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1Department of Neurosurgery, State University of New York-Upstate Medical University, Syracuse, New York 13210; 2Pittsburgh Veterans Affairs Medical Center, 3Center for the Neural Basis of Cognition, Departments of 4Neurobiology, 5Neurological Surgery, and 6Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261
Submitted 26 May 2004; accepted in final form 27 July 2004
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ABSTRACT |
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INTRODUCTION |
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, 1996; Galea and Darian-Smith 1994; Russell and DeMyer 1961; Toyoshima and Sakai 1981). Approximately one-third of the corticospinal system also originates from cortical areas in the parietal lobe (Galea and Darian-Smith 1994; Russell and DeMyer 1961; Toyoshima and Sakai 1981). The efferents that form the corticospinal system are largely crossed and terminate most heavily in contralateral regions of the spinal cord (Brinkman and Kuypers 1973; Dum and Strick 1991, 1996; Liu and Chambers 1964). The ipsilateral components of the corticospinal system are small and thought to have little influence over the control of distal movements (Brinkman and Kuypers 1973; Galea and Darian-Smith 1994; Liu and Chambers 1964; Toyoshima and Sakai 1981; however, see Lacroix et al. 2004).
Comparable data on the corticospinal tract of the human are limited (Jane et al. 1967; Lassek 1948; see Kuypers 1981; Porter and Lemon 1993). Based on the findings that are available and those in the monkey, one would expect that a unilateral cerebrovascular accident (CVA) in the human would have little or no effect on the performance of distal movements by the limb ipsilateral to the lesion (i.e., the "ipsilesional" limb). However, there have been occasional reports that patients with a unilateral ischemic stroke displayed bilateral movement abnormalities. For example, hemiplegic subjects were impaired in operating a steering wheel with their ipsilesional limb (Jones et al. 1989). Brodal (1973) observed that his handwriting was less coordinated after a stroke in the internal capsule ipsilateral to his dominant hand. Colebatch and Gandevia (1989) found that unilateral damage to motor cortex or its descending projections produced some weakness in the ipsilesional limb. These and other results (e.g., Carey et al. 1998; Desrosiers et al. 1996; Fisk and Goodale 1988; Haaland and Harrington 1989; Hermsdörfer et al. 1999; Winstein and Pohl 1995) suggest that damage to one hemisphere may have bilateral effects on the control of movement. A bilateral component to distal motor control is further supported by recent observations that functional activation is present bilaterally in cortical areas, including the primary motor cortex (M1), during unilateral finger movements (e.g., Cramer et al. 1999; Dassonville et al. 1997; Kim et al. 1993a, b; Salmelin et al. 1995; Solodkin et al. 2001).
In this study, we examined whether unilateral damage to cortical areas in the frontal lobe or their efferents produced deficits bilaterally in the generation and control of distal limb movements. We selected step-tracking movements of the wrist for this analysis because we have previously characterized the kinematics and patterns of muscle activity that are associated with these movements in normal human subjects (Hoffman and Strick 1986, 1990, 1993, 1999). Step-tracking movements of the wrist are associated with distinct and reproducible patterns of activity in forearm muscles. The muscle activity is graded in a systematic manner for movements of different amplitudes, speeds, loads, and directions. The extensive information on normal step-tracking movements provided the critical framework for our analysis of deficits in patients with cortical lesions.
Our results indicate that patients with a contralateral hemiparesis of the upper limb resulting from a unilateral CVA had profound deficits in their ability to perform skilled movements of the ipsilesional wrist. These deficits were present following damage to the dominant or nondominant hemisphere. Overall, our observations indicate that the movement abnormalities induced in the ipsilesional limb by a unilateral lesion are more extensive than previously thought. Portions of these data were presented previously in abstract form (Yarosh et al. 1996).
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METHODS |
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Our results are based on an examination of step-tracking movements of the wrist in seven patients and in seven normal subjects. The studies were approved by the institutional committees overseeing human experiments. All subjects gave informed consent according to the Declaration of Helsinki.
