FOR PATIENTS AFTER stroke, recovering the ability to

1753 Recovery of Standing Balance and Functional Mobility After Stroke S. Jayne Garland, PhD, Deborah A. Willems, MSc, Tanya D. Ivanova, PhD, Kimberly J. Miller, MSc ABSTRACT. Garland SJ, Willems DA, Ivanova TD, Miller KJ. Recovery of standing balance and functional mobility after stroke. Arch Phys Med Rehabil 2003;84:1753-9. Objective: To examine the extent to which recovery of functional balance and mobility is accompanied by change in a few specific physiologic measures of postural control. Design: Longitudinal prospective study. Setting: Laboratory setting in Ontario. Participants: Twenty-seven volunteers (age, 64.2 13.7y) undergoing 4 weeks of rehabilitation after stroke participated. At initial testing, patients were 32.7 18.4 days poststroke and exhibited a moderate level of motor recovery (lower-extremity and postural control, stages 3 4 on the Chedoke-McMaster Stroke Assessment Impairment Inventory). Interventions: Not applicable. Main Outcome Measures: Three functional measures (Berg Balance Scale, Clinical Outcome Variables Scale, gait speed) were assessed. Three physiologic measures (electromyographic data of hamstrings and soleus muscles bilaterally, postural sway, arm acceleration) were taken while subjects stood quietly on a force platform and while they performed a rapid shoulder flexion movement of the nonparetic upper extremity. Results: After 1 month of rehabilitation, there was an overall significant improvement in all outcome measures (functional, physiologic). However, 10 patients failed to show any improvement in the electromyographic activation of hamstrings muscle on the paretic side in response to the rapid arm movement. These patients compensated by increasing the anticipatory activation of the nonparetic hamstrings. Conclusion: After stroke, patients showed improvement in both physiologic and functional measures of balance and mobility over a 1-month period. We have identified some patients who may be using compensatory strategies to increase function. The factors that may predict those patients who are likely to use compensatory strategies awaits further study. Key Words: Balance; Cerebrovascular accident; Rehabilitation. 2003 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation FOR PATIENTS AFTER stroke, recovering the ability to stand and walk is critical. Standing and walking require complex postural control mechanisms, the nature of which has not been fully determined. Numerous strategies have been suggested for the treatment of postural control deficits that result from stroke. 1-4 Although objective clinical evidence exists that functional ability can be improved by participating in a rehabilitation program after stroke, 5,6 this improvement could be caused by the following mechanisms: true neurologic recovery, compensatory strategies acquired by the patient, or a combination of both. One way to investigate the nature of the relationship among the different mechanisms is to compare the clinical change in patients by using validated functional outcome measures, 7-9 with physiologic measures of postural control obtained in a controlled laboratory setting. 10,11 For instance, Lee et al 12 used a cross-sectional design to investigate the relationships between patterns of muscle activation and center of pressure (COP) sway during a sit-to-stand transfer and functional mobility assessed with the FIM instrument. Lee found that both electromyographic and force platform data correlated well with the functional mobility capability in subjects after stroke. In a previous cross-sectional study, 11 we also found relationships between electromyographic and force platform measurements and a clinical evaluation of balance (Berg Balance Scale [BBS]) in persons with chronic hemiparesis after stroke. The primary objective of this project was to extend our previous study to determine whether changes over a 4-week period in clinical measures of functional ability were accompanied by changes in specific laboratory-based measures of postural control in patients after an acute stroke. We hypothesized that if functional change was accompanied by no change in physiologic measures of postural control, compensatory strategies acquired by the patient must have occurred. If functional change was accompanied by physiologic change, then neurologic recovery had taken place. Preliminary results of this study have been presented in abstract form. 13 METHODS From the School of Physical Therapy (Garland, Ivanova, Miller), University of Western Ontario; London Health Sciences Centre, University Campus (Willems), London, ON, Canada. Miller is currently affiliated with the School of Physiotherapy, University of Melbourne, Parkville Victoria, Australia. Preliminary data presented at the Canadian Physiotherapy Association Congress, June 30, 2001, Calgary, AB. Supported by the Physiotherapy Foundation of Canada and the London Health Sciences Centre. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Reprint requests to S. Jayne Garland, PhD, Sch of Physical Therapy, Elborn College, University of Western Ontario, London, ON N6G 1H1, Canada, e-mail: jgarland@uwo.ca. 0003-9993/03/8412-7904$30.00/0 doi:10.1016/j.apmr.2003.03.002 Participants Twenty-seven subjects participated in the study (see table 1 for demographics). All subjects who were admitted to the stroke rehabilitation unit at the London Health Sciences Centre, University Campus, London, ON, between 1997 and 1999 were asked to participate either on admission or once they achieved the inclusion criteria. Subjects met the inclusion criteria if they were able to maintain independent unsupported stance for 20 seconds, had a unilateral hemiparesis as a result of stroke and reported no cardiac, respiratory, or neuromuscular condition (eg, peripheral neuropathy, ankle sprain, shoulder tendinitis) that would interfere with the testing protocol. The study was approved by the university ethics review board.

