Brain (1992), 115, 1849-1874

IMPAIRMENTS OF MOVEMENT INITIATION AND EXECUTION IN UNILATERAL NEGLECT DIRECTIONAL HYPOKINESIA AND BRADYKINESIA by JASON B. MATTINGLEY, JOHN L. BRADSHAW and JAMES G. PHILLIPS

SUMMARY Patients with unilateral neglect may exhibit slowness in the initiation of contralesionally directed movements in peripersonal space (directional hypokinesia). The present study used a sequential movement task to characterize any such impairment in a group of 24 patients with right hemisphere lesions, 18 of whom had left neglect. A further five patients with left hemisphere lesions, one of whom had right neglect, were also tested. We measured movement initiation and execution times for leftward and rightward movements in either hemispace and across the body midline. Most left neglect patients, particularly those with lesions involving posterior cortex, showed directional hypokinesia. Left neglect patients with anterior and/or subcortical lesions also showed directional bradykinesia, i.e. a slowing in the execution phase of contralesionally directed movements. This impairment occurred regardless of the spatial location of the apparatus and was exacerbated as patients moved closer to their neglected side. The patient with right neglect showed directional hypokinesia but not directional bradykinesia. Right hemisphere and left hemisphere lesion patients without neglect performed in a manner comparable to controls, who did not exhibit directional hypokinesia or directional bradykinesia. These results suggest that directional hypokinesia is associated with both left hemisphere and right hemisphere damage, but only in the context of unilateral neglect. Moreover, the site of hemispheric lesion may determine the temporal characteristics of movement impairments in neglect. Damage to posterior cortex produces deficits in detecting contralesional targets and initiating movements toward them, while damage to anterior or subcortical structures may disrupt the internal representation of an intended trajectory.

INTRODUCTION

Unilateral neglect provides a unique opportunity to study the mechanisms underlying space related behaviour. Although the impairments exhibited by patients with neglect have been described in terms of a failure to direct attention into or toward the contralateral hemispace (Mesulam, 1981; Heilman et al., 1987; Posner et al., 1987), the disorder is not restricted to stimuli occurring in the external sensory environment. The disorder also appears to disrupt the internal representation of space in the visual (Bisiach and Luzzatti, 1978; Bisiach et al., 1981; Ogden, 1985a) and auditory (Altman et al. ,1979; Bisiach et al., 1984) modalities. Thus, most current theories of unilateral neglect postulate either a disruption to systems responsible for mediating directed attention, or a defect in the neural apparatus responsible for generating representations of real (or imagined) space. The purpose of this study is to demonstrate the existence of an intentional defect Correspondence to: Jason B. Mattingley, Department of Psychology, Monash University, Clayton, Victoria 3168, Australia. © Oxford University Press 1992

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(From the Department of Psychology, Monash University, Clayton, Victoria, Australia)

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in unilateral neglect, i.e. an impairment in the initiation and execution of goal-directed actions. Since most current theories emphasize the importance of purely sensory or 'input' factors in neglect, they do not adequately account for impairments of goal-directed action which may accompany, or be responsible for, neglect behaviour. For example, the phenomenon of non-sensory or motor neglect has been reported in both animals (Watson et al., 1978; Valenstein et al., 1982) and humans (Laplane and Degos, 1983; Ogden, 1988). It involves a disturbance of spontaneous movement of the contralesional limbs in the absence of hemiplegia. This should be distinguished for direction-specific impairments in the spatial extent of voluntary movements and direction specific slowness in initiating movements toward the contralateral side of space. Unlike motor neglect, these impairments are manifest in movements carried out both by the contralesional and by the ipsilesional limbs, and are not necessarily restricted to movements performed in the contralateral hemispace. Despite the emergence of relevant empirical data, the taxonomy used to classify direction-specific motor or intentional impairments in neglect has not been formally specified. Thus, the term 'directional hypokinesia' has hitherto been used to refer to a slowness in the initiation of contralesional movements (Heilman et al., 1985; Meador et al., 1986), reduced spatial exploration toward the contralesional side (Mijovic, 1991; Tegner and Levander, 1991) and insufficient amplitude of contralesional limb movements (Bisiach et al., 1990). In contrast to this apparent over-inclusiveness, the terms 'directional motor neglect' (Butter et al., 1988), 'hemispatial motor neglect' (Meador et al., 1986) and 'hemispatial limb hypometria' (Meador et al., 1988) have been used to denote specific impairments of movement, each of which might be more readily subsumed under a different heading. Before examining the evidence relevant to the present study, therefore, it may be instructive to consider a more systematic means by which to classify motor and intentional impairments in neglect. Our approach is to draw a distinction between spatial and temporal aspects of performance. Thus, most previous studies have been concerned with directionspecific impairments in the spatial extent of movement, whereas those conducted by Heilman et al. (1985) and Meador et al. (1986) have employed temporal measures as an index of impaired performance. This distinction is rarely drawn, even though the neural operations involved in the timing of movement initiation and execution (kinematics) may be distinct from those involved in scaling amplitude (Kerr, 1992). In the present study, we employed only temporal performance indices. Consequently, the terminology we have adopted here is based upon an established nomenclature in the neurological literature, specifically that relating to the temporal aspects of performance in movement disorders such as Parkinson's disease (e.g. Hallett and Khoshbin, 1980; Hallett, 1990; Phillips and Stelmach, 1992). Thus, we use (directional) hypokinesia to denote slowing in the initiation of movement and (directional) bradykinesia to refer to slowing in the execution of movement (i.e. after response initiation). In accordance with this more restrictive taxonomy, neglect studies in which the spatial extent of movement was measured (e.g. Bisiach et al., 1990) will be considered separately, under the heading directional hypometria (i.e. insufficient amplitude or spatial extent of movement toward the contralesional side). Of course, while there is nothing in these terms that explicitly acknowledges the spatial/temporal distinction, these more specific

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descriptors may facilitate further refinements in our understanding of direction-specific movement deficits in neglect.

