4361 (1283) 5102 (1688)TPV (ms) 377 (56) 379 (26) 324 (40) 309 (35) 333 (52) 422 (90) 362 (50) 337 (62) 292 (65) 318 (70)PV (mm/s) 801 (77) 736 (52) 645 (74) 625 (70) 730 (150) 658 (177) 605 (119) 546 (122) 519 (67) 572 (141)

GripTGA (ms) 674 (142) 648 (122) 558 (122) 562 (99) 566 (122) 851 (137) 691 (85) 656 (91) 606 (97) 682 (132)MGA (mm) 49.7 (7.5) 49.4 (7.2) 49.5 (8.3) 53.3 (9.0) 59.3 (11.0) 40.7 (6.0) 41.2 (6.5) 40.6 (6.2) 43.8 (6.9) 49.4 (10.8)

Mean values and standard deviations (in brackets) of movement parameters considered in the fixed condition as a function of group (RBD− and RBD+) and position of the target object (abbreviationsas in the text).

748A

.Fa

rnee

ta

l./Ne

uro

psych

olog

ia4

1(2

00

3)

73

9–

75

7

Table 3Kinematic parameters of reach-to-grasp movements in the perturbed condition: RBD patients

RBD− (position) RBD+ (position)

−20◦ −10◦ 0◦ +10◦ +20◦ −20◦ −10◦ 0◦ +10◦ +20◦

RT (ms) 528 (85) 565 (23) 580 (43) 584 (38) 628 (142) 940 (414) 1073 (506) 1213 (741) 1288 (809) 1209 (539)MT (ms) 1478 (159) 1271 (161) 831 (87) 1184 (58) 1326 (83) 2361 (930) 1994 (672) 1218 (409) 1737 (903) 2100 (1023)

TransportTPA (ms) 186 (34) 181 (34) 196 (49) 180 (70) 189 (82) 235 (60) 209 (72) 200 (40) 155 (27) 173 (49)PA (mm/s2) 4974 (477) 4747 (814) 4801 (396) 4524 (682) 4703 (1075) 2714 (757) 2606 (1356) 3068 (827) 3100 (767) 3205 (756)TPV (ms) 298 (35) 287 (15) 319 (58) 276 (24) 290 (63) 397 (64) 373 (73) 384 (65) 315 (72) 315 (27)PV (mm/s) 633 (100) 649 (128) 672 (61) 644 (89) 655 (91) 470 (139) 456 (140) 510 (128) 484 (132) 472 (140)TPV2 (ms) 889 (65) 774 (89) 319 (58) 684 (87) 743 (29) 1500 (627) 1434 (665) 384 (65) 871 (289) 1108 (473)PV2 (mm/s) 510 (13) 407 (22) 672 (61) 389 (73) 738 (84) 387 (143) 283 (92) 510 (128) 253 (54) 432 (114)

GripTGA (ms) 511 (16) 478 (31) 514 (56) 440 (45) 444 (22) 820 (209) 743 (150) 732 (103) 602 (104) 673 (111)MGA (mm) 43.0 (7.4) 43.4 (8.7) 49.2 (1.6) 41.6 (6.5) 42.1 (7.0) 33.2 (6.1) 35.4 (8.8) 39.0 (5.6) 32.5 (6.1) 31.6 (9.2)TGA2 (ms) 1178 (78) 959 (80) 514 (56) 838 (6) 973 (33) 1894 (670) 1761 (765) 732 (103) 1250 (486) 1531 (560)MGA2 (mm) 46.5 (3.7) 45.8 (4.1) 49.2 (1.6) 51.2 (5.4) 59.9 (6.7) 41.8 (6.9) 39.7 (6.1) 39.0 (5.6) 43.1 (4.1) 46.7 (4.8)

Mean values and standard deviations (in brackets) of movement parameters considered in the perturbed condition as a function of group (RBD− and RBD+) and position of the target object (abbreviationsas in the text). Note that values reported in TGA2 and MGA2 for the control position (0◦) are taken, for comparative purposes, from control movements (TGA and MGA).


Fig. 4. Mean values of maximum grip-aperture (MGA) as a function of ob-ject position and experimental condition (fixed, perturbed) in (A): healthysubjects (Elderly and Young collapsed) and (B): RBD patients (with andwithout neglect collapsed). The second MGA (MGA2) is reported for theperturbed condition. (C): The individual performance of RBD patients inthe fixed condition is reported to show that the non-linear pattern (man-ifest when comparing (B) with (A)) was not due to a floor effect. Notethat the individual thumb-index distance was subtracted from MGA.

longer for −10◦ (1360 ms) than for+10◦ (1044 ms,P <

0.04), the same tendency being present between more ec-centric positions (−20◦: 1536 ms;+20◦: 1252,P = 0.056).As in the fixed condition, the pattern of MGA2 was asym-metric. The Group X Position interaction [F(4, 20) = 4.45;P < 0.01] showed that MGA2 significantly differed fromthe central 0◦ to the right+20◦ perturbed position in bothgroups (P < 0.002) while, in RBD− patients, the MGA2in +10◦ position was also smaller than in+20◦ position

Fig. 5. Mean values of time to peak velocity in the perturbed condition asa function of object position in (A): healthy subjects (Elderly and Youngcollapsed); (B): RBD patients (with and without neglect collapsed); (C):individual performances of RBD patients. Note that one patient manifesteda quite symmetric pattern (patient P5−, thicker line), as compared to theasymmetric pattern of the group.

(P < 0.0002). Thus, the common feature to both groupswas a significant increase of the MGA2 from the central tothe rightmost position, without any difference between thecentral and the two left-sided positions.