Patients were selected based on the following criteria: 1) the presence of hemiparesis after a single cerebral ischemic event; 2) the absence of any additional neurological disorder, other than that caused by the ischemic event; 3) the presence of a unilateral lesion as documented by imaging studies that included at least one or more of the following: computer-assisted tomography, nuclear MRI and cerebral angiography; 4) the ability to understand simple commands; and 5) the absence of pain in the tested limb. Control subjects had no history of neurological problems or pain affecting either wrist. They were matched as closely as feasible with the patients on the basis of sex, age, and handedness (Table 1). The patient and control groups each included three males and four females. Subjects' ages ranged from 27 to 73 yr (mean, 56.7 ± 18.4 yr for patients; mean, 56.9 ± 18.1 yr for controls). Handedness was quantified using the Edinburgh Inventory (Oldfield 1971). The inventory resulted in a laterality quotient (L.Q.) that ranged from –100 to +100, with left-handedness defined as a L.Q. <0. All subjects were right-handed except for P1 and C1.
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). Two patients (P1, P2) had no voluntary power at the wrist. Five patients (P3–P7) had varying degrees of weak movement. Two patients (P3, P6) had substantial increases in wrist tone. The patients with profound weakness (P1, P2) or substantially increased tone (P3, P6) were unable to perform the step-tracking task with the contralesional wrist. The patients with more mild weakness or mild changes in tone (P4, P5, P7) were able to perform the task. However, <50% of the movements with their contralesional wrist were smooth and well directed.
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Lesions were located in the left hemisphere of four patients and in the right hemisphere of three patients (Table 3). Six patients sustained a stroke that involved the middle cerebral artery (MCA). The lesion in one of these patients also included territory of the anterior cerebral artery (P5). Among the patients with an MCA stroke, two (P2, P4) had lesions that were restricted to the lateral frontal and parietal gray matter and the underlying white matter. Four (P1, P3, P5, P6) had more extensive lesions that also included the temporal lobe and, in some cases, portions of the basal ganglia and the internal capsule. The remaining patient (P7) had a small lacunar infarct involving the right globus pallidus and the posterior limb of the internal capsule. This patient was included because it is likely that the posterior portion of the internal capsule contains many of the descending efferents from the cortical motor areas (Fries et al. 1993). Note that the lesions were located in the dominant hemisphere in three subjects (P2, P3, P4) and in the nondominant hemisphere in the remaining subjects (P1, P5, P6, P7; Table 4).
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Step-tracking movements of the wrist were performed with the ipsilesional limb in patients. The same limb was tested in control subjects who were matched to each patient in age, sex, and handedness. Each subject sat in a chair which supported the forearm and elbow of the tested limb. The forearm was held midway between full pronation and full supination. Subjects grasped the handle of a light-weight manipulandum that rotated freely about the horizontal and vertical axes. The handle position was adjusted to align the wrist joint with two potentiometers that are coupled to this low-friction device. The potentiometers enabled measurement of wrist angle in the two planes of wrist joint rotation: flexion-extension and radial-ulnar deviation. A complete description of the manipulandum was presented in a prior study (Fig. 1 in Hoffman and Strick 1986).
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, 1990, 1999). Briefly, the task began with the subject positioning the cursor in a central target location for a variable hold period (1.0–1.5 s). Then, the target jumped to one of eight different locations arranged in a circle around the central hold position. Subjects were instructed to move the cursor "as fast and as accurately as possible" to the peripheral target location. If subjects asked whether they should emphasize speed or accuracy, we instructed them to emphasize speed. The peripheral targets required a 20° change in the angle of the wrist joint. To examine whether undershoot of the target was specific to a 20° change in the angle of the wrist joint, we asked some subjects to perform additional movements to the 10° target (e.g., Fig. 2). The eight peripheral target locations were presented in a pseudo-randomized manner. The patients and control subjects made practice movement until they felt comfortable with the manipulandum and with the task. Subjects performed the task in blocks of 40 trials (5 trials to each target) separated by brief rest periods.
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EMG activity was recorded using surface electrodes (Liberty Mutual Myoelectrodes, Boston, MA) taped onto the skin overlying four wrist muscles: extensor carpi radialis longus (ECRL), extensor carpi radialis brevis (ECRB), extensor carpi ulnaris (ECU), and flexor carpi radialis (FCR). The raw EMG signals were amplified (2666x or 2800x), full-wave rectified, and filtered (
= 10 ms; see Gottlieb and Agarwal 1970). These signals were amplified again by two to five times. EMG and the potentiometer signals from the manipulandum were digitized at 1.25 kHz by a Digital Equipment Corporation PDP 11/34 computer using custom designed software or at 1.0 kHz by an IBM-compatible PC using Tempo software (Reflective Computing, St. Louis, MO).
