| | Recovery of Standing Balance and Health-Related Quality of Life After Mild or Moderately Severe StrokePreliminary data presented to the World Congress in Physical Therapy, June 3, 2003, Barcelona, Spain. Abstract Garland SJ, Ivanova TD, Mochizuki G. Recovery of standing balance and health-related quality of life after mild or moderately severe stroke. ObjectiveTo examine the physiologic and functional recovery of standing balance and health-related quality of life (HRQOL) in people after mild and moderate stroke. DesignInception cohort study with evaluations at 1 month and 3 months poststroke. ParticipantsTwenty-nine volunteers who had sustained a stroke. Subjects were categorized into mild and moderate groups. InterventionsNot applicable. Main Outcome MeasuresFunctional balance was assessed (Clinical Outcome Variables Scale [COVS]) and physiologic measures (electromyography, postural sway) were taken when subjects stood quietly on a force platform and when they performed a rapid unilateral arm-raise perturbation. The Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36) was administered to evaluate HRQOL. ResultsSubjects in the mild group were approaching maximal scores on the COVS (87.7±4.1/91) at 3 months poststroke, yet had significant impairment in paretic muscle activation patterns when compared with healthy subjects. Subjects in the moderate group had increased paretic muscle activation over the 2 months, accompanied by significant increases of 10.7±5.9 points on the COVS. For both groups, there was significantly less postural sway on the paretic than the nonparetic leg and significant improvements in the SF-36 (physical component) over time. ConclusionsSubjects recovering from a stroke showed a significant improvement in physical HRQOL and functional and physiologic balance, yet the physiologic balance recovery was not complete even in the mild group. PATIENTS UNDERGOING REHABILITATION form a select group of patients after stroke.1 These patients fall into a “middle band” with moderately severe strokes and significant hemiparesis, other impairments, or environmental factors that require an extended rehabilitation experience. There is evidence that functional balance ability increases after 1 month of rehabilitation in this middle band of stroke patients.2, 3 People in the upper band with mild strokes or young age are typically managed at home and do not receive extensive rehabilitation services. It is not known whether these patients show physiologic impairments in standing balance or whether their physiologic balance responses change over time. No observational studies have been reported that describe the natural recovery of standing balance in people after mild stroke. Furthermore, although it is often assumed that improvements in functional balance and mobility will enhance a person’s quality of life (QOL), the relation between balance and QOL has yet to be established. There is a growing body of literature describing the use of posturography to explore the mechanisms underlying recovery of standing balance after stroke,4 yet there are relatively few longitudinal investigations2, 5, 6 of the ability of the central nervous system (CNS) to remodel muscle activation patterns in the recovery process after stroke. Those studies report shifts in latency of muscle activation to internally2 and externally produced5, 6 perturbations. Standing balance requires the activation of postural muscles; in response to perturbations, this activation must be fast enough and large enough to maintain stability. The deleterious effects of disuse and muscle weakness7, 8 may play a role in postural control after stroke, including a loss of fast twitch motor units that produce large forces with fast contraction times.9 Any loss of these fast twitch motor units might affect balance negatively because muscle force in the leg and trunk that must be produced quickly in response to internal or external perturbations is likely dependent on fast twitch motor units. Measures of electromyographic burst amplitude and burst slope may indicate whether there is any impairment in motor unit recruitment, separate from the latency of muscle activation. The reorganization of muscle activation patterns associated with rapid single-arm movements in standing has been found in response to experimentally induced back pain.10 The feed-forward activation of deep trunk abdominal muscles was delayed or reduced in amplitude both under conditions of acute pain10 and in subjects with chronic back pain (who were pain-free at the time of testing), suggesting a compensatory motor control strategy.11 Indeed, even anticipation of back pain delayed the activation of deep trunk abdominal muscles, consistent with a protective postural control strategy.12 The purpose of this study was to use an inception cohort design to investigate the recovery of standing balance, with emphasis on muscle activation patterns, and health-related QOL (HRQOL) in subjects after mild and moderately severe stroke. Preliminary results of this study have been presented in abstract form.13 Methods  Participants Thirty-two subjects (21 men, 11 women) aged 23 to 85 participated in the study (table 1). All subjects admitted to the London Health Sciences Centre, University Campus, for stroke between December 2001 and January 2004 were screened to determine suitability for the study within 1 week of their stroke. Subjects were excluded if they had (1) a bilateral stroke or a previous stroke in the other hemisphere because