3.2.1. DiscussionDespite the relatively small group-size (4RBD+ versus

3RBD−), the analysis revealed clear differences betweenneglect and non-neglect patients. In the perturbed condition,RBD+ patients showed lower PA and longer TGA thanRBD− patients. However, the kinematics of both groupswas similarly affected by object position. In fixed trials,

750A

.Fa

rnee

ta

l./Ne

uro

psych

olog

ia4

1(2

00

3)

73

9–

75

7

Table 4Kinematic parameters of reach-to-grasp movements in the fixed condition: healthy subjects

Elderly (position) Young (position)

−20◦ −10◦ 0◦ +10◦ +20◦ −20◦ −10◦ 0◦ +10◦ +20◦

RT (ms) 261 (48) 260 (40) 248 (40) 257 (43) 276 (44) 288 (55) 278 (60) 268 (35) 275 (56) 305 (63)MT (ms) 627 (114) 603 (110) 557 (119) 563 (112) 556 (119) 600 (102) 546 (70) 523 (77) 548 (81) 549 (75)

TransportTPA (ms) 111 (10) 114 (12) 114 (14) 111 (14) 113 (17) 108 (16) 108 (14) 100 (12) 97 (12) 101 (11)PA (mm/s2) 7950 (1004) 7411 (1366) 8208 (2255) 8640 (2381) 9533 (2137) 9715 (3372) 10,374 (3082) 10,356 (3127) 10,954 (2533) 13,105 (4004)TPV (ms) 254 (21) 247 (22) 223 (28) 208 (28) 200 (21) 243 (30) 225 (20) 206 (21) 182 (21) 184 (20)PV (mm/s) 1088 (153) 1001 (162) 948 (157) 861 (147) 923 (158) 1114 (203) 1029 (162) 971 (162) 907 (178) 1036 (262)

GripTGA (ms) 421 (69) 386 (55) 347 (60) 339 (57) 340 (54) 389 (70) 358 (61) 321 (43) 316 (56) 316 (50)MGA (mm) 49.3 (9.6) 51.2 (7.0) 54.6 (8.2) 55.5 (7.6) 61.4 (6.1) 49.6 (9.7) 50.9 (11.0) 53.6 (8.7) 55.0 (10.9) 60.3 (13.6)

Mean values and standard deviations (in brackets) of movement parameters considered in the fixed condition as a function of group (Elderly and Young) and position of the target object (abbreviationsas in the text).


leftward movements (particularly to the leftmost position)were slower, displaying longer TPA, TPV and TGA, lowerPA and higher PV than rightward movements. In perturbedtrials, both groups failed to show a shortening of the TPA,and their performance was clearly asymmetric, the longestTPA being observed in leftmost perturbed trials. Instead,rightward movements of both groups were characterisedby an important shortening of the TPV (∼50 ms), whichwas absent on leftward movements. Also asymmetric wasthe pattern of MGA that, in both groups, increased onlyfrom the central to right-sided positions in both conditions.Therefore, the presence of neglect (although severe in mostcases) did not seem responsible of patients’ asymmetricperformance. These results were consistent in all patientswith the exception of patient P5 (RBD− group), whoseperformance was comparable to that of Elderly controls(i.e. symmetrical) for the transport phase of perturbedmovements. However, the same asymmetric pattern on thegrasping component emerged also in this patient.

3.3. A comparison between Elderly and Young controls

As mentioned inSection 1, the paradigm of sudden dis-placement of target position has been usually conducted onYounger subjects than the Elderly group investigated here.Therefore, the absence of fast reactions in leftward perturbedmovements both in patients and Elderly controls could de-pend (at least partially) on the normal ageing, the lesion,or both. In the same line of reasoning, the presence of fastcorrections in rightward perturbed movements found in pa-tients, but not in Elderly controls, would be difficult to inter-pret without disambiguating the role of age on visuo-motorcontrol in normal subjects. To this aim, the performance ofhealthy controls in both conditions was submitted to simi-lar ANOVAs with Age (Young, Elderly) as between-subjectfactor. For sake of brevity, only the results relevant to elu-cidate age-related effects will be reported. Mean values ofthe kinematic parameters are fully detailed inTables 4 and 5that also allow for a comparison between Young and Elderlygroups.

In the fixed condition, the factor Age did not influence anyparameter, and the previous results were replicated (Section3.1) also confirming that MGA was clearly modulated byobject position, being smaller for both left-sided positions(−20◦: 49.5 mm;−10◦: 51 mm) with respect to the centralposition (0◦: 54.1 mm, bothP < 0.005) which, in turn, wassmaller than the rightmost position (+20◦: 60.9 mm,P <

0.0002). The Age X Position interaction [F(4, 40) = 3.71;P < 0.02] revealed that PA of perturbed movements (±20,±10◦) occurred earlier than in control movements (0◦, allP < 0.0003) in the Young group, but not in the Elderlygroup. The Age X Position interaction [F(4, 40) = 4.02;P < 0.01] showed that in perturbed movements (−20,−10and+10◦) TPV was shorter than in control movements inboth groups (allP < 0.05), the same being true for+20◦perturbation in Young, but not Elderly subjects, although

showing the same tendency (P = 0.053). Age did not influ-ence TGA2 or MGA2, the progressive increase of the latterbeing fully confirmed by the present analysis (Table 4).