All data analysis was performed on individual trials of wrist angular position and EMG. The amplitude of the initial trajectory was measured as the change in wrist angle between the starting position and the position at the next zero crossing of tangential velocity. Tangential velocity was calculated from the two potentiometer signals. The signals were low-pass filtered (cut-off at 12 Hz for data from the DEC PDP 11/34 and at 15 Hz for data from the IBM-compatible PC) and differentiated. Tangential velocity was calculated as (a2 + b2)1/2, where a = velocity in the horizontal plane (wrist flexion-extension) and b = velocity in the vertical plane (wrist radial-ulnar deviation). Student's paired and unpaired t-tests were used to examine the statistical significance of kinematic data between patients and matched controls.
We aligned EMG data on movement onset, determined as the time when tangential velocity reached 15% of its peak. We calculated a baseline level of EMG during a 200-ms interval in the hold period. The onset of an EMG burst was defined as the time relative to movement onset when the EMG signal exceeded the baseline +2 SD and remained above this level for 
25 ms. The 25-ms minimum period that we used to define an EMG burst in this study is much shorter than the duration of the average agonist or antagonist burst (70–100 ms) that we observed in the wrist muscles of normal, young subjects (Hoffman and Strick 1999). For the illustrations, EMG activity was normalized to the maximum peak activity observed in that muscle for movements in any direction.
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RESULTS |
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, 1990, 1993, 1999). Wrist movements of normal subjects
The age-matched control subjects made wrist movements that were smooth and were well directed toward each of the targets (Fig. 1, A and B; see also Fig. 1 in Hoffman and Strick 1999). The amplitude of the initial movement step in the controls usually overshot the target (Fig. 2, A and B) and averaged 25.1 ± 6.0° (n = 520 trials) to targets that required a 20° change in wrist angle. The tangential velocity curve had a single large peak in the direction of movement, followed by a smaller peak in the reverse direction (Fig. 2, C and D). Most wrist movements in the controls were quite fast (Fig. 3) and had a peak velocity that averaged 378.6 ± 145.0°/s (n = 560 trials) to targets that required a 20° change in wrist angle.
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, 1990, 1993, 1999). The step-tracking movements of the older (>60 yr) and younger age-matched control subjects in this study differed in two ways. The amplitude of the initial movement step (20° target) in the older controls was smaller (22.1 ± 4.6°, n = 280 trials) than that of the younger controls (28.4 ± 6.0°, n = 320 trials, P < 0.001). Not surprisingly, the peak movement velocities of the older subjects were considerably reduced (277.9 ± 64.5°/s, Fig. 3, gray symbols) compared with those of the younger subjects (458.6 ± 143.3°/s, P < 0.001, Fig. 3, open symbols). Thus the older subjects did not move as fast or as far as the younger subjects. Ipsilesional wrist movements of patients
All patients made some ipsilesional wrist movements that were not well directed toward the target and lacked smoothness. This difficulty occurred regardless of whether the lesion was in their dominant (Fig. 1, C and D) or nondominant (Fig. 1, E and F) hemisphere. Frequently, the initial trajectory of a movement made by the ipsilesional wrist began in the wrong direction. As a consequence, an abrupt change in direction occurred to bring the wrist trajectory back on course (Figs. 1, C–F, 4, B and C, and 5, B and C). This gave some of the movements a highly irregular appearance. The patients had particular difficulty in moving toward targets that required wrist extension (or flexion) combined with radial or ulnar deviation (i.e., "diagonal" movements; Fig. 1, D and F). Movements made by the ipsilesional wrist to targets in the horizontal and vertical planes were less irregular, but even some of these movements were initially misdirected and exhibited abrupt changes in direction (Fig. 1, C and E).
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A third difference between the movements of patients and those of age-matched controls was that ipsilesional movements were much slower than those of control subjects (Figs. 2, G and H, and 3). In general, the peak velocities of the ipsilesional movements were only 38% of those of the wrist movements performed by age-matched controls. The average peak velocity in the patient group was only 144.9 ± 56.7°/s (n = 520 trials) when the target locations required 20° of wrist rotation. This was significantly lower than the movement velocity of control subjects to the same targets (378.6 ± 145.0°/s, P < 0.001). The reduction in movement velocity occurred regardless of whether the lesion was located in the dominant or nondominant hemisphere. Five patients (P1, P2, P3, P4, P6) made ipsilesional movements that were significantly slower than those of their matched control subjects for all eight movement directions (P < 0.05). Two patients (P5, P7) moved more slowly than their matched controls to most targets (P < 0.05), except when the target required a combination of extension + ulnar deviation (P5, P7) or pure extension (P5).