Directional hypokinesia The only evidence of directional hypokinesia comes from a study conducted by Heilman et al. (1985), in which patients with left or right hemisphere lesions were required to use their ipsilesional hand to move a handle along a fixed linear pathway in the horizontal plane. Patients with right hemisphere lesions were significantly slower to initiate leftward compared with rightward movements (as measured by the patients' reaction time) even when the movements were carried out entirely within the right hemispace. Once the movement had been initiated, however, there was no difference in the time required to execute leftward and rightward movements, as measured by patients' movement times; thus, there was no evidence of directional bradykinesia. On the basis of their findings, Heilman et al. (1985) suggested that each hemisphere is responsible for activating the motor apparatus necessary for making a movement toward the contralateral hemispace, but that the right hemisphere also controls movements toward the ipsilateral hemispace. This notion accords well with models of spatial cognition which assume that the 'dominance' of the right hemisphere is attributable, at least in part, to its ability to attend and intend toward both sides of space (Mesulam, 1981, 1985; Heilman et ai, 1987; Weintraub and Mesulam, 1987). Despite the paucity of evidence in favour of the concept of directional hypokinesia in patients with unilateral neglect, it is nevertheless likely that the direction of a planned movement is used by the brain as a parameter to control movement (de Graaf et al., 1991). Studies of arm movements in monkeys have shown that the direction of an intended movement in peripersonal space is encoded by directionally selective cells in motor cortex (Georgopoulos et al. ,1988; Kettner et al., 1988; Schwartz et al., 1988). Moreover, in humans, it has been suggested that the accuracy of goal-directed movements toward visual targets is determined by information derived from an internal representation of the trajectory of the intended movement (Vincken and Denier van der Gon, 1985; van Sonderen and Denier van der Gon, 1990; de Graaf et al., 1991).

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Directional hypometria There would appear to be ample evidence in support of the concepts of directionspecific deficits in spatial exploration and movement amplitude, i.e. directional hypometria, as defined above. For example, patients with unilateral neglect may show hypometric saccades toward their neglected side (Butter et al., 1988). They may also exhibit hypometric arm movements toward the contralesional side when asked to reproduce horizontal displacements (Meador et al., 1988). Tegner and Levander (1991) used a 90° angle mirror to dissociate direction of visual attention from direction of arm movement in a line cancellation task. They found that left neglect patients with anterior lesions moved their responding hand towards, but not into, left hemispace, even though their attention was supposedly being drawn towards the non-neglected (right) hemispace. Finally, Bisiach et al. (1990) have shown that, among neglect patients, especially those with lesions involving anterior (prerolandic) brain regions, directional hypometria may contribute to rightward errors in a modified version of the line bisection test.

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METHODS Subjects A total of 29 patients (19 males, 10 females) and 23 healthy controls (14 males, 9 females) served as subjects. All subjects gave their informed consent to participate in the study prior to testing. Patients had unilateral cerebral lesions as inferred from clinical examination and confirmed by computerized tomography (CT) scan. Patient imaging studies were conducted initially within 24 h of symptom onset and subsequently at an interval of between 1 and 4 wks post-cerebrovascular accident. Since the final boundary of infarcted tissue is best visualized 7—10 d after stroke (Donnan, 1992), the second or later sets of scans were used to delineate the lesion site. All subjects were right-handed for unimanual skills (e.g. writing, throwing) prior to their stroke.

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Directional hypokinesia and space representation If neglect patients are unable to form an adequate internal representation of external space (and presumably, therefore, the trajectories of goal-directed movements across that space), it might be predicted that they would show direction-specific impairments of movement that are consistent with Heilman's notion of directional hypokinesia. In an attempt to test this prediction we assessed patients with unilateral neglect on a sequential movement task in which responses could be directed either toward or away from the neglected side of space. The present experiment employed two temporal measures of performance, 'down time' and 'movement time'. These indices reflect fundamental properties of serial movement (Bradshaw et al., 1988, 1990, 1992; Stelmach et al., 1989; Franks and Van Donkelaar, 1990; Montgomery and Buchholz, 1991). Down time reflects the time taken to detect the next visual cue in a sequence and to initiate a response towards it. Previous studies conducted with the same apparatus have shown that down time also provides an index of preparatory processes, during which the motor program for the next movement in a sequence is assembled (Bradshaw et al., 1992; Jones et al., 1992). Movement time, on the other hand, exhibits a well-established relationship with target size and movement amplitude (Fitts' Law; Fitts, 1954). Movement time reflects the time spent in motion between target buttons and provides an index of continued programming during movement execution (Jones et al., 1992). The use of temporal indices which separate movements into components of initiation (down time) and execution (movement time) is particularly important, since different neural processes are involved in these motor acts (Montgomery and Buchholz, 1991). Our paradigm also permitted us to address questions that have not been answered by previous work. For example, Heilman et al. (1985) did not assess right hemisphere lesion patients without neglect. It is therefore not possible to determine whether directional hypokinesia (if it exists) is directly associated with unilateral neglect, or whether it occurs independently in patients with unilateral cerebral damage who show no evidence of neglect on standard measures. We therefore tested groups of right hemisphere lesion patients with and without unilateral neglect, in addition to a group of left hemisphere lesion patients, one of whom had neglect. Moreover, since Heilman et al. (1985) did not measure leftward movements made in left hemispace, they were unable to determine whether directional hypokinesia could be modified by the hemispatial location in which movements are performed. We asked patients to perform unidirectional movement sequences at the midline and in left and right hemispace in order to address this issue.