3.3.1. DiscussionBesides the positional modulation of MGA (present in

both conditions and groups) Elderly subjects failed to showthe shortening of TPA in perturbed trials that was present inthe Young group. Contrary to the first analysis1, however, asignificant shortening the TPV was present in perturbed tri-als in both groups (except for the+20◦ location). By repli-cating the findings of previous studies on double-step taskson Young subjects, the analysis revealed that older peopletake into account the position-change somewhat later, at thelevel of the TPV, instead of the TPA. This helps clarifyingthe results of the direct comparison between patients andElderly controls (Section 3.1). In the case of leftward per-turbation, patients’ kinematics was genuinely comparableto that of age-matched controls when considering the TPA,since the Elderly group did not show anticipated TPA whencompared with Younger subjects. In contrast, patients’ lackof TPV anticipation seems not to be solely due to normalageing, since this shortening was found both in Elderly andYoung subjects. The possibility that patients’ performancein the left hemispace was impaired by the lesion is supportedby the results of rightward perturbed movements, wherebypatients’ shortening of TPA and TPV was more similar to theperformance of Young than that of Elderly subjects, that pa-tients somewhat outperformed (since TPA anticipation wasnot significant in Elderly).

Thus, across all the analyses performed, the main findingscharacterising RBD patients’ kinematics with respect to thatof age-matched and Younger controls is (1) the asymmet-rical modulation of the MGA (seeFig. 4A and B), clearlypresent only in the perturbed condition and (2) the absenceof TPV shortening in leftward, but not rightward perturbedmovements, compared to control movements (seeFig. 5Aand B).

4. General discussion

To evaluate the right hemisphere’s (RH) involvement inthe visuo-motor control of the ipsilateral hand we requiredRBD patients (with and without neglect), and normal sub-jects (Elderly and Young) to grasp with their dominant righthand an object, whose location either remained stationary(single-step task), or was suddenly displaced (double-steptask). The results of the latter, more demanding taskshowed that hand pre-shaping, and redirection of movement“in-flight” were selectively affected when RBD patients

1 The reason of the discrepancy between analyses might depend upon alower statistical power in the RDB vs. Elderly analysis, where mean andvariability largely differed between groups, as compared to the Young vs.Elderly analysis (seeTables 3 and 5).

752A

.Fa

rnee

ta

l./Ne

uro

psych

olog

ia4

1(2

00

3)

73

9–

75

7

Table 5Kinematic parameters of reach-to-grasp movements in the perturbed condition: healthy subjects

Elderly (position) Young (position)

−20◦ −10◦ 0◦ +10◦ +20◦ −20◦ −10◦ 0◦ +10◦ +20◦

RT (ms) 245 (49) 241 (54) 236 (50) 245 (41) 243 (65) 295 (76) 280 (85) 280 (81) 289 (73) 296 (78)MT (ms) 948 (181) 839 (143) 533 (110) 830 (118) 935 (167) 848 (103) 733 (106) 525 (97) 749 (100) 887 (121)

TransportTPA (ms) 114 (12) 117 (12) 120 (11) 118 (13) 119 (14) 92 (10) 97 (11) 107 (11) 94 (9) 97 (10)PA (mm/s2) 9011 (2348) 9294 (3051) 8870 (2499) 8886 (2486) 9101 (2806) 9817 (2690) 9643 (2345) 9713 (2366) 9976 (2747) 9666 (2379)TPV (ms) 213 (27) 217 (34) 225 (32) 217 (25) 216 (31) 198 (20) 201 (15) 218 (18) 195 (17) 208 (14)PV (mm/s) 995 (167) 1007 (185) 995 (177) 985 (180) 1003 (185) 954 (189) 930 (157) 945 (159) 960 (194) 947 (178)TPV2 (ms) 595 (84) 517 (69) 225 (32) 499 (58) 556 (68) 556 (35) 505 (44) 218 (18) 467 (39) 540 (51)PV2 (mm/s) 658 (116) 467 (119) 995 (177) 451 (132) 742 (135) 629 (139) 445 (103) 945 (159) 421 (189) 757 (183)

GripTGA (ms) 349 (66) 341 (58) 338 (69) 325 (45) 336 (62) 296 (27) 301 (46) 330 (52) 289 (27) 304 (35)MGA (mm) 52.1 (9.8) 51.5 (10.6) 52.1 (8.6) 49.9 (11.2) 50.7 (12.0) 53.7 (18.5) 53.4 (19.0) 54.3 (13.4) 52.4 (19.1) 53.6 (17.5)TGA2 (ms) 754 (144) 623 (104) 338 (69) 674 (91) 756 (116) 667 (117) 571 (118) 330 (52) 581 (93) 704 (111)MGA2 (mm) 42.5 (9.7) 45.0 (8.4) 52.1 (8.6) 49.0 (9.4) 55.1 (10.9) 48.5 (14.6) 51.1 (22.2) 54.3 (13.4) 55.9 (17.8) 62.4 (19.9)

Mean values and standard deviations (in brackets) of movement parameters considered in the perturbed condition as a function of group (Elderly and Young) and position of the target object (abbreviationsas in the text). Note that values reported in TGA2 and MGA2 for the control position (0◦) are taken, for comparative purposes, from control movements (TGA and MGA).


grasped objects in the left contralesional hemispace, irre-spective of the presence of visual neglect. These findingsstrongly suggest that relevant information for controlling theright hand into the contralateral hemispace is partly providedby the ipsilateral hemisphere. They also suggest that ipsile-sional disturbances in acting in the contralesional space, inthe case of right brain damage, are independent of visual ne-glect. These results and their implications will be discussedin the following paragraphs.

4.1. Healthy subjects

Normal subjects’ performance confirmed recent findingsof an influence of object position on finger grip formation[18,75]. Paulignan et al.[75] found an almost linear increaseof MGA as subjects grasped equally-sized cylinders fromleft (−10◦) to right locations (+40◦). Here, we showed thispositional tuning of grip formation to be manifest also whenobjects are symmetrically distributed across hemispaces (40◦from left- to right-most position), thus strengthening theidea that prehension is organised in a non-homogeneousworkspace[18,64,75].