The wrist movements of control subjects displayed some variation in peak velocity for different directions of movement. Movements in the vertical plane (radial-ulnar deviation) tended to have higher peak velocities than those in the horizontal plane (flexion-extension; Fig. 3, open and gray symbols). The ipsilesional movements of patients did not exhibit this variation. Plots of velocity versus movement direction were "flattened" for patients (Fig. 3, black symbols) relative to the plots of movements of control subjects (Fig. 3, open and gray symbols).
Muscle activity in normal subjects and in patients
Step-tracking movements of the wrist in the age-matched controls were associated with the well-known triphasic pattern of muscle activity that consisted of alternating bursts of activity in agonist and antagonist muscles (e.g., Fig. 5A, for additional examples, references, and discussion, see Hoffman and Strick 1990, 1999). Agonist bursts led movement onset by 30–50 ms (e.g., Fig. 6, A and B). Antagonist bursts began at or just after (0–45 ms) movement onset (e.g., Fig. 6B). Frequently, one or more synergist muscles were activated simultaneously with agonist and antagonist muscles (Figs. 5A and 6A; see also Hoffman and Strick 1999). The age-matched controls showed considerable trial-to-trial consistency in the timing of activity onset and duration (Fig. 6, A and B). Overall, the pattern of muscle activity during step-tracking movements in these age-matched controls was the same as that observed in the younger subjects that we previously studied (Hoffman and Strick 1990, 1999).
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25 ms). The remaining five patients (P2, P4, P5, P6, P7) displayed bursts of activity, but less frequently than age-matched controls (i.e., in only 42% of the instances when an agonist or antagonist burst was generated by control subjects). In the patients many movements were initiated by activity in single muscles, without co-activation of synergists (compare Fig. 6, A and C). For example, two patients (P2, P5) initiated 25–40% of their movements using activity in a single agonist muscle, and the remaining patients (P4, P6, P7) initiated 70% of their movements in this way. In contrast, age-matched controls initiated about 90% of their movements using co-activation of synergists.
When patients did exhibit activity in synergist muscles, the activity was often inappropriately timed. For example, synergistic and nearly simultaneous activity in ECRB and ECRL, along with agonist activity in ECU, was necessary to direct movement accurately to a target that required wrist extension + ulnar deviation (Figs. 4A and 6A). However, ECRB and ECRL activity occurred well before or well after the onset of ECU activity when a patient moved to the same target (Figs. 4, B and C, and 6C). The lack of co-activation of agonist and synergistic muscles resulted in movements that were misdirected (Fig. 4, B and C). Eighty-four percent (38/45) of the movements made by patients (P2, P4, P5, P6, P7) to the target that required extension + ulnar deviation were associated with a delayed onset of activity in either agonist or synergistic muscles. In contrast, only 26% (13/50) of the movements to the same target by the age-matched controls exhibited delayed activation of either agonist or synergistic muscles.
The alternation of agonist and antagonist activity found in the triphasic EMG pattern also was disrupted for movements of the ipsilesional wrist. For example, patients sometimes incorrectly attempted to perform a flexion movement using a brief burst in an antagonist muscle (Fig. 5B, ECU; Fig. 6D) or a co-activation of an agonist and an antagonist muscle (Fig. 5C, FCR, ECRL). In contrast, control subjects generally initiated wrist flexion movements with a distinct agonist burst in FCR, followed by pronounced antagonist bursts in ECU and ECRL (Fig. 5A). Overall, 38% (17/45) of the wrist flexion movements performed by patients (P2, P4, P5, P6, P7) exhibited abnormal sequences of agonist and antagonist muscles (for example, compare Fig. 6, B and D). The early, abnormal activation of antagonist muscles by patients resulted in movements that were grossly misdirected (Fig. 5, B and C).
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DISCUSSION |
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, 1999). Our results add to a growing body of literature which demonstrates that the supposedly "unaffected" ipsilesional limb does not function normally after a unilateral stroke of the cerebral motor areas (e.g.,Brodal 1973; Carey et al. 1998; Desrosiers et al. 1996; Fisk and Goodale 1988; Haaland and Harrington 1989; Winstein and Pohl 1995; Wyke 1971). The step-tracking task that we employed to test patients is a simple one that involves movements limited to a single joint. Thus the deficits we observed represent difficulties in generating motor output at a fundamental level of motor control. Prior studies of the motor capabilities of the ipsilesional limb often have found difficulties with movements that require more complex coordination of the entire upper arm (e.g., Desrosiers et al. 1996; Haaland and Harrington 1989; Hermsdörfer et al. 1999; Winstein and Pohl 1995; Wyke 1971).