1754 STANDING BALANCE AFTER STROKE, Garland Table 1: Description of Total Group and Subgroups at Admission Characteristic Total Group (N 27) Group I (n 5) Group IIa (n 10) Group IIb (n 12) Age (y) 64.2 13.7 56.8 18.2 63.6 13.2 67.8 12.0 Gender, n Male 17 5 5 7 Female 10 0 5 5 Side of paresis, n Right 13 2 5 6 Left 14 3 5 6 Stage of recovery Leg 4.0 1.3 5.5 1.0 4.1 1.2 3.4 1.2 Foot 3.1 1.4 4.8 1.3 3.2 1.2 2.5 1.2 Trunk 4.3 0.6 5.3 0.5 4.2 0.6 4.1 0.3 Time post-cva at initial assessment (d) 32.7 18.4 19.4 6.0 27.3 13.8 42.7 20.4 Time between testing (d) 27.5 6.7 25.0 5.2 30.4 8.4 26.1 5.2 NOTE. Values are mean standard deviation (SD) unless otherwise noted. Abbreviation: CVA, cerebrovascular accident. Experimental Procedure Berg Balance Scale. The BBS is composed of 14 tasks, graded on a 5-point scale, that require the subject to maintain a static position, to change the orientation of the center of mass with respect to base of support, and to diminish base of support. The BBS has been established as a valid and reliable tool for measuring functional balance in patients who present with cerebrovascular accident. Its reliability in patients with acute stroke is excellent (intraclass correlation coefficient [ICC].99). 14 Analysis of minimal detectable change suggests that a change of 6 points on the BBS is necessary to be 90% confident of genuine change in the patient s functional balance abilities. 15 Clinical outcome variables scale. The Clinical Outcome Variables Scale (COVS) is a functional mobility scale with 13 items (eg, rolling, transfers, ambulation) each measured with a 7-point scale (by a therapist) for a total score of 91. The reliability of the COVS has been established (ICC.97). 8 A clinically important change in COVS score is 5 of 91 points. 16 Gait speed. Gait speed was assessed by asking subjects to walk 7m at a comfortable walking pace. 17 Only the middle 5m were timed, allowing for alterations in velocity related to starting and stopping. Time was recorded by a digital stopwatch, measuring to the nearest.01 second, triggered to start and stop by 2 infrared beams and photosensors mounted on stands 3m apart in the middle of the walkway, at a height of 1.2m above floor level so that the sensors would not be triggered by walking aids or the subject s hands. Subjects used the same walking aid on both testing sessions. Four subjects were unable to walk 7m during the first testing; a gait speed of 0m/s was recorded for these subjects on initial testing. A digital stopwatch has been shown to have high reliability of determining gait speed (Pearson product correlation.97). 18 Chedoke-McMaster Stroke Assessment Impairment Inventory. Stages of recovery of the leg, foot, and postural control were assessed by using the Chedoke-McMaster Stroke Assessment (CMSA) Impairment Inventory. The CMSA provides an indication of the level of impairment of motor control at admission. High intrarater (r range,.94.98) and interrater (r range,.85.96) reliability have been reported for the CMSA Impairment Inventory items. 19 Physiologic Measures Each subject wore a safety harness 20,21 and stood on a force platform (OR6-5-1 a ) in a standardized stance (feet approximately 18-cm apart). A linear accelerometer a was taped to the web space between the first and second digits of each subject s nonparetic arm to measure the peak tangential arm acceleration during the upper-extremity flexion movement. Activity of bilateral hamstrings and soleus was recorded by using surface electromyography technology. b For each muscle group, 2 surface electrodes (diameter, 0.8cm) were placed vertically in the midline of the distal third of the muscle. The force platform measure of postural control in quiet stance was recorded in 5 trials of 20 seconds in duration. Each subject was instructed to look straight ahead and stand as still as you can. Rest periods between trials were allowed if necessary. Internally produced perturbations to standing balance were examined by having each subject perform a rapid forward arm flexion movement of the nonparetic arm and then maintain the elevated position until instructed to return to the starting position. The instruction, when you are ready, swing your arm as fast as possible over your head and hold it there was given to each subject. After a couple of practice trials, 20 trials were performed with rest periods of 15 to 30 seconds between trials. Subjects were allowed to sit as often as necessary to prevent fatigue. Data Analysis BEDAS-2 software, version 3.11, a was used to determine the COP. The COP measurement was obtained from the force platform for 0.5 second before movement and for 1.5 seconds after movement onset. The velocity of the COP excursion was selected as the outcome for the force platform component based on the recommendations of 2 reliability studies of force platform indicators of postural control. 