Most interestingly, the present study revealed thatgrip-aperture is very effectively and dynamically tuned,the left to right MGA increase being present independentof the occurrence of an unpredictable change of objectposition. The second MGA is usually comparable to thatobtained in control movements[13,14,74]. Here, we foundthat the positional modulation of grip-size is tightly linkedto the perturbed location; the second MGA was re-scaledto reproduce the same pattern of left to right increase ofgrip-aperture obtained when subjects grasped stationaryobjects (single-step task). Since in the present and previousstudies[74,75], the object-wrist distance decreased fromleft to right, further studies are needed to clarify whether thepositional modulation of grip-size, and its dynamic tuning,depends upon movement direction or amplitude.

Changing object position clearly affected the trans-port component. In agreement with previous findings[9,14,32,74], we confirm and extend the notion that changesin movement execution are achieved very early, about100 ms after movement had started. The first detectable re-action to perturbation was the peak of acceleration, whichoccurred earlier in perturbed than control movements. Ourresults also showed that early changes are insensitive tothe distance and side where the new target object appeared.The comparable fast reactions observed for 10 and 20◦ po-sitions in both hemispaces support the notion that, due toan error-signal about target location, the planned movementis interrupted very rapidly, to allow movement redirection[27,53].

This pattern of movement reorganisation, however, is notcompletely invariant with respect to subjects’ age. Indeed,the only relevant difference between Elderly and Younggroups was that in the Elderly group the first reaction toperturbation was manifest in the TVP instead of the TPA

(i.e. about 100 ms later), in agreement with the fact thatvisuo-motor ability is both qualitatively and quantitativelywell preserved in normal ageing[4–6,11].

4.2. RBD patients

The performance of RBD patients, besides showing ratherobvious and expected findings due to the brain lesion suchas reduced velocity and prolonged movement time, alsoshowed a strikingly asymmetric pattern of results. First, thepositional tuning of grip-size in the double-step task wasabsent from left-sided to the central location. At variancewith controls, the grip-size performed by RBD patients tograsp both leftward perturbed objects was absolutely com-parable to that used to grasp the central object, a similartendency being present in the single-step task (seeFig. 4).Second, patients showed signs of early corrective changes(on TPV) when reaching objects perturbed in the ipsilesionalhemispace, similarly to healthy subjects. In contrast, fastcorrections were completely absent when reaching objectsperturbed in the contralesional hemispace, again showing aremarkably asymmetric pattern (seeFig. 5).

However, the general kinematic pattern was not disruptedby the brain lesion. In the single-step task for example,RBD patients showed later TPV and MGA, and longer MTwhen grasping objects located in the left as opposed to theright hemispace. These differences, though, are not due tolateralised brain damage, since they were also shown bynormal subjects. Despite the relatively preserved move-ment kinematics, RBD patients performance revealed moresubtle disturbances in leftward aimed movements. Sincepatients’ lesion was restricted to the RH and they used theiripsilesional limb, the sensory-motor functions of the lefthemisphere, contralateral to that limb, were quite intact.Therefore, the specific alteration of kinematic parameterscan be conceived as reflecting the lack, or the distortedcontribution of the RH to ipsilateral visuo-motor control.The deficits documented in the present study are specificin two respects. First, they selectively concern high-orderaspects of visually-guided motor control (namely, in-flightpositional re-scaling of grip-size and in-flight movementredirection). Second, they are selectively manifest when theipsilesional hand acts into the contralesional hemispace.

4.3. Right-hand deficits in grasping following ipsilateralbrain lesion

One may ask whether patients’ asymmetry on grip-sizeincrease in the perturbed condition actually represents a“deficit”. In fact, patients were not functionally defective;they correctly grasped and lift the leftward perturbed targetobjects, despite this aspect of the grasping phase was notnormal. In principle, the phenomenon of positional tuning ofgrip-size could depend upon (a) bio-mechanical constraints,(b) the different distance of objects from the wrist, or (c)the central influence of object’s position on grip formation.


By showing symmetric positional grip-size modulation innormal, but not in RBD patients perturbed movements, thepresent study reveals that this phenomenon is far from beinga mere bio-mechanical by-product of kinematics. Similarly,the general slowing in movement execution exhibited by pa-tients cannot account for this asymmetry since the lack ofgrip-size modulation was selective for the left hemispace.In addition, the slowing of leftward compared to rightwardmovements would have actually favoured a progressive re-duction in the MGA for left-sided objects[92,93]. There-fore, the grasping “deficit” manifested by RDB patients canbe best conceived as the product of an absent, or distortedcontribution of the damaged ipsilateral hemisphere to theprocessing of grasp-related visuo-motor information.

4.4. Right-hand deficits in reaching redirection followingipsilateral brain lesion

The ability to redirect in-flight the ipsilesional hand to-wards the contralesional hemispace was also impaired inRBD patients. In contrast, redirection of reaching towardsthe ipsilesional hemispace was comparatively well pre-served. This finding considerably extends our knowledgeabout the effects of a RH lesion on the reprogramming ofon-going movements with the ipsilesional hand. To the bestof our knowledge, very few studies are reported in the liter-ature that adopted a paradigm of positional perturbation inRBD patients. By asking RBD patients to update the direc-tion of alternating reciprocal movements, Mattingley et al.[68] found that patients were impaired in reprogrammingmovement direction towards unexpected contralesional tar-gets (see also[19]). In agreement with this finding, our re-sults also show that RBD patient’s deficit in reprogrammingcontralesional movements affects more complex, prehensilemovements.