We observed impairments of ipsilesional wrist function in patients with lesions in either hemisphere. In addition, we found no evidence that the type of deficit differed for lesions in the dominant and nondominant hemispheres. However, this issue should be explored further with a larger sample size. Some prior studies did find differences in motor function that depended on whether the right or left hemisphere was damaged (e.g., Fisk and Goodale 1988; Haaland and Harrington 1989; Haaland et al. 1987; Hermsdörfer et al. 1999; Winstein and Pohl 1995; Wyke 1971; but see Winstein et al. 1999). In general, these studies used tasks that required coordination between different parts of the forelimb and found a left hemisphere specialization for the efficient timing of movement subcomponents (Winstein and Pohl 1995).
Wrist movements of the ipsilesional limb had a much smaller peak velocity and a smaller initial amplitude than the wrist movements of control subjects. This result might be explained by a weakness of the ipsilesional wrist. Although we did not directly measure muscle strength, our results are consistent with a prior study that found an 
70% weakness of ipsilesional wrist flexion and extension in hemiparetic patients compared with normal control subjects (Colebatch and Gandevia 1989). In addition to weakness, we observed that the agonist burst in muscles of the ipsilesional wrist was very much reduced in duration and that the patients often failed to appropriately co-activate synergist muscles along with agonists. Both of these alterations reflect an altered central command to muscles that would result in reduced force generation and smaller, slower movements.
The most striking deficit seen in ipsilesional wrist movements was that they often had irregular trajectories, which meant that the movement was not smoothly directed toward the target. The nature of this deficit was similar to the misdirected movements seen in the contralesional wrist of monkeys following a large unilateral lesion of primary motor cortex (Hoffman and Strick 1995). In the lesioned monkey, the irregular trajectories resulted from a lack of synchronous onset of activity in agonist and synergist muscles. In some instances, the misdirected movements of the ipsilesional wrist of the patients were caused by a comparable problem (Fig. 4, B and C). In other trials, the misdirected movements of the ipsilesional wrist were associated with an inappropriate sequence of activity in agonist and antagonist muscles (Fig. 5, B and C). Taken together, our observations clearly suggest that a unilateral lesion of the cortical motor areas can cause bilateral disruptions in the appropriate temporal sequencing of activity in agonist, synergist, and antagonist muscles. In support of this suggestion, repetitive transcranial magnetic stimulation (TMS) of M1 to create a "temporary lesion" in normal subjects was found to induce temporal errors in the performance of ipsilateral finger movements (Chen et al. 1997).
In summary, we found evidence for two types of motor deficits in the ipsilesional wrist. One type of deficit is characterized by an insufficient magnitude of muscle activation at the onset of movement. This results in movements that are slow and undershoot the target. The second type is a temporal incoordination of multiple bursts of muscle activity. This results in movements that are misdirected and have irregular trajectories. Thus rather elementary aspects of step-tracking movements, i.e., their magnitude and direction, are affected by a lesion of motor areas in the ipsilateral hemisphere (see also Velicki et al. 2000).
Because a unilateral cortical lesion can disrupt processing at multiple levels of the neuraxis, the motor abnormalities we observed are likely to have a complex explanation that involves multiple, interrelated neural mechanisms. In the interest of brevity, our discussion will focus on potential mechanisms that may operate at the cortical level. One mechanism is that the deficits in ipsilesional wrist movements might reflect the extent to which one hemisphere and even the primary motor cortex exerts bilateral descending control over distal movements. The corticospinal tract is well known to have a small ipsilateral component, as well as a large contralateral pathway. The ipsilateral projection amounts to 10–15% of the corticospinal fibers from one hemisphere in the human (Nyberg-Hansen and Rinvik 1963). In the monkey, the ipsilateral corticospinal projection originates from all of the cortical motor areas and includes efferents from some of the largest pyramidal neurons in the hand representation of M1 (Hutchins and Strick 1987; Lacroix et al. 2004; R. P. Dum and P. L Strick, unpublished observations). Some M1 neurons are active prior to movements of the ipsilateral digits (Aizawa et al. 1990; Tanji et al. 1988). Activation is present bilaterally in functional imaging studies of M1 when subjects perform a unilateral finger tapping task (Cramer et al. 1999; Dassonville et al. 1997; Kim et al. 1993a, b; Salmelin et al. 1995; Solodkin et al. 2001). Thus the loss of ipsilateral descending output that accompanies a unilateral cortical lesion may contribute to the deficits seen in the wrist ipsilateral to a cortical stroke.