22,23 COP excursion was sampled at 50Hz. Electromyographic signals were amplified and filtered (10 2000Hz). Acceleration and electromyographic signals were recorded on videotape c for off-line digitization (sampling rate, 5000Hz). Electromyographic data were rectified and averaged by using DataWave Technologies software. d The presence of an electromyographic burst was determined when the electromyographic amplitude became greater than twice that found for baseline activity. The onset of the burst was defined as the point when the amplitude exceeded the upper limit of the baseline tracing. All latencies were calculated relative to the onset of movement that was defined as the point where progressive increases in arm acceleration were observed by using

STANDING BALANCE AFTER STROKE, Garland 1755 Table 2: Outcome Measures at Admission and After 4 Weeks of Rehabilitation Outcome Measure Time Overall Group I Group IIa Group IIb BBS (/56) Admission 28.3 11.7 45.0 4.5* 26.1 9.4 23.1 9.2 Retest 42.2 10.1 53.6 3.0* 44.6 7.8 35.5 8.6 COVS (/91) Admission 56.9 12.5 73.2 6.9* 54.8 8.5 51.8 11.8 Retest 70.2 11.0 83.6 4.7* 71.1 9.6 68.9 8.8 Gait speed (m/s) Admission 0.38 0.42 0.76 0.32* 0.28 0.2 0.31 0.52 Retest 0.60 0.41 1.10 0.46* 0.54 0.29 0.44 0.33 COP velocity quiet stance (cm/s) Admission 0.84 0.24 0.63 0.18* 0.81 0.17 0.95 0.27 Retest 0.71 0.17 0.59 0.14 0.69 0.11 0.77 0.19 COP velocity during arm raise (cm/s) Admission 2.06 0.49 1.97 0.48 2.13 0.42 2.04 0.56 Retest 2.14 0.62 1.93 0.34 2.12 0.30 2.26 0.86 Arm acceleration (m/s 2 ) Admission 12.4 9.4 24.0 15.3* 10.2 4.4 9.4 5.5 Retest 18.2 11.1 30.6 13.3* 17.0 9.3 14.0 8.2 Ipsilateral hamstrings EMG burst area (AU) Admission 2.19 1.02 3.21 1.20* 2.07 1.00 1.87 0.72 Retest 2.73 1.23 3.46 1.44* 2.61 1.35 2.52 0.99 Contralateral hamstrings EMG burst area (AU) Admission 1.46 0.52 2.09 0.70 1.48 0.38 1.19 0.26 Retest 2.16 1.10 3.02 1.85 2.26 0.94 1.73 0.61 Ipsilateral hamstrings EMG latency (ms) Admission 96.7 81.8 152.4 109.5* 99.7 47.8 66.1 83.4 Retest 146.3 78.6 198.0 104.0* 133.6 64.5 121.0 72.9 Contralateral hamstrings EMG latency (ms) Admission 0.67 90.8 37.2 48.2* 31.2 98.0 49.6 110.0 Retest 42.6 86.8 84.8 53.8 77.1 61.6 37.8 97.6 NOTE. Values are mean SD. Abbreviations: AU, arbitrary units; EMG, electromyographic. *Group I differed significantly from group IIa and IIb. Retest differed significantly from admission. the same criteria as for the electromyographic burst onset. The full-wave rectified electromyographic signal was integrated, and the area for 1 second was calculated for the quiet stance and arm raise task. The electromyography area for 1 second in quiet stance was used to normalize the electromyography area of the bursts of the corresponding muscle during the arm raise task. Trials were excluded from the data analysis on the basis of obvious movement artifacts or technical problems. Trials were also excluded if the magnitude of peak arm acceleration for an individual movement was less than 2 standard errors below the person s mean acceleration (on average, 1 2 trials per testing). Only 1 subject was not able to complete all 20 arm movements. The averages for this subject were from 8 and 10 trials at admission and retest, respectively. All subsequent analyses were performed on the average of the remaining trials. Subjects were characterized with descriptive statistics. For the total group, paired t tests were used to compare the admission testing and the 4-week retesting for the 6 outcome measures (BBS, COVS, gait speed, COP velocity, arm acceleration, electromyographic latency). Subgroups were assessed by using 2-way repeated-measures analysis of variance (ANOVA) with time (admission, 4-wk later) and group (I, IIa, IIb) as factors for each of the 6 outcome measures. Significant interactions were assessed with Scheffé post hoc comparisons. One-way ANOVA with Scheffé post hoc comparisons were used to examine the differences in subject characteristics across groups at initial testing. Associations between variables were determined with Pearson correlations. All statistical procedures were carried out by using SPSS software e with a significance level set at P equal to.05. RESULTS The subject characteristics are presented in table 1 with the initial assessment values (mean standard deviation) for each of the outcomes. Twenty-seven subjects (17 men, 10 women), aged 34 to 84 years, were assessed initially approximately 1 month after the stroke (32.7 18.4d) and reassessed approximately 4 weeks later (27.5 6.7d). The subjects exhibited moderate impairment in postural control and lower-extremity motor control. Functional Measures All subjects showed an improvement in