subjects needed 1 nonparetic arm to perform the force platform testing or (2) severe comorbidity that was likely to dominate the pattern of care and result in serious health decline or death within the study period (eg, metastatic disease, end-stage renal disease, cardiorespiratory disease). After this screening, all subjects were interviewed to determine if they met the inclusion criterion of unilateral hemiparesis as a result of stroke or had other exclusion criteria such as (1) coexisting peripheral neuropathies because these are known to affect postural responses,14 (2) acute musculoskeletal problems (ie, swollen ankle joint or shoulder tendonitis) that would impede the force platform testing, and (3) insufficient ability to communicate in English. All subjects who consented to participate were contacted again 3 weeks after stroke to arrange for initial testing at 1 month poststroke and to ensure that they had the ability to maintain independent unsupported stance for 20 seconds. At this point, some subjects were undergoing inpatient rehabilitation, whereas others were living in the community. The study was approved by the university ethics review board. Experimental Procedure Baseline measures of motor impairment and balance The level of motor impairment of the leg, foot, and postural control at 1 month after stroke was evaluated by using the Chedoke-McMaster Stroke Assessment (CMSA) Impairment Inventory.15 This Impairment Inventory has separate scales for the leg, foot, and postural control, with each scale being scored out of 7. Standing balance was evaluated functionally by using the Berg Balance Scale (BBS), a tool that has been established as valid and reliable for measuring functional balance in patients after acute stroke.16 The BBS is composed of 14 tasks, graded on a 5-point scale for a total score of 56, that require the subject to maintain a static position, change the orientation of the center of mass with respect to the base of support, and diminish the base of support. Functional balance and mobility Functional mobility was assessed with the Clinical Outcome Variables Scale (COVS), a scale with items ranging from rolling to ambulation of long distances.17 The COVS has 13 items, each measured with a 7-point scale for a total score of 91. Quality of life HRQOL was measured by using the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36).18, 19 It was administered by using a telephone interview by trained interviewers. This tool has proven reliability and validity and has been used extensively with people after stroke.20 The SF-36 has 8 subscales including physical functioning, physical role, bodily pain, general health, vitality, social functioning, emotional role, and mental health. All subscales, except bodily pain, were affected even with mild stroke.21 The SF-36 also has 2 summary scores: physical component summary (PCS) and mental component summary (MCS). The summary scores are norm based and set to a standard score of 50±10 points. Age- and sex-matched normative data for the SF-3622 were used to compare with those of subjects after stroke. Physiologic balance measures Each subject was fitted into a safety harness23, 24 and stood with each foot on a separate force platform.a The position of the feet was traced to enable them to be placed in the same position on repeated trials. A linear accelerometerb was taped to the web space between the first and second digits of each subject’s nonparetic arm to provide a measure of the peak tangential arm acceleration during the arm flexion movement. The activity of bilateral biceps femoris, soleus, rectus femoris, and tibialis anterior was monitored by using surface electromyography.b Two surface electrodes (diameter, 0.8cm) in a bipolar configuration were fixed in a vertical orientation approximately 2cm apart to the prepared skin of each site. Postural control in quiet stance was determined over 20-second trials in which each subject was instructed to “look straight ahead and stand as still as you can.” Five trials were performed with rest periods between trials as necessary. Next, each subject was asked to perform a forward shoulder flexion of the nonparetic arm as quickly as possible and hold the arm at shoulder height for 1 second before slowly returning the arm to the starting position. The instruction “when you are ready, swing your arm as fast as possible to shoulder height and hold it there” was given to each subject. After 1 or 2 practice trials, 20 arm-raise trials were performed with rest periods of 5 to 30 seconds between trials. Subjects were allowed to sit as often as they wished to prevent fatigue. Data Analysis Two force platforms (model OR6-6-1) with BioSoft software (version 2.00)a were used to determine the center of pressure (COP) for each leg. The area of the 95% confidence ellipse for COP position was selected as the outcome for the force platform component to represent the amount of postural sway (fig 1A). During quiet stance, the COP ellipse area and the vertical ground reaction force (Fz) on each leg were measured for the middle 10 seconds of the 20-second trial and averaged across the 5 trials. The ratio between the paretic and nonparetic side ground reaction forces was calculated to evaluate the weight distribution. During the arm-raise perturbation, the COP ellipse area (duration, 2s) was obtained from the force platform for 0.7 seconds before movement and for 1.3 seconds after movement onset (see fig 1A). In both the quiet stance and arm flexion conditions, force