Another possible mechanism for the deficits in ipsilateral wrist movements is that damage to one hemisphere may alter callosal signals and disrupt neural processing in the opposite hemisphere. Anatomical studies in monkeys and other animals have shown that the corpus callosum densely interconnects the motor cortices of the two hemispheres (Gould et al. 1986; Jenny 1979; Pappas and Strick 1981; Rouiller et al. 1994; Zant and Strick 1978). Within M1, only the regions that contain a representation of the digits lacked dense callosal connections (e.g., Gould et al. 1986; Jenny 1979; Pappas and Strick 1981; Zant and Strick 1978). Neurons in proximal and distal regions of M1 responded to electrical stimulation of the callosum, although the latencies for activation of the neurons related to distal movements were longer than those related to proximal movements (Matsunami and Hamada 1984). Thus even regions of M1 without direct callosal connections receive interhemispheric information. Interhemispheric interactions have been examined in normal human subjects by measuring the motor-evoked potentials that result from TMS in a paired pulse paradigm. Interhemispheric inhibition was larger and easier to elicit with TMS than was facilitation (e.g., Chen et al. 2003; DiLazzaro et al. 1999; Ferbert et al. 1992; Hanajima et al. 2001; Meyer et al. 1998). These TMS observations in human subjects are similar to the specific facilitatory and broader inhibitory transcallosal effects recorded in M1 of cats after stimulation of the contralateral M1 (Asanuma and Okuda 1962).
Given the dense callosal connections that link M1 in the two hemispheres and the prominence of inhibitory effects mediated by this interconnection, one might expect a stroke in one hemisphere to alter the excitatory-inhibitory balance in the opposite hemisphere. Indeed, TMS studies using a paired pulse paradigm found that M1 in the nondamaged hemisphere of stroke patients displayed less inhibition than M1 in control subjects (e.g., Bütefisch et al. 2003; Liepert et al. 2000; Shimizu et al. 2002; Traversa et al. 1998). An increased excitability of the nonstroke hemisphere also was observed in M1 of mice following an experimental stroke produced by occluding the middle cerebral artery (e.g., Que et al. 1998). Thus the level of inhibition in M1 in the nonstroke hemisphere appears to be changed by the removal of callosal input. In monkey experiments, the amount of inhibition in M1 has been altered experimentally by injecting the GABAA antagonist, bicuculline, or the GABAA agonist, muscimol, into the arm area (Matsumura et al. 1991, 1992). These injections caused a marked disruption of the spatiotemporal patterns of muscle activity and resulted in the loss of smooth, well-directed limb movements. Taken together, these experimental observations lead us to suggest that a loss of the normal pattern of interactions between the stroke hemisphere and the nonstroke hemisphere could underlie the temporal discoordination of muscle activity that we observed in the ipsilesional wrist of hemiparetic subjects.
Overall, our findings show that damage to one hemisphere results in abnormal patterns of movement and muscle activity not only in the wrist contralateral to a stroke but also in the ipsilesional wrist. At the cortical level, a unilateral stroke could interfere with the bilateral control of motor output that originates from a single hemisphere. In addition, a unilateral stroke could alter the excitability of the opposite hemisphere and change the function of the otherwise intact hemisphere. Both of these proposed mechanisms would result in abnormal descending signals. In addition, spinal reflexes can show bilateral, long-lasting changes in hemiparetic subjects (Dewald et al. 1999; Thilmann and Fellows 1991). Thus descending commands in stroke patients are likely to interact with a segmental network of interneurons and motoneurons with abnormal levels of excitability. The combination of abnormal descending commands and altered spinal excitability could contribute to the bilateral deficits in voluntary movements of the wrist that we observed. Clearly, cortical motor areas in the nonstroke hemisphere are by themselves unable to generate normal distal movements after damage to their counterparts in the opposite hemisphere. An understanding of the mechanisms responsible for the movement abnormalities may lead to new approaches for facilitating recovery of motor function following cortical damage.
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GRANTS |
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Address for reprint requests and other correspondence: P. L. Strick, Univ. of Pittsburgh School of Medicine, W1640 Biomedical Science Tower, 200 Lothrop St., Pittsburgh, PA 15261 (E-mail: strickp{at}pitt.edu).
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