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Right hemisphere lesion group. There were 18 patients with unilateral right-hemisphere lesions and left neglect. Clinical details of these patients are provided in Table 1. The performance of these patients using their preferred (ipsilesional) hand was to be compared with the performance of 18 healthy controls using the same hand. The two groups were matched with respect to sex and there was no significant age difference between the groups [Left Neglect Group = 64.1 yrs, Control Group = 62.5 yrs, 1(34) = 0.36, n.s.].

TABLE I. PERSONAL AND CLINICAL DATA FOR LEFT NEGLECT PATIENTS Sex F

2

71

M

12

Ischaemia

3

65 82 41 65

M M M M

21 2 1 4

Ischaemia Ischaemia Haemorrhage Ischaemia

8 9

65 66 65

M M F

5 49 56

Ischaemia Haemorrhage Haemorrhage

10 11

93 51

F M

5 22

Ischaemia Ischaemia

12

67

M

13 14 15

43 74 63

M F F

13 2 14 6

Ischaemia Ischaemia

16

57

F

12

17

60

F

4

Ischaemia

18

47

M

7

Haemorrhage

4

5 6

7

1

Etiology Ischaemia

Ischaemia Ischaemia and haemorrhage Haemorrhage

CT scan R lentiform nucleus and corona radiala R periventricular lucencies R parietotemporal R parietal R lentiform nucleus R frontal, anterior limb of internal capsule, lentiform nucleus R parietal R frontoparietal R corona radiata, lentiform and caudate nuclei R occipitoparietal R temporo-parieto-occipital junction R occipitoparietal R frontal R occipitotemporal R frontoparietal, posterior limb internal capsule, corona radiata R anterior limb internal capsule, caudate and lentiform nuclei R frontoparietal, temporal and corona radiata R temporoparietal

VF NAD NAD LHH NAD LHH LHH

LHH NAD LHH LHH LHH LHH NAD LHH Unknown

LHH NAD LHH

Poststroke = time (weeks) between cerebrovascular event and testing; VF = visual fields; LHH = left homonymous hemianopia; NAD = no abnormalities detected; R = right.

An additional group of six patients with right hemisphere lesions but without left neglect on standard screening measures (see below) was tested in the same manner as the Left Neglect Group (see Table 2). The right-hand performance of this group was also to be compared with that of six matched subjects selected from the normal Control Group. The mean age of the Right Hemisphere Lesion Group (53.8 yrs) was not significantly different from the normal Control Group [54.5 yrs, /(10) = 0.09, n.s.]. Left hemisphere lesion group. A further five patients with unilateral left hemisphere lesions were tested (Table 3), one of whom (Case 1) had right unilateral neglect. The performance of these patients using their non-preferred (ipsilesional) hand was to be compared with the performance of five healthy controls

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Age 79

Poststroke

1

Case

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J. B. M A T T I N G L E Y AND O T H E R S

TABLE 2 . PERSONAL AND CLINICAL DATA FOR RIGHT HEMISPHERE LESION PATIENTS WITHOUT NEGLECT Age 67

F

Poslslroke 5

2

55

M

7

3 4 5

65 57 33

M M M

2 22 6

Ischaemia Ischaemia Ischaemia and haemorrhage

6

46

M

29

Ischaemia

Etiology Ischaemia

Ischaemia

CT scan R parietal, genu of internal capsule, lentiform nucleus. thalamus R frontal, temporal, anterior limb of internal capsule, lentiform nucleus R temporoparietal R frontoparietal R anterior limb of internal capsule, lentiform and caudate nuclei R parietal

VF LHH

NAD

LHH LHH NAD

Unknown

Poststroke = time (weeks) between cerebrovascular event and testing; VF = visual fields; LHH = left homonymous hemianopia; NAD = no abnormalities detected; R = right.