functional balance (BBS) and mobility (COVS) of 14 7.1 points and 13 7.3 points, respectively, over the course of the 4 weeks of rehabilitation (P.001). Gait speed in the total group also increased significantly by.22.25m/s (P.001), an increase of 58%. Physiologic Measures After a month of rehabilitation, patients were able to stand quietly on the force platform with a significantly reduced COP velocity of.13.15cm/s, indicating less postural sway (P.001) (table 2). In the arm raise task, there was a significant increase in arm acceleration of 5.8 6.0m/s 2 (P.001) (table 2). This internal perturbation to balance was associated with a significant decrease in the latency of hamstring activation by 60.4 47.1ms and 39.8 71.9ms on the nonparetic (ipsilateral) and paretic (contralateral) leg, respectively, indicating an improvement in the feed-forward anticipatory response to the upper-extremity flexion movement (P.001). The soleus muscle group did not show statistically significant change because only 15 of 27 and 12 of 27 subjects had bursts in soleus muscle on the first testing in the nonparetic and paretic legs, respectively (fig 1). Figure 1 clearly shows the leftward shift in hamstring latency toward a more feed-forward (anticipatory) response. Furthermore, it shows that many subjects gained the ability to produce an electromyographic burst on retesting. Because the hamstring muscle was the prime muscle in producing a feed-forward response to the arm raise perturbation, 10,11 we looked more closely at these data. Subjects could be categorized into subgroups based on functional balance

1756 STANDING BALANCE AFTER STROKE, Garland Fig 1. (A) The latency of the muscle burst in ipsilateral (nonparetic) and contralateral (paretic) hamstrings (HAMi, HAMc) and soleus (SOLi, SOLc) muscles. Data from each subject are presented in separate rows (admission, F; retest values after 4wk of rehabilitation, E). The solid line at time 0 represents the time at which the forward arm movement started (ie, onset of arm acceleration). Muscle groups that were activated in a feed-forward anticipatory fashion have negative latencies and muscle groups that were activated in a feedback manner have positive latencies (after the arm begins to move). If the arm movement was not associated with any muscle burst, this is denoted by an, placed arbitrarily at 400ms when there is no burst at either testing. If there was no burst at admission but there was at retest, the symbol is placed beside the retest latency. (B) The mean values for all subjects. Note the improved feed-forward control of hamstrings muscles after rehabilitation, indicated by significantly more negative latencies. scores and changes in paretic hamstrings electromyographic latency. Five patients (group I) were functioning at a high level at admission to rehabilitation (tables 1, 2). They had initial BBS scores above 40, COVS scores above 70, and a gait speed twice as fast as group II. The top panel in figure 2A shows that all patients in group I improved on the BBS and had at least a 20-ms increase in the feed-forward response of hamstrings bilaterally in the arm raise task. Improvement in both measures is reflected in the diagonal arrows pointing up and to the left. The other 22 patients (group II) had lower scores on the outcome measures than group I, with a mean initial BBS score just over 20 seconds, COVS score at about 50 seconds, and gait speed of only 0.3m/s (table 2). Half of the patients in group II improved on the BBS and showed at least a 20-ms increase in the paretic hamstrings electromyographic latency (group IIa), but half improved only on the BBS (group IIb) (figs 2B, 2C). Note that although group IIb showed less improvement on the BBS than the other 2 groups, that group showed similar improvement in gait speed and COVS scores (table 2). Group IIb were admitted to rehabilitation later than group I (42.7 20.4d poststroke vs 19.4 6.0d, P.04) with a tendency to be admitted later than group IIa (42.7 20.4d poststroke vs 27.3 13.8d, P.10) (table 1). Because the patients had a wide range in postural control at admission, it was not possible in our experiment to standardize the arm acceleration in the arm raise task across patients and across testing sessions. It was hypothesized that an increase in arm acceleration after rehabilitation would be an indicator of improved balance and improved confidence. We were curious as to how much of the improvement in electromyographic activation could be attributed to the increased arm acceleration 24 versus improved physiologic function. This cannot be answered directly with our present design, but we have 3 indicators that the arm acceleration alone does not dictate the electromyographic improvement in this study. First, both group IIa and IIb