4.5. Ipsilateral visuo-motor control of the right hand

Besides a general impoverishment in movement perfor-mance, already reported in previous studies[49–67], nogross impairment was found as a consequence of the RHlesion in simple single-step movements. Instead, the lesionaffected fine-grained aspects of more complex double-stepmovements in the contralesional hemispace, namely, theon-line correction of the ispsilesional hand’s trajectory, andthe on-line positional re-scaling of the fingers’ grip-aperture.These more subtle impairments seem not to reflect adeficit in RH mechanisms involved in visual localisationof leftward targets. Indeed, RBD patients never misreachedleft-sided objects whose detection, as measured by RTs,was not slowed as compared to right-sided objects, rulingout possible explanations on the present findings in termsof “prior-entry” [86] for right-sided objects. In addition,a decreased awareness of left-sided stimuli should havemostly affected the performances of neglect patients, butthe sudden leftward perturbation similarly influenced the

kinematics of both RBD groups. Finally, it is worth re-membering that on-line movement redirection may occurautomatically, taking place without the subject being per-ceptually aware of the target displacement[35,76,78,80],the awareness of the perturbation largely lagging behind themotor correction[13,14].

Since RBD patients’ asymmetric performance cannot bereadily explained by deficits in the selection of contralesionalvisual inputs, nor by a general disturbance in motor outputselection (see[69]), we suggest that our findings are morelikely to reflect the result of the lesion upon the processes ofvisuo-motor transformations of the ipsilateral hemisphere.In this respect, Desmurget et al.[24] showed that subjects’ability to perform on-line corrections with their right handin the right hemispace was disrupted by TMS applied overthe left parietal cortex during perturbation of target position,thus suggesting that the left hemisphere controls the updat-ing of right-hand trajectories in the right hemispace[25].Similar on-line corrections were not disrupted by this tempo-rary ‘lesion’ when subjects acted with their left ‘ipsilesional’hand. Taken together, Desmurget et al’s findings and thepresent results suggest the intriguing possibility that the lefthemisphere might be crucial for the contralateral hand act-ing in the contralateral hemispace, whereas the RH mightbe relevant for the ipsilateral hand acting in the contralat-eral hemispace, although this hypothesis need to be verifiedin future studies. In agreement with functional imaging andTMS studies showing bilateral hemispheric involvement inthe control of distal finger movements[15,20,56,95], thepresent study showed that both transport and grasping phasesof perturbed movements were affected, although distal fin-ger joints have stronger contralateral innervation[8,17]. Incontrast, non-visually controlled movement redirection canrely on “pure” contralateral inputs[25].

A final result deserving discussion is the low impactof neglect on RBD patients kinematics. On the basis ofprevious studies (seeSection 1), we expected that neglectcould, at least, worsen patients’ performance. This appar-ently obvious prediction was partially confirmed by ourresults. However, on the basis of the well established no-tion of dissociable mechanisms subserving perception andaction [71], it can be suggested that visuospatial neglectwould not negatively influence the ipsilesional visuo-motorcontrol of RBD patients, especially when the task requiresrapid input/output sensorimotor transformations. Actually,the visuo-motor performance of neglect patients has beenshown to compensate[90], or outperform their perceptualabilities [28,84,85]. In keeping with the idea that dorsalvisuo-motor systems are less affected by neglect than ven-tral representational systems (see[55]), Pritchard et al.[81] reported a neglect patient affected in a perceptual, butnot in a visuo-motor task. In particular, while the patientvisually under-estimated the size of an object located inthe left compared to the right hemispace, she was ableto accurately grasp the same object in both hemispaces.Therefore, the comparable performance we found in RBD


patients with and without neglect may be only apparentlycounterintuitive.

In conclusion, the right hemisphere seems to be involvedto some degree in visually guiding the right hand into the lefthemispace. This involvement is manifest after a lesion whenvisuo-motor transformations become rather demanding, andprobably reflects the reduced or distorted inter-hemisphericinterplay[65] of the dorsal streams for in-flight modulationof positional grip-size and trajectory amendment. After righthemisphere damage, movement kinematics appear to be al-tered independent of visual neglect, and future studies willhopefully clarify whether similar deficits can be revealedfollowing left hemisphere damage.

Acknowledgements

We wish to thank all the subjects for their collaboration.We also thank Marc Thevenet for the development of the OP-TODISP software, Francesca Frassinetti for her assistancein the reconstruction of lesion. Patrick Monjaud and Chris-tian Urquizar are acknowledged for their help in construct-ing the experimental set-up and software assistance. Thiswork was supported by I.N.S.E.R.M. and Université ClaudeBernard. A.F. was supported by a European NeuroscienceProgramme fellowship, under the umbrella of the EuropeanScience Foundation.

References

[1] Albert ML. A simple test for visual neglect. Neurology 1973;23:658–64.

[2] Balint R. Die Seelenhahmung des “Schauens”. MonatsschriftPsychologische Neurologie 1909;25:57–71.

[3] Baskett JJ, Marshall HJ, Broad JB, Owen PH, Green G. The goodside after stroke: ipsilateral sensory motor function needs carefulassessment. Age and Ageing 1996;25:239–44.

[4] Bennett KM, Castiello U. Reach to grasp: changes with age. Journalof Gerontology 1994;49:1–7.

[5] Bennett KM, Castiello U. Reorganization of prehension componentsfollowing perturbation of object size. Psychology of Aging1995;10:204–14.

[6] Birren JE, Fisher LM. Aging and speed of behavior: possibleconsequences for psychological functioning. Annual Review ofPsychology 1995;46:329–53.

[7] Brain WR. Visual disorientation with special reference to lesions ofthe right hemisphere. Brain 1941;64:244–72.