TABLE 3. PERSONAL AND CLINICAL DATA FOR LEFT HEMISPHERE LESION PATIENTS Case 1*

Age

78

Sex F

Poststroke 2

Etiology Ischaemia

2

59

F

Unknown

Ischaemia

3 4 5

48 58 46

M M M

37 58 6

Haemorrhage Ischaemia Ischaemia

CT scan L thalamus, periventricular lucencies L anterior limb of internal capsule, lentiform nucleus L frontoparietal L parietal L anterior limb and genu of internal capsule, caudate nucleus, corona radiata

VF NAD NAD RHH NAD NAD

*Patient had right unilateral neglect. Poststroke = time (weeks) between cerebrovascular event and testing; VF = visual fields; RHH = right homonymous hemianopia; NAD = no abnormalities detected; L = left.

using the same hand. The two groups were matched with respect to sex and there was no significant age difference between the groups [Left Hemisphere Lesion Group = 57.8 yrs, Control Group = 57.2 yrs, ;(8) = 0.07, n.s.]. Screening for unilateral neglect An identical screening procedure was followed for all patient groups prior to conducting the main experimental investigation. Patients were given a line cancellation task (Albert, 1973), a circle cancellation task (Ellis et at., 1987), and the Star Cancellation task from the Behavioural Inattention Test (Wilson et al., 1987). Each sheet was placed directly in front of the patient and centred at the body midline. All patients used their ipsilesional limb to hold the pen. Patients were also given a line bisection test, consisting of 10 horizontal lines varying in length from 80 mm to 170 mm in 10 mm increments. These lines were centred on a single sheet of A4 paper in pseudorandom order and drawn through a mask with a central window which exposed one line at a time. Deviation from the true midpoint of each line was measured to the nearest millimetre. Subjects were classified as having unilateral neglect if they made two or more omissions on one or more of the cancellation tasks on the half of the page contralateral to the lesion, or if they showed an average bias greater than 3 mm from the midpoint toward the side of the lesion on the line bisection test.

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Case 1

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Patients included in the right hemisphere and left hemisphere lesion groups (without neglect) made no omissions on the cancellation tasks and showed only a very small mean deviation on line bisection, i.e. less than 2 mm on either side of the true midpoint. Apparatus The response board consisted of a laminated wooden surface measuring 480 x 100 mm, into which were set 23 spring-loaded, circular buttons (see Fig. 1). Each button was made from highly visible white plastic

o o o o o o o o o o o o o o o o o o o o o o F

S2

480 mm FIG. 1. Response board used in the experiment, viewed from above. Subjects began by pushing SI then S2, followed by a sequence of 10 movements between successive pairs of buttons, finishing at F.

and was situated within a translucent circular annulus. Red light-emitting diodes (LEDs) were embedded within the annuli and served as visual cues. Twenty of these buttons were arranged in two parallel rows of 10, with three additional buttons, two of which were always pressed at the start (SI, S2) and finish (F) of the movement sequence. Each pair of buttons was separated by 30 mm, the rows themselves were 30 mm apart, and each button was 13 mm in diameter. Procedure All aspects of visual cue production and sequence structure were controlled by a Toshiba T3100e Lap Top computer. Maximum duration of cue illumination was set at 1000 ms for both patients and controls. Down time and movement time measures were recorded on-line to the nearest millisecond for each element of the movement sequence. All patients responded with their ipsilesional hand in order to eliminate the detrimental effects of primary motor and sensory deficits present on the contralesional side of the body. Individual control subjects were required to use the same hand as the patient with which they were matched. Control subjects and most patients sat at a table throughout the experiment. A small number of patients were tested while sitting upright in bed, with a height-adjustable table located at a comfortable distance in front of them. The apparatus was positioned in the horizontal plane, approximately 300 mm in front of the subject. This distance was adjusted between individuals to accommodate for variations in reach of the upper limb. The subjects' task was to press a sequence of buttons with the index finger as quickJy as possible in response to the visual (LED) cues located in the annulus at the base of each target button. In all trials, subjects began by pressing two single buttons (first SI then S2) to initiate the task. Thereafter, the computer generated a sequence of light cues in which one member of each of the 10 pairs of buttons was illuminated, one at a time. During the time for which each cue remained illuminated, the subject was required to move toward and press the target button as quickly as possible. Upon pressing the target button, the next cue in the sequence was activated and the subject was required to make a movement toward the appropriate target button, and so on along the board. Each movement sequence (one trial) consisted of iO cued movements, all proceeding in the same direction from start to finish, either from left to right or right to left. Thus, each movement in a sequence was directed only as far as the next pair of buttons. Trials were terminated at the final button (F), which was located at the end of the board opposite the starting buttons.

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S1

r\

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Data treatment Data obtained from the starting and finishing buttons were not analysed, since there was no uncertainty associated with these movements. The computer calculated means and standard deviations of the two dependent variables (down time and movement time) for each of the 10 cued movements in a sequence. These values were analysed separately as a function of Spatial Location (left, midline and right), Movement Direction (left to right, right to left) and Sequence (buttons 1 to 10 across the response board). Data obtained from each of the subject groups were analysed in separate, mixed-model analyses of variance (ANOVAs). The factors included in each ANOVA, including subanalyses, are provided in the context of the results. RESULTS AND DISCUSSION

Right hemisphere lesion group with left neglect Analysis of down times. The down time measure indicated the time taken to detect the next visual cue in a sequence, and to initiate a response towards it. The mean down time for each group represented data obtained from 10 cued movements across 48 trials, i.e. a total of 480 separate movements. The mean down time for controls and left neglect patients is shown in Fig. 2 as a function of Movement Direction and Spatial Location. Data were submitted to a four-way ANOVA with repeated measures on the factors of Spatial Location, Movement Direction and Sequence and non-repeated measures on Group. Patients with left neglect took significantly longer to initiate movements (164 ms) than normal controls (99 ms) [F(l,34) = 6.23, P < 0.05]. There was also a significant main effect of Movement Direction [F(l,34) = 11.35, P < 0.01]. This result should be interpreted in terms of the significant Group x Movement Direction interaction [F(l ,34) = 5.14, P < 0.05]. Both groups were slower to initiate leftward (146 ms) compared with rightward (116 ms) movements. Two repeated measures ANOVAs (Spatial Location x Movement Direction x Sequence) were performed separately on the down time data obtained from each group. Controls were significantly slower to initiate leftward (104 ms) compared with rightward (94 ms) movements [F(l,17) = 9.42, P < 0.01]. Patients with left neglect were also slower to initiate leftward (188 ms) compared with rightward (139 ms) movements [F(l,17) = 8.207, P < 0.05]. Thus, the significant interaction indicates that patients with left neglect were disproportionately slower than controls, i.e. a 49 ms versus 10 ms leftward movement inferiority for left neglect patients and controls, respectively.