had a similar improvement in arm acceleration, yet there was no improvement in the electromyographic latency in the paretic leg in group IIb. Second, some subjects in each group showed little change in arm acceleration between the 2 testings, yet the electromyographic latency increased to more feed-forward values after rehabilitation (eg, fig 3). Third, some subjects in group IIb (fig 3) had substantial increases in arm acceleration without change in the electromyographic latency on the paretic side. Furthermore, these patients had a large increase in the size and latency of the nonparetic hamstrings burst, suggestive of a compensatory strategy. Thus, we are confident that the electromyographic changes are a true reflection of changes of physiologic function. Correlation Between Functional and Physiologic Measures We sought to determine whether any of the initial functional measures correlated with final physiologic measures. For the correlation analysis, we used the entire group of 27 subjects. We found that the COP velocity in quiet stance at retest correlated with the initial leg stage of recovery (r.40) and the initial postural control stage of recovery (r.41). The arm acceleration at retest correlated with the BBS at admission (r.38) and the initial postural control stage of recovery (r.44). In addition, the latency of the paretic hamstrings at retest correlated with the initial leg and foot stages of recovery at admission (r.47, r.43, respectively).

STANDING BALANCE AFTER STROKE, Garland 1757 Fig 2. The relationship between the functional balance data and the physiologic measures of standing balance for each subject in (A) group I, (B) group IIa, and (C) group IIb. The BBS score is on the y axis and hamstring latency is on the x axis with ipsilateral (nonparetic) values on the left and contralateral (paretic) data on the right. Closed circles (F) represent data taken at admission; retest measurements are in open circles (E); and indicates no burst. Arrows are placed between the admission and discharge data for each subject to enable visualization of change over time. Diagonal arrows going up and to the left indicate improvements in both functional and physiologic measures of standing balance. Arrows going vertically up indicate improvement in functional balance without concomitant improvement in physiologic indicators of standing balance. DISCUSSION Postural control and functional mobility are key focus areas for therapeutic intervention after acute stroke. 25 Our study concurs with previous investigations and clinical observations 6,26 confirming that significant improvement in clinical measures of balance, mobility, and gait are observed with inpatient rehabilitation after acute stroke. The improvements established over the 4 weeks of rehabilitation were not only statistically significant, but also clinically meaningful. The mean improvements of 14 of 56 points on the BBS and 13 of 91 points on the COVS far exceeded the minimum of 6 and 5 points, respectively, necessary for clinically important change in the functional balance and mobility of patients after stroke. 15,16 Improvements in function have been ascribed to true physiologic recovery when the patient more closely approximates normal balancing responses, compensatory strategies, or a combination of both. Compensatory motor patterns are adaptive movements that reflect the effects of the lesion, the mechanical characteristics of the motor system, and the environmental demands on the individual. 27 Clinically based functional measures cannot differentiate between physiologic recovery and compensatory strategies. Electromyographic and force platform measures of postural stability provide 1 way to

1758 STANDING BALANCE AFTER STROKE, Garland Fig 3. A representative subject from (A) group I, (B) group IIa, and (C) group IIb is presented with admission data as a solid line and retest data as a dotted line. In each panel, the top trace is arm acceleration during the forward arm raise, the bottom 2 traces are the ipsilateral (nonparetic) and contralateral (paretic) hamstrings electromyographic burst. The dashed line at time 0 represents the onset of arm acceleration. Note the improved feed-forward response in both nonparetic and paretic hamstrings bursts in group I despite a lower arm acceleration. In group IIa, the subject had an improved electromyographic burst in the paretic hamstrings muscle without any notable change in arm acceleration. In group IIb, the subject was able to raise the arm with increased acceleration, accompanied by a large increase in the nonparetic hamstrings and little change in the paretic hamstrings. This represents a compensatory strategy involving the nonparetic limb. measure physiologic recovery of standing balance. For example, Kirker