platform data were sampled at 100Hz. All electromyographic signals were amplified and filtered (10−2000Hz) and digitized by using Spike 2 (version 4.1) software.c A pulse produced by the force platform system at the beginning of each trial was recorded together with the electromyograms and was used to synchronize the recordings. All electromyographic and accelerometer data were digitized by using a sampling rate of 5000Hz. All signals were calibrated before analysis. Muscle activity was also recorded while subjects were sitting quietly. The amplitude of this signal would reflect the characteristics of the recording site (ie, electrode placement, skin resistance), separate from the characteristics of the signal that are related to recovery from stroke. The electromyographic signals in sitting did not differ significantly between groups or testing sessions, indicating that the recording conditions were comparable on all occasions. During quiet stance, the five 20-second trials were full wave rectified, averaged, and integrated; the mean area for 1 second is reported. On some occasions, subjects moved during a trial so these trials were excluded before averaging. For the arm-raise task, the 20 trials were averaged, relative to the onset of movement, which was defined as the point in which progressive increases in arm acceleration were seen (fig 1B, solid vertical line). The electromyographic and arm acceleration data were averaged for 2 seconds, from 0.7 seconds before movement onset to 1.3 seconds after the movement onset. Trials were excluded from the data analysis if there were obvious movement artifacts or mechanical problems. Furthermore, trials were excluded if the magnitude of peak arm acceleration for an individual movement was 2 standard errors (SEs) below the individual’s mean acceleration (on average, 1−2 trials per test). The presence of a burst in the muscle activity was determined when the amplitude of the electromyographic signal became greater than twice that found for baseline activity in the first 200ms of the trial (from 0.7 to 0.5s before the arm movement) (see fig 1B, filled trace). The onset of the burst was defined as the point when the amplitude exceeded the upper limit of the baseline tracing and a progressive increase of muscle activity was seen. The computer-generated onset times were verified with visual inspection of the data, as recommended by Hodges and Bui.25 The end of the burst was taken as the point when the falling phase of the burst was no longer progressive (ie, was interrupted by a steady level or increase in muscle activity) (see fig 1B, filled traces of bursts). The area of the burst and the baseline were recalculated for 1 second, and, subsequently, the area of the baseline was subtracted from the area of the burst to represent a modulation in muscle activation in response to the balance perturbation. The slope of the burst was calculated as the amplitude (from baseline to peak) divided by the duration of the rising phase of the burst (see fig 1B, dashed line). To report a slope measurement that was independent of the amplitude of the burst, the slope of the burst was divided by its amplitude. This normalized slope parameter was used for statistical analysis. All onset latencies of the electromyographic bursts were calculated with respect to the onset of arm acceleration (see fig 1B, dotted lines). Statistical Analysis Descriptive statistics were used to characterize the subjects. Subjects were divided into 2 groups according to the BBS score and CMSA leg and foot score at 1 month. Subjects who had a BBS score of 50/56 or higher and CMSA combined leg and foot scores of at least 12/14 were allocated to the mild group (n=14); the rest were allocated to the moderate group. The groups were assessed by using 2-way repeated-measures analysis of variance (ANOVA), with time (1mo and 3mo as the repeated measure) and group (mild, moderate) as factors for each of the following dependent variables: COVS, Fz ratio during quiet stance, arm acceleration, and QOL (PCS, MCS). Three-way repeated-measures ANOVAs were performed with time as the repeated measure and group and side (nonparetic, paretic) as factors for COP ellipse area and muscle activity parameters (area of electromyogram during quiet stance, burst latency, burst area, slope of burst) for each of the tested muscles. A Newman-Keuls multiple comparisons test was used for post hoc analyses.26 Independent Student t tests were used to examine the differences in subject characteristics between groups at the initial 1-month testing. One-way ANOVA was used to assess the differences in PCS and MCS scores among the subjects at 1 month poststroke, 3 months poststroke, and matched normative data, for each group separately. Associations between QOL and balance were determined for all subjects combined with Pearson correlations. All statistical procedures were performed by using SPSSd and SASe software with a significance level set at P equal to .05. All data presented in the text are mean ± standard deviation (SD). Data in figures are presented as mean ± SE. Results Thirty-two subjects participated in the study. Three subjects (2 men, 1 woman) did not return for the 3-month testing; 2 subjects were not interested in returning for retesting, and 1 subject was having an episode of acute knee pain unrelated to the stroke. Therefore, 29 subjects are included in the data analysis. Subjects were tested at 1 month poststroke (32.5±5.1d) and reassessed at 3 months (92.1±6.9d) after