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The exact sequence of movements from button to button varied across trials so that subjects were unable to predict their next movement prior to receiving a visual cue. The numbers of linear and diagonal movements between successive pairs of buttons were balanced, such that the total distance covered in each trial was constant. There were eight equidistant sequence paths (four original and four mirror-reversed). All subjects received a minimum of eight practice trials (four in each direction) with the board located across the midline. Some patients required additional practice trials, which were allowed as necessary. During experimental trials, the board was located either across the body midline, with half the response buttons in each hemispace, or with its entire extent located within either hemispace, i.e. fully to left or right of the body midline. Subjects completed two blocks of eight trials in each spatial location (left, midline and right) making a total of 48 trials per subject. The order in which the board was positioned in the three spatial locations was counterbalanced within each group of subjects. Starting position (and therefore movement direction) was alternated every two trials, such that there were four trials in each direction within each block. If, during a movement sequence, a subject missed a cue or pushed a button that had not been cued, the same trial was repeated from the beginning. In the event, all subjects performed well and most returned an errorless performance.

M O V E M E N T I M P A I R M E N T S IN N E G L E C T 240 n

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240 -i B

A

Left

Midline

Right

Left

Midline

Right

FIG. 2. Mean down time (with 1 SE indicated) as a function of spatial location for rightward (solid bars) and leftward (hatched bars) movement sequences, A, controls; B, left neglect patients.

There was no main effect of Spatial Location [F(2,68) = 1.05, P > 0.05] and no interactions involving this variable, indicating that the longer mean down time for leftward movements in both groups (and especially in patients with left neglect) occurred independently of the region of peripersonal space from which they were obtained. By plotting the mean down time for each of the 10 cued movements, it is possible to examine the extent to which this temporal index changes as a function of button position across the response board. Figure 3A shows the mean down times for left neglect patients and controls, at the three spatial locations, for movements made from left to right. For both groups, mean down time decreased from left to right, although this trend was more salient in the left neglect group. Thus, movements made toward the right (i.e. away from the patients' neglected left side) became progressively easier to initiate, regardless of the spatial location in which the limb was operating. In contrast, although movements from right to left {see Fig. 3B) were initiated progressively faster by the control group in each spatial location, and by the left neglect group in left hemispace, performance of the latter group with the board located at the midline and in right hemispace became somewhat more erratic as they approached the left side. Taken together, the down time functions indicate that the time required by left neglect patients to detect a visual target and initiate a movement towards it tended to change during the movement sequence. The extent of this change was dependent upon whether the movement was made toward or away from the neglected side. It will be seen that such effects were far more pronounced with movement times. Analysis of movement times. The movement time measure indicated the time spent in motion between target buttons, i.e. it reflected the execution phase of each visually cued movement. The mean movement time represented data obtained from 10 cued movements across 48 trials, i.e. a total of 480 separate movements per subject. Data were submitted to a four-way ANOVA with the same design as the down time analysis.

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40-

1858

J. B. MATTINGLEY AND OTHERS Spatial location 240 n

Right

Midline

Left

r240

«• 2 0 0 "

-200

E 5 6 0 : •I 5 2 0 :: ^ 480 a) 440-

10

MOVEMENT IMPAIRMENTS IN NEGLECT

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These correlational analyses revealed that there was no significant relationship between line bisection/cancellation task performance and the degree of directional movement bias shown in patients' down time and movement time profiles (all non-significant at oc = 0.05). These results, which held for both the Anterior/Subcortical Lesion Group and the Posterior Cortical Lesion Group, indicated that the direction specific slowing in initiation and execution of movement sequences exhibited by left neglect patients was not consistently reflected in their performances on clinical screening measures.