[8] Brinkman J, Kuypers HG. Cerebral control of contralateral andipsilateral arm, hand and finger movements in the split-brain rhesusmonkey. Brain 1973;96:653–74.

[9] Carnahan H. Manual asymmetries in response to rapid targetmovement. Brain and Cognition 1998;37:237–53.

[10] Carnahan H, Goodale MA, Marteniuk RG. Grasping versus pointingand the differential use of visual feedback. Human Movement Science1993;12:219–34.

[11] Carnahan H, Vandervoort AA, Swanson LR. The influence of agingand target motion on the control of prehension. Experimental AgingResearch 1998;24:289–306.

[12] Carson RG. Putative right hemisphere contributions to the preparationof reaching and aiming movements. In: Elliott D, Roy EA, editors.

Manual asymmetries in motor performance. Boca Raton: CRC Press;1996. p. 159–72.

[13] Castiello U, Jeannerod M. Measuring time to awareness. NeuroReport1991;2:797–800.

[14] Castiello U, Paulignan Y, Jeannerod M. Temporal dissociation ofmotor responses and subjective awareness. A study in normalsubjects. Brain 1991;114:2639–55.

[15] Chen R, Gerloff C, Hallett M, Cohen LG. Involvement of theipsilateral motor cortex in finger movements of different complexities.Annals of Neurology 1997;41:247–54.

[16] Chieffi S, Gentilucci M, Allport A, Sasso E, Rizzolatti G. Study ofselective reaching and grasping in a patient with unilateral parietallesion. Dissociated effects of residual spatial neglect. Brain 1993;116:1119–37.

[17] Colebatch JG, Gandevia SC. The distribution of muscularweakness in upper motor neuron lesions affecting the arm. Brain1989;112:749–63.

[18] Connolly JD, Goodale MA. The role of visual feedback of handposition in the control of manual prehension. Experimental BrainResearch 1999;125:281–6.

[19] Corben LA, Mattingley JB, Bradshaw JL. A kinematic analysis ofdistractor interference effects during visually guided action in spatialneglect. Journal of the International Neuropsychological Society2001;7:334–43.

[20] Cramer SC, Finklestein SP, Schaechter JD, Bush G, Rosen BR.Activation of distinct motor cortex regions during ipsilateral andcontralateral finger movements. Journal of Neurophysiology 1999;81:383–7.

[21] Damasio H, Damasio AR. Lesion analysis in neuropsychology.Oxford: Oxford University Press; 1989.

[22] De Renzi E. Apraxia. In: Boller F, Grafman J, editors. Handbook ofclinical neuropsychology. Amsterdam: Elsevier; 1990. p. 245–63.

[23] De Renzi E, Motti F, Nichelli P. Imitating gestures: a quantativeapproach to ideomotor apraxia. Archives of Neurology 1980;37:6–10.

[24] Desmurget M, Epstein CM, Turner RS, Prablanc C, Alexander GE,Grafton ST. Role of the posterior parietal cortex in updating reachingmovements to a visual target. Nature Neuroscience 1999;2:563–7.

[25] Desmurget M, Gréa H, Grethe JS, Prablanc C, Alexander GE, GraftonST. Functional anatomy of nonvisual feedback loops during reaching:a positron emission tomography study. Journal of Neuroscience2001;21:2919–28.

[26] Diller L, Weinberg J. Hemi-inattention in rehabilitation: Theevolution of a rational remediation program. Advances in Neurology1977;18:63–82.

[27] Elliott D, Binstead G, Heath M. The control of goal-directedmovements: Correcting errors in the trajectory. Human MovementScience 1999;18:121–36.

[28] Edwards MG, Humphreys GW. Pointing and grasping in unilateralvisual neglect: effect of on-line visual feedback in grasping.Neuropsychologia 1999;37:959–73.

[29] Fisk JD, Goodale MA. The effects of unilateral brain damage onvisually guided reaching: hemispheric differences in the nature ofthe deficit. Experimental Brain Research 1988;72:425–35.

[30] Gainotti G, Messerli P, Tissot R. Qualitative analysis of unilateralspatial neglect in relation to laterality of cerebral lesions. Journal ofNeurology Neurosurgery and Psychiatry 1972;35:545–50.

[31] Gauthier L, Dehaut F, Joanette Y. The bells test: a quantative andqualitative test for visual neglect. International Journal of ClinicalNeuropsychology 1989;11:49–54.

[32] Gentilucci M, Chieffi S, Scarpa M, Castiello U. Temporalcoupling between transport and grasp components during prehensionmovements: Effects of visual perturbation. Behavioral Brain Research1992;47:71–82.

[33] Goodale MA. Brain asymmetries in the control of reaching. In:Goodale MA, editor. Vision and action: the control of grasping.The Canadian Institute for Advanced Research series in artificialintelligence and robotics. Norwood (NJ): Ablex Publishing Corp.;1990. p. 14–32.


[34] Goodale MA, Milner AD, Jakobson LS, Carey DP. Kinematicanalysis of limb movements in neuropsychological research: subtledeficits and recovery of functions. Canadian Journal of Psychology1990;44:180–95.

[35] Goodale MA, Pelisson D, Prablanc C. Large adjustments in visuallyguided reaching do not depend on vision of the hand or perceptionof target displacement. Nature 1986;320:748–50.

[36] Haaland KY, Harrington D. The role of the hemispheres in closedloop movements. Brain and Cognition 1989;9:158–80.

[37] Haaland KY, Harrington DL. Limb-sequencing deficits after left butnot right hemisphere damage. Brain and Cognition 1994;24:104–22.