stroke. The subjects were categorized as having either a mild stroke or moderate stroke, a determination made on the basis of functional and impairment scores at 1 month (see Methods). Subjects in the moderate group (n=15) received, on average, 1 month of inpatient rehabilitation services (24.5±22.3d) after the initial 1-month testing, whereas the mild group received only 4.1±8.7 days. Consistent with the results of Garraway et al,1 the mean age of subjects in the mild group (52.8±15.2y) was significantly less than those in the moderate group (64.9±13.2y). The subject characteristics are found in table 1. Functional Balance and Mobility The 2-way ANOVA revealed a significant effect of time and group, with subjects in the mild group scoring significantly higher than subjects in the moderate group. Subjects in the mild group had a significant improvement on the COVS of 3.6±5.4 points over the 2-month period. There was no significant change (1 point) in the BBS scores; subjects in the mild group had a mean of 54.8/56 at the 1-month testing. All subjects except 3 (who scored 55) scored 56/56 at the 3-month testing. Because of this ceiling effect, the BBS score was not used as a primary outcome measure. Subjects in the moderate group had significant improvements in functional balance and mobility measures with change scores of 10.7±5.9 points and 8.7±7.4 points on the COVS and BBS, respectively (table 2). Health-Related Quality of Life Twenty-four subjects completed the SF-36 questionnaires at both the 1- and 3-month tests; 5 subjects could not be reached by the telephone interviewer at one of the tests. There was a significant effect of time and group for the PCS, with the mild group having significantly higher scores than the moderate group. In contrast, the MCS scores did not differ significantly by time or group. At 1 month, subjects in the mild group (n=13) had PCS scores of 38.3±9.1 (see table 2), and there was a small but significant improvement in the PCS scores of 3.7±8.4 at 3 months poststroke. In the moderate group (n=11), the PCS scores at 1 month (32.9±7.6) increased significantly by 3.7±4.9 points. The PCS scores for both groups at 1 month and 3 months were significantly lower than that found in normative data in Canada.22 The average PCS scores for age- and sex-matched healthy subjects in the 2 groups were 50.0±3.4 and 47.2±4.0 points, respectively. There was no difference in the MCS scores between age- and sex-matched healthy subjects and subjects after stroke in either group. Physiologic Balance Measures For quiet stance, the 3-way ANOVA revealed a significant effect of time, group, and side, with subjects in the mild group having significantly less sway, as measured by the COP ellipse area, than subjects in the moderate group and the paretic leg having significantly less sway than the nonparetic leg. Both groups showed a significant reduction in the COP ellipse area at 3 months (except for the paretic side in the mild group), indicating less postural sway and better balance than at 1 month (table 3). When the ratio between the ground reaction forces under both legs was analyzed, it was shown that subjects in the moderate group bore more weight through the nonparetic side, whereas subjects in the mild group showed more even weight distribution during standing. The pattern remained unchanged for both groups at 3 months (see table 3). Overall, the muscles on the paretic side were significantly less activated compared with the nonparetic side during quiet standing (fig 2). There was a significant interaction between group and time for all the muscles (ie, the subjects in the mild group maintained the upright posture with less muscle activation on the nonparetic side than the moderate group at 1 month, but the moderate group displayed a significant reduction in the muscle activation, except for soleus, on the nonparetic side at 3 months, indicating better postural control). During the arm-raise perturbation, there was a significant effect of side (with the paretic side having less sway than the nonparetic side) but no significant effect of group or time in the COP ellipse area. There was a tendency (P<0.1) for subjects in the mild group to have less sway than the moderate group at 1 month and for moderate group to show a reduction in the COP ellipse area on the paretic side at 3 months. Figure 1 shows the COP excursion in a single subject during an arm-raise perturbation. The COP ellipse area is a composite of the lateral and anteroposterior sway, and the lateral sway is noticeably larger on the nonparetic side. There was a significant effect of time and group in arm acceleration of the arm-raise perturbation, with subjects in the mild group producing higher arm acceleration than subjects in the moderate group. A significant increase of 9.5±13.9m/s2 was observed for the mild group; the acceleration changing from 44.4±19.0m/s2 at 1 month poststroke to 53.9±19.0m/s2 at 3 months poststroke. For the moderate group, the arm acceleration significantly increased by 7.0±10.6m/s2 at 3 months poststroke, from 31.3±12.4m/s2 to 38.2±16.8m/s2. Figure 3 summarizes the data for the electromyographic burst area. The number of subjects showing bursts of activity in each muscle is shown within the bars in figure 3. An electromyographic burst was consistently generated in the hamstrings muscle on the paretic side (ie, in all but 1 subject in the moderate group at 1 month poststroke). The burst areas were significantly larger on the nonparetic than the paretic