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Left hemisphere lesion group According to Heilman et al. (1985), the right hemisphere activates mechanisms responsible for initiating movements towards either hemispace, whereas the left hemisphere is only able to initiate contralateral movements. If this model is correct then patients with left hemisphere lesions should not show directional hypokinesia for contralesionally directed movements, since their intact right hemisphere should be able to initiate movements in either direction. In order to address this prediction, the performances of five patients with left hemisphere lesions were compared with those obtained from five matched controls. Since patients could only use their ipsilesional (non-preferred) hand, control subjects were also required to use their non-preferred hand. Two separate ANOVAs, one for down time and one for movement time, were conducted with Group as a non-repeated measure and with repeated measures on Spatial Location, Movement Direction and Sequence. There were no significant main effects or interactions in the down time analysis. Importantly, left hemisphere lesion patients were no different to normal controls in the time required to locate a visual target and initiate a movement towards it. With respect to movement time, there was a significant effect of Movement Direction [F(l,4) = 15.8, P < 0.05] with rightward movements (374 ms) being executed faster than leftward movements (408 ms). However, there was no Group x Movement Direction interaction, indicating that both groups exhibited the same rightward superiority in executing visually cued movements. These results accord well with previous observations on young normal subjects, where adductive movements have been shown to be faster than abductive movements (Bradshaw et al., 1990). To summarize, the down time and movement time profiles of patients with left hemisphere lesions were the same as those obtained from normal controls. It should be noted, however, that four of the five patients showed no evidence of unilateral neglect. The performance of the single patient with right-sided neglect {see Table 3, Case 1) was sufficiently different from the other left hemisphere lesion patients to warrant further consideration. The down time profiles for rightward and leftward movements for Case 1 are shown in Fig. 10 compared with her own matched control. Although the patient was slower in both directions, her movements toward the neglected right side became progressively more difficult to initiate. This pattern, which is similar to that observed in the movement time profiles of the left neglect group, suggests that problems of cue detection and movement initiation towards the neglected side may occur following both right hemisphere and left hemisphere lesions, but only in the presence of unilateral neglect. In terms of movement execution, Fig. 11 shows the movement time profiles of the same patient and matched control, for rightward and leftward movements. The

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Spatial location Midline

Left

1200-i

Right

M1 1000800E

600- •

I

400-

Q

2002345678910

1 2 3 4 5 6 7 8 9 1 0

tim

1000800600c 400Q 2001 0 9 8 7 6 5 4 3 2

1 1 0 9 8 7 6 5 4 3 2 1 Button number

1 0 9 8 7 6 5 4 3 2 1

FIG. 10. Mean down time for 10 cued movements across the response board, plotted separately for the three spatial locations. Filled and open circles represent the performance profiles of a right neglect patient and matched control, respectively, A, rightward movements; B, leftward movements. Note change in vertical scale for this figure.

performance of each subject was very similar for movements in either direction, with the possible exception of the erratic rightward movements made by the patient at the midline. GENERAL DISCUSSION

Unilateral neglect patients were slow to detect a visual target and to initiate a movement towards it when the movement was directed toward the neglected (contralesional) side. This pattern was particularly evident in neglecting patients with right-sided posterior cortical lesions and in the single neglecting patient with left hemisphere damage. Left neglect patients also failed to show the leftward superiority of movement execution exhibited by normal subjects. More importantly, such patients with lesions of anterior cortical and subcortical structures tended to be slower in executing leftward compared with rightward movements. This represents a reversal of the pattern exhibited by normals and those patients with posterior lesions. These deficits are not simply a consequence of unilateral hemispheric damage, since separate groups of right hemisphere and left hemisphere lesion patients without neglect performed in a manner comparable to normal controls.

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1 23456789101

MOVEMENT IMPAIRMENTS IN NEGLECT

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Spatial location Midline

L

1 2 3 4 5 6 7 8 9 1 0

1

r1600 -1400

B

-1200

-1000 -800 -600 -400 -200 -0

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FIG. 11. Mean movement time for 10 cued movements across the response board, plotted separately for the three spatial locations. Filled and open diamonds represent the performance profiles of a right neglect patient and matched control, respectively, A, rightward movements; B, leftward movements. Note change in vertical scale for this figure.

The extent of the direction-specific impairments exhibited by our neglect patients on the sequential movement task was not correlated with their errors on line bisection, nor with the number of omissions made on the three cancellation tasks. Thus, at least for our sample of patients, we must conclude that deficits of movement are not necessarily related to, or predictable from, performance on neglect screening tasks. Moreover, although there were significant differences on our temporal performance indices between patients with anterior/subcortical and posterior cortical lesions, the two groups could not be distinguished on the basis of their performance on clinical screening tasks. While there may be several explanations for this discrepancy, it seems most likely that our sequential movement task provided a more sensitive means by which to assess directional bias in visuomotor control which is not readily indexed by screening tasks. Several previous studies have suggested that in order to demonstrate the existence of directional hypokinesia (or indeed directional hypometria), the direction of movement (e.g. of the operating limb) should be dissociated from the direction in which the attentional focus is to be moved (Bisiach et al., 1990; Mijovic, 1991; Tegner and Levander, 1991). To the extent that such manipulations are able to produce a corresponding directional antagonism between attention and intention along a sensorymotor continuum, these experiments constitute the only empirical evidence relevant to

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Movement initiation A previous demonstration of 'intentional' impairment in neglect was provided by Heilman et al. (1985), in which subjects were required to produce a single, open-loop movement toward left or right hemispace along a fixed trajectory. Patients with left neglect were slower to initiate leftward compared with rightward movements, even though they used their ipsilesional (right) upper limb. Subsequent studies have attempted to confirm the presence of what we have called directional hypometria among neglect patients. Results have been obtained which would seem to support the existence of such deficits in neglect (Butter et al., 1988; Bisiach et al., 1990; Coslett et al., 1990; Tegner and Levander, 1991), although there is also evidence to the contrary (Mijovic, 1991). Unfortunately, resolution of this issue has been clouded as a consequence of the broad range of definitions ascribed to the concept of directional hypokinesia. In this regard, it is worth restating the distinction drawn earlier between the spatial and temporal parameters of movement. In our study, directional hypokinesia is used to denote slowness in the initiation of movements in the contralesional