[38] Haaland KY, Harrington DL, Yeo R. The effects of task complexity onmotor performance in left and right CVA patients. Neuropsychologia1987;25:783–94.

[39] Haaland KY, Yeo RA. Neuropsychological and neuroanatomicaspects of complex motor control. In: Bigler ED, Yeo RA, TurkheimerR, editors. Neuropsychological function and brain imaging. Criticalissues in neuropsychology. New York (NY): Plenum Press; 1989.p. 219–44.

[40] Haggard P. Perturbation studies of coordinated prehension. In:Bennett KMB, Castiello U, editors. Insights into the reach tograsp movement. Advances in psychology, vol. 105. Amsterdam(Netherlands): North-Holland/Elsevier; 1994. p. 151–70.

[41] Haggard P, Wing AM. Coordinated responses following mechanicalperturbation of the arm during prehension. Experimental BrainResearch 1995;102:483–94.

[42] Halligan PW, Marshall JC. How long is a piece of string? A studyof line bisection in a case of visual neglect. Cortex 1988;24:321–8.

[43] Harrington DL, Haaland KY. Hemispheric specialization for motorsequencing: Abnormalities in levels of programming. Neuro-psychologia 1991;29:147–63.

[44] Harvey M, Milner AD, Roberts RC. Spatial bias in visually-guidedreaching and bisection following right cerebral stroke. Cortex1994;30:343–50.

[45] Hecaen H, de Ajuriaguerra J. Balint’s syndrome (psychic paralysisof visual fixation) and its minor forms. Brain 1954;77:373–400.

[46] Heilman KM, Bowers D, Coslett HB, Whelan H, Watson RT.Directional hypokinesia: Prolonged reaction times for leftwardmovements in patients with right hemisphere lesions and neglect.Neurology 1985;35:855–9.

[47] Hermsdörfer J, Mai N, Spatt J, Marquardt C, Veltkamp R, GoldenbergG. Kinematic analysis of movement imitation in apraxia. Brain1996;119:1575–86.

[48] Hermsdörfer J, Laimgruber K, Kerkhoff G, Mai N, Goldenberg G.Effects of unilateral brain damage on grip selection, coordination, andkinematics of ipsilesional prehension. Experimental Brain Research1999;128:41–51.

[49] Hermsdörfer J, Ulrich S, Marquardt C, Goldenberg G, Mai N.Prehension with the ipsilesional hand after unilateral brain damage.Cortex 1999;35:139–61.

[50] Hodges NJ, Lyons J, Cockell D, Reed A, Elliott D. Hand, spaceand attentional asymmetries in goal-directed manual aiming. Cortex1997;33:251–69.

[51] Holmes G. Disturbances of visual orientation. British Journal ofOphthalmology 1918;2:449–68.

[52] Jackson SR, Newport R, Husain M, Harvey M, Hindle JV.Reaching movements may reveal the distorted topography of spatialrepresentations after neglect. Nuropsychologia 2000;38:500–7.

[53] Jeannerod M. Visuomotor channels: their integration in goal-directedprehension. Human Movement Science 1999;18:201–18.

[54] Karnath H-O, Dick H, Konczak J. Kinematics of goal-directed armmovements in neglect: Control of hand in space. Neuropsychologia1997;35:435–44.

[55] Karnath H-O, Ferber S, Himmelbach M. Spatial awareness is afunction of the temporal not the posterior parietal lobe. Nature2001;411:950–3.

[56] Kim SG, Ashie J, Hendrich K, Ellerman JM, Merkle H, UgurbilK, et al. Functional magnetic resonance imaging of motor cortex:hemispheric asymmetry and handedness. Science 1993;261:615–7.

[57] Kimura D. Left-hemisphere control of oral and brachial movementsand their relation to communication. Philosophical Transactions ofthe Royal Society of London 1982;B298:135–49.

[58] Kolb B, Milner B. Performance of complex arm and facial movementsafter focal brain lesions. Neuropsychologia 1981;19:491–503.

[59] Konczak J, Himmelbach M, Perenin MT, Karnath HO. Do patientswith neglect show abnormal hand velocity profiles during tactileexploration of peripersonal space? Experimental Brain Research1999;128:219–23.

[60] Konczak J, Karnath HO. Kinematics of goal-directed arm movementsin neglect: Control of hand velocity. Brain and Cognition1998;37:387–403.

[61] Leiguarda RC, Marsden CD. Limb apraxias. Higher-order disordersof sensorimotor integration. Brain 2000;123:860–79.

[62] Liepmann H. Drei Aufsatze aus dem Apraxiegebiet. Berlin: Karger;1908.

[63] Liepmann H. Motor aphasia, anartria and apraxia. In: Proceedings ofthe 17th International Congress of Medicine, Part 2, London, 1913.p. 97–106 [transl.].

[64] Marteniuk RG, MacKenzie CL. Invariance and variability in humanprehension: implications for theory development. In: Goodale MA,editor. Vision and action: the control of grasping. The CanadianInstitute for Advanced Research series in artificial intelligence androbotics. Norwood (NJ): Ablex Publishing Corp.; 1990. p. 49–64.

[65] Marzi CA, Fanini A, Girelli M, Ipata AE, Miniussi C, Prior M,et al. Is extionction following parietal damage an interhemisphericdisconnection phenomenon? In: Thier P, Karnath HO, editors. Parietallobe contributions to orientation in 3D space. Berlin: Springer; 1997.p. 431–46.

[66] Mattingley JB, Bradshaw JL, Phillips JG. Impairments of movementinitiation and execution in unilateral neglect. Directional hypokinesiaand bradykinesia. Brain 1992;115:1849–74.