et al 28 applied lateral perturbations to the pelvis when standing to examine the electromyographic responses and ground reaction forces serially in 13 patients after acute stroke (first testing median, 6wk; last testing median, 16wk). They found evidence of compensatory strategies, namely, overuse of the nonparetic musculature. Whereas Kirker 28 evaluated patients who showed slow clinical recovery at longer intervals than those who progressed quickly, our study evaluated all patients 1 month apart. When the 27 subjects were analyzed as a group, subjects showed significant improvement on physiologic measures over the 1-month period. They had less postural sway as they stood quietly on the force platform. During the arm raise task, they were able to move their nonparetic arm with greater acceleration and with an earlier activation of their nonparetic and paretic hamstring muscles, showing improvement in the feedforward response to the arm raise perturbation. It was clear that both functional measures of balance and mobility and physiologic measures of postural control improved significantly over the 4 weeks. When normal subjects performed this task (unilateral upperextremity elevation to horizontal as quickly as possible), ipsilateral hamstrings muscle preceded the onset of movement by 205ms. 29 Patients in our study exhibited ipsilateral (nonparetic) hamstring activity that approximated that of normal subjects on retest (overall and group I means, 146.3 78.6ms, 198.0 104.0ms, respectively), but not at admission (overall mean, 96.7 81.8ms). In normal subjects, the contralateral hamstrings muscle was activated later than the ipsilateral muscle, but still before movement onset by approximately 40ms. 29 Furthermore, the probability of recording an electromyographic burst in the contralateral hamstring muscle was.98. 29 Only 70% of patients in our study exhibited an electromyographic burst in the paretic (contralateral) hamstring muscle during initial testing; this burst occurred with an overall mean onset of 0.67 90.8ms, that is, coincident with the onset of movement. This changed to anticipatory muscle activation at retest (overall mean, 42.6 86.8ms; 93% of patients demonstrated a burst), with the exception of subjects in group IIb. When the subjects were divided into subgroups, based on their BBS scores at admission, we found 12 patients (group IIb) with low initial BBS scores whose paretic musculature did not improve over the course of rehabilitation despite significant improvement in BBS and COVS at retest (fig 2). According to our hypothesis, this combination of functional change without physiologic change was indicative of the use of compensation. Note also that these patients demonstrated significantly more feed-forward activation of the nonparetic hamstrings muscle with the arm raise perturbation. This pattern of activation is consistent with previous reports of the use of a compensatory strategy. 28 Preference for initiating a stabilizing response with the nonparetic lower extremity for postural stability has been reported in subjects with chronic hemiplegia as result of stroke. 29,30 The remaining 10 subjects (group IIa) with low BBS scores at admission showed significant improvement in the feed-forward activation of the paretic hamstrings without significant change in the nonparetic side (table 2). This pattern of activation is consistent with true physiologic recovery. Associations have been found between measures of motor recovery by using the Fugl-Meyer Assessment and physiologic measures of postural stability on a single occasion. 31,32 The sample size in our experiment limits the extent to which we can determine the initial subject characteristics that may influence physiologic recovery. Nevertheless, there was a statistically significant correlation between the BBS score at admission and

STANDING BALANCE AFTER STROKE, Garland 1759 the arm acceleration at retest. The correlation coefficient was relatively weak (r.38), and it is possible the ceiling effects of the BBS negatively impacted this relationship, particularly in group I. 33 The admission stages of recovery of the leg and foot as measured by the CMSA Impairment Inventory correlated with the latency of the paretic hamstrings electromyographic burst at retesting. This supports the common assumption that low levels of motor control in the lower extremity negatively impact the ability to produce effective postural responses to internal perturbation. CONCLUSION This study showed that force platform and electromyography technology can be useful in differentiating between physiologic improvements in postural control and compensatory strategies that may underlie improvements in functional outcome scores. 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