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the distinction of 'input' versus 'output' factors in neglect. However, it has been suggested that there is a complex interdependence of processes involved in attentional orienting and the preparation of action (Allport, 1989; Neumann, 1990). At present, it is not clear whether such experimental paradigms actually achieve their purported aim of decoupling these processes. Perhaps the dissociation between direction of attention and direction of intended movement is most clearly realized in novel, incongruous tasks. Later, with increasing automaticity, the two may become congruent, as tends to occur after practice in most stimulus-response incompatible tasks (e.g. Brebner, 1973). Since our paradigm did not create a directional antagonism between the directions of cue detection and limb movement, it does not distinguish between the so-called 'inputand output-related factors' of neglect. The major advantage of our paradigm is that it closely models the demands of normal motor activities in which attentional and intentional mechanisms are mobilized toward a common goal (Allport, 1989). We preserved the congruity of attentional and motor processes by allowing the subject to perform a series of goal-directed movements in which the factors of attentional shifting and movement initiation (down time) were distinguished from those of movement execution (movement time). These results may help to resolve a number of important issues regarding the mechanisms underlying the motor behaviour of patients with unilateral neglect. We acknowledge that the term directional hypokinesia has been used in the context of paradigms which measure the spatial aspects of performance. However, given the potential complexities of mechanisms involved in motor control, implementation of a more refined taxonomy may facilitate the process of identifying specific movement deficits in subgroups of patients with neglect. Thus, in addition to our findings of contralesional slowing in movement initiation among neglect patients (directional hypokinesia), several recent experiments have provided valuable data concerning deficits in the amplitude of upper limb (Bisiach et al., 1990) and eye movements (Butter et al., 1988), and on direction-specific deficits in spatial exploration (Mijovic, 1991; Tegner and Levander, 1991). The extent to which temporal and spatial aspects of performance may be related in these patients has yet to be determined.

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Movement execution In addition to showing directional hypokinesia, left neglect patients failed to exhibit the previously established adductive (leftward, with the right hand) movement time superiority found in normal control subjects (Bradshaw et al., 1990). Of potentially greater theoretical importance, however, is the finding that left neglect patients with anterior/subcortical damage exhibited a reversal of the normal directional asymmetry, such that leftward movements were executed slower than rightward movements in all three regions of peripersonal space. Moreover, such a bias was not found in those patients with lesions restricted to posterior cortex. This represents, we believe, the first demonstration of directional bradykinesia, i.e. a direction-specific slowness in the time required to execute a goal-directed movement. The patients tested by Heilman et al. (1985) failed to show a movement time slowing for leftward movements. This may reflect the fact that movements executed by patients in their task were always predictable (open loop) and did not require visual guidance. Thus, specification of the movement trajectory was controlled externally (by the apparatus) and did not have to be generated, as here, by mechanisms involved in target acquisition. It is these latter mechanisms that are important determinants of movement time and are known to be disrupted in patients with movement disorders (Montgomery and Buchholz, 1991). The finding of directional bradykinesia in patients with anterior/subcortical lesions is unlikely to reflect a direction-specific problem in executing eye movements toward the target buttons. Pierrot-Deseilligny et al. (1991), in a study of patients with unilateral infarction, found that lesions of frontal cortex did not affect the latency of visually guided saccades. In addition, all our patients were screened for gaze disturbances prior to testing. Moreover, the impairment of movement execution in these patients was measured independently of any disturbance of attentional orienting or pre-movement planning, factors which are largely, if not wholly, incorporated in the down time index. Thus, the movement time index reflects the time spent in motion after detection of the next

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direction. Directional hypokinesia is not necessarily tied to hemispatial coordinates, although the hemispace in which directional movements are executed could conceivably exert some additional influence on the existing directional asymmetry. There is at least one explanation for the prolonged down time profiles in the contralesional movements of neglect patients. It is known that patients with parietal lesions have difficulty disengaging their attention from its present location in preparation for a shift towards the contralesional side (Posner et al., 1984). The down time phase of our task encompasses operations involved in shifting attention (locating the next target button) in addition to movement preparation time. Slowness in the initiation of movements toward the contralesional side may therefore reflect disruption of processes involved in the orienting of attention, rather than a 'pure' deficit of motor initiation. However, Heilman et al. (1985) have demonstrated directional hypokinesia using a paradigm which did not require direction-specific attentional orienting toward spatial cues. Moreover, it has been established that down time, as measured with our apparatus, provides a reliable index of movement planning in normals (Bradshaw et al., 1990) and in patients with movement disorders (Bradshaw et al., 1992; Jones et al., 1992). Thus, although patients may have difficulty in directing their attention towards the contralesional side, this alone is unlikely to account for their direction-specific impairment of movement initiation.