[67] Mattingley JB, Bradshaw JL, Bradshaw JA, Nettleton NC. Recoveryfrom directional hypokinesia and bradykinesia in unilateral neglect.Journal of Clinical and Experimental Neuropsychology 1994;16:861–76.

[68] Mattingley JB, Corben LA, Bradshaw JL, Bradshaw JA, Phillips JG,Horne MK. The effects of competition and motor reprogrammingon visuomotor selection in unilateral neglect. Experimental BrainResearch 1998;120:243–56.

[69] Mattingley JB, Driver J. Distinguishing sensory and motor deficitsafter parietal damage: an evaluation of response selection biases inunilateral neglect. In: Thier P, Karnath HO, editors. Parietal lobecontributions to orientation in 3D space. Berlin: Springer; 1997.p. 309–38.

[70] Mattingley JB, Husain M, Rorden C, Kennard C, Driver J. Motorrole of human inferior parietal lobe revealed in unilateral neglectpatients. Nature 1998;392:179–82.

[71] Milner AD, Goodale MA. The visual brain in action. Oxford (UK):Oxford University Press; 1995.

[72] Nico D. Detecting directional hypokinesia: the epidiascope technique.Neuropsychologia 1996;34:471–4.

[73] Oldfield RC. The assessment and analysis of handedness: TheEdinburgh inventory. Neuropsychologia 1971;9:97–113.

[74] Paulignan Y, MacKenzie CL, Marteniuk RG, Jeannerod M. Selectiveperturbation of visual input during prehension movements. 1. Theeffects of changing object position. Experimental Brain Research1991;83:502–12.

[75] Paulignan Y, Frak VG, Toni I, Jeannerod M. Influence of objectposition and size on human prehension movements. ExperimentalBrain Research 1997;114:226–34.

[76] Pelisson D, Prablanc C, Goodale MA, Jeannerod M. Visual controlof reaching movements without vision of the limb. II. Evidenceof fast unconscious processes correcting the trajectory of the hand


to the final position of a double-step stimulus. Experimental BrainResearch 1986;62:303–11.

[77] Perenin MT. Optica ataxia and unilateral neglect: clinical evidencefor dissociable visual functions in posterior parietal cortex. In: ThierP, Karnath HO, editors. Parietal lobe contributions to orientation in3D space. Berlin: Springer; 1997. p. 289–308.

[78] Pisella L, Grea H, Tilikete C, Vighetto A, Desmurget M, Rode G,et al. An ‘automatic pilot’ for the hand in human posterior parietalcortex: Toward reinterpreting optic ataxia. Nature Neuroscience2000;3:729–36.

[79] Pohl PS, Winstein CJ, Onla-or S. Corrigendum: Sensory-motorcontrol in the ipsilesional upper extremity after stroke. Neurore-habilitation 1997;9:57–69.

[80] Prablanc C, Martin O. Automatic control during hand reachingat undetected two-dimensional target displacements. Journal ofNeurophysiology 1992;67:455–69.

[81] Pritchard CL, Milner AD, Dijkerman HC, MacWalter RS.Visuospatial neglect: veridical coding of size for grasping but notfor perception. Neurocase 1997;3:437–43.

[82] Riddoch G. Visual disorientation in homonymous half-fields. Brain1935;58:376–82.

[83] Robertson IH, Marshall JC, editors. Unilateral neglect: clinical andexperimental studies. Hove (UK): Lawrence Erlbaum Associates Inc.;1993.

[84] Robertson IH, Nico D, Hood BM. The intention to act improvesunilateral left neglect: two demonstrations. NeuroReport 1995;7:246–8.

[85] Robertson IH, Nico D, Hood BM. Believing what you feel:using proprioceptive feedback to reduce unilateral neglect. Neuro-psychology 1997;11:53–8.

[86] Rorden C, Mattingley JB, Karnath H-O, Driver J. Visual extinctionand prior entry: Impaired perception of temporal order with intactmotion perception after unilateral parietal damage. Neuropsychologia1997;35:421–33.

[87] Rothi LJG, Heilman KM, editors. Apraxia: the neuropsychologyof action. Hove (UK): Psychology Press/Erlbaum (UK) Taylor &Francis; 1997.

[88] Rushworth MFS, Nixon PD, Renowden S, Wade DT, PassinghamRE. The left parietal cortex and motor attention. Neuropsychologia1997;35:1261–73.

[89] Schluter ND, Krams M, Rushworth MFS, Passingham RE. Cerebraldominance for action in the human brain: the selection of actions.Neuropsychologia 2001;39:105–13.

[90] Shaw A, Jackson SR, Harvey M, Newport R, Kramer T, Dow L.Grip force scaling after hemispatial neglect. NeuroReport 1997;8:3837–40.

[91] Thier P, Karnath HO, editors. Parietal lobe contributions to orientationin 3D space. Berlin: Springer; 1997.

[92] Wallace SA, Weeks DL. Temporal constraints in the controlof prehensive movements. Journal of Motor Behavior 1988;20:81–105.

[93] Wing AM, Turton A, Fraser C. Grasp size and accuracy of approachin reaching. Journal of Motor Behavior 1986;18:245–60.

[94] Winstein CJ, Phol PS. Effects of unilateral brain damage onthe control of goal-directed hand movements. Experimental BrainResearch 1995;105:163–74.

[95] Ziemann U, Ishii K, Borgheresi A, Yaseen Z, Battaglia F, HallettM, et al. Dissociation of the pathways mediating ipsilateral andcontralateral motor evoked potentials in human hand and armmuscles. Journal of Physiology 1999;518:895–906.

Documents

Visuo-motor control of the ipsilateral hand: evidence from right brain-damaged patients