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visual cue and during which the desired movement trajectory is programmed (Bradshaw etal., 1990, 1992; Jones etal., 1992). The fact that directional bradykinesia was only exhibited by a particular subgroup of left neglect patients suggests that it exists as a separate entity from directional hypokinesia. Although the reasons for this impairment are not yet clear, we can offer some speculations. It has been suggested that the behavioural manifestations of unilateral neglect may reflect disruption to specific components of a network subserving spacerelated behaviour (Mesulam, 1981, 1985). Indeed, previous studies of patients with left neglect following frontal lesions have provided evidence to suggest that they are particularly impaired on tasks requiring movement in a contralesional direction (Butter et al., 1988; Bisiach et al., 1990; Tegner and Levander, 1991). We decided to isolate and combine just the data from our left neglect patients with anterior cortical lesions and/or subcortical lesions, since these structures are known to be involved in the coordination of movement (Rothwell, 1987). The finding of directional bradykinesia in this patient subgroup, therefore, provides additional support for Mesulam's model, in which the motor aspects of space-related behaviour are subserved by the frontal cortex and striatum. With respect to the mechanisms which are possibly responsible for producing directional bradykinesia, previous studies have established that the direction of a visually guided movement is used as a parameter for motor control (de Graaf et al., 1991). In particular, goal-directed movements may be controlled via an internal representation of their intended trajectory (Vincken and Denier van der Gon, 1985; van Sonderen and Denier van der Gon, 1990; de Graaf et al., 1991). If unilateral neglect is due to a failure to form a complete internal representation of real (or imagined) space (Bisiach and Luzzatti, 1978; Bisiach and Berti, 1987), then directional bradykinesia could reflect a disruption to internally generated movement trajectories. Moreover, it has been suggested that neglect resulting from unilateral striatal dopamine depletion may be due to disruption of the spatial coding of responses, or of the representation of space in which responses are directed (Brown and Robbins, 1989; Carli et al., 1989). Of course, since directional bradykinesia is a direction-specific impairment in the execution of movements, disruption of a desired trajectory would also need to be direction specific. We are currently investigating this possibility using kinematic analyses of ipsilesional limb movements in a group of left neglect patients. Finally, we turn to the movement time profiles exhibited by our unilateral neglect patients. Movement times for leftward movements in any spatial location became progressively longer towards the end of the sequence. This result suggests that the patients experienced relatively more difficulty in executing each component of the sequence as they approached their neglected side, regardless of the starting-point. This directionspecific gradient in movement time slowing could not be due simply to biomechanical factors (e.g. stretching into the opposite hemispace), since an almost identical trend was evident when the limb was moving adductively at the midline and in its own hemispace. A more plausible explanation is that unilateral neglect produces a pathological gradient in the processing of spatial information. Kinsbourne (1987) has suggested that the opposing orienting tendencies of the two cerebral hemispheres produce an attentional

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Conclusions We have demonstrated the existence of direction-specific impairments in both the initiation and execution of visually cued movements. These results confirm previous reports of directional hypokinesia in unilateral neglect, and additionally document directional bradykinesia in the execution of contralesionally directed movements. These impairments may contribute to, or arise as a consequence of, unilateral neglect, but are absent in left hemisphere and right hemisphere lesion patients without neglect. Directional hypokinesia is stronger in neglect patients with posterior cortical lesions while directional bradykinesia is more salient in those patients with anterior/subcortical lesions. This implies that the location of a cerebral lesion may alter the behavioural manifestations of unilateral neglect. Finally, the performance gradient for movements towards the contralesional side suggests that the transformation of spatially coded information into a movement trajectory is selectively impaired in certain types of unilateral neglect. We are currently using kinematic analyses to examine the quality of goal-directed movements in these patients.

ACKNOWLEDGEMENTS We gratefully acknowledge the assistance of administration and staff of the following institutions: Alfred Hospital, Austin Hospital, Hampton Rehabilitation Hospital, Heidelberg Repatriation Hospital, Monash Medical Centre, Royal Talbot Rehabilitation Hospital and The Royal Guide Dogs Association. We sincerely thank Bob Wood and Frank Devlin for designing and constructing the apparatus and Mike Durham for writing the software. Thanks also to Judy Bradshaw for her assistance with data collection and analysis. We are particularly grateful for the valuable comments of two anonymous reviewers on an earlier version of this manuscript. This study was supported by a grant from the Australian Research Council. Part of this research was presented at the meeting of the International Neuropsychological Society, Queensland, 1991.

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gradient across the whole of extrapersonal space in normals. Unilateral right hemisphere damage may release the vector of the spared left hemisphere, thereby producing a steep gradient in the level of attention across extrapersonal space. Several investigators have found evidence in support of this model (Bisiach et al., 1984; De Renzi et al., 1989; Ladavas et al., 1990; Warrington, 1991), although ours is the first to document its occurrence in the execution phase of directional movements. It is not clear why this gradient was so strong in the leftward movement time profile and relatively weak (or at least inconsistent) in the leftward down time profile. One possibility is that, since the main emphasis of the task was on movement, it was the movement time index which was maximally sensitive to any anisotropy in processing resources across space. Furthermore, previous demonstrations of an attentional gradient in neglect patients have employed paradigms in which unpredictability existed between stimuli along the left-right axis {see, for example, De Renzi et al., 1989). In our task, although each movement towards the next target button could not be predicted prior to receiving a cue, this unpredictability involved a decision between 'top or bottom', rather than 'left or right'. Of course, neither of these explanations provides the reason as to why our patient with right neglect showed a tendency for slower down times as she approached the contralesional side.

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(Received June 3, 1992. Accepted July 18, 1992)

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Impairments of movement initiation and execution in unilateral neglect. Directional hypokinesia and bradykinesia.

Patients with unilateral neglect may exhibit slowness in the initiation of contralesionally directed movements in peripersonal space (directional hypo...
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