sides. Although the areas of the bursts were not compared across muscles with statistical analyses, the magnitude of the muscle activity in the ankle muscles appeared smaller than the hip musculature. The paretic soleus burst area and the nonparetic tibialis anterior burst area were significantly larger in the moderate group than in the mild group at 3 months. The moderate group showed a significant increase in the burst area of all 4 muscles on the paretic side at 3 months, whereas the mild group had significant increases in the paretic tibialis anterior muscle and the nonparetic quadriceps. The data for burst slope are presented in figure 4. Similar to the area of the burst, the burst slope was significantly larger on the nonparetic than the paretic sides and significantly larger in the mild than the moderate group. More specifically, the paretic hamstrings and quadriceps burst slopes were significantly larger in the mild than the moderate group at both 1 month and 3 months poststroke, as well as the nonparetic hamstrings burst slope at 1 month poststroke. There was a significant increase in the burst slope in the paretic soleus muscle in the moderate group and the paretic hamstrings and the nonparetic soleus muscles in the mild group between 1 month and 3 months poststroke. Note that even though the slope of the soleus muscles increased substantially at 3 months poststroke, the magnitude of the burst remained quite small, just above baseline. Figure 5 summarizes the latency results for all muscles. There was no significant difference in the latencies of the bursts between groups; this is evident by the overlap in values between the mild (squares) and moderate (diamonds) groups. There was a significant decrease in the latency of hamstring activation at 3 months poststroke of 25.3±49.6ms for the nonparetic (ipsilateral) leg in the mild group, indicating an improvement in the feed-forward response to the arm raise perturbation (P<.001). On the paretic side, there was no significant difference in the latency of muscle activation at 3 months poststroke in any muscle or group. To show further the muscle activation patterns during an arm raise perturbation, Fig 6, Fig 7 depict individual subject data. Balance is maintained by the orderly activation of posterior and anterior muscle groups (eg, from a healthy subject in fig 7). Figure 6 presents the data from 2 representative subjects at the 1-month testing. The subject in the moderate group showed limited feed-forward activation of leg muscles in advance of the arm movement and considerable cocontraction between the quadriceps and hamstrings muscles. The subject in the mild group produced more distinct and feed-forward bursts of muscle activity than the subject in the moderate group for an internal perturbation of comparable magnitude (similar arm acceleration). Both subjects showed a lack of coordination of muscle activation across the joint, particularly at the ankle joint when compared with the healthy subject in figure 7. Figure 7 shows the same subject in the mild group from figure 6 at the 3-month testing, in addition to data from an age- and sex-matched healthy subject performing the same task in a previous study.27 The subject at 3 months after stroke has BBS and COVS scores of 56/56 and 90/91, respectively. Despite this high level of motor recovery, he is moving his arm “as fast as he can” with an acceleration approximately 50% of maximal acceleration of the age- and sex-matched healthy subject. Comparing the individual poststroke with the healthy subject moving at 50% of maximal acceleration, the nonparetic hamstrings activation is similar between the 2 subjects, yet the rest of the electromyographic bursts have lower amplitude and altered timing in the individual poststroke. Comparing the 50% acceleration with the 100% acceleration in the healthy subject, the amplitude of the bursts scales with the magnitude of the perturbation but the timing of the bursts does not change significantly. Correlation Between Balance and QOL We sought to determine whether any of the functional or physiologic balance measures were correlated with HRQOL. Subjects in both groups were pooled for this analysis. We found moderate correlations between several baseline and functional balance measures and the PCS scores at 1 month poststroke (table 4). Moderate correlations were observed also between PCS scores and some physiologic measures (see table 4, last 3 rows). There was no correlation between MCS scores and either functional or physiologic balance measures. The correlations were somewhat smaller at the 3-month retesting, possibly because of a reduction in the range of values at 3 months. There was no significant correlation between the change in PCS scores and either the initial (1mo) or the change in functional or physiologic balance measures. | | |  | Outcome Measure | Time | PCS | MCS | |
|---|
| BBS | 1 month | .51, P=.014 | −.22,P=.34 | | | | 3 months | .37,P=.087 | −.12,P=.55 | | | COVS | 1 month | .53,P=.01 | −.14,P=.53 | | | | 3 months | .56,P=.005 | −.12,P=.57 | | | Stage of recovery | 1 month | .46,P=.03 | −.30,P=.17 | | | Leg | 3 months | .39,P=.06 | −.17,P=.44 | | | Area of COP ellipse in quiet stance (cm2) | 1 month | −.40,P=.05 | .01,P=0.9 | | | Nonparetic side | 3 months | −.15,P=.47 | −.28,P=0.9 | | | Area of COP ellipse in quiet stance (cm2) | 1 month | −.35,P=0.1 | .07,P=.74 | | | Paretic side | 3 months | −.08,P=.72 | .07,P=.74 | | | Ground reaction force | 1 month | .42,P=.04 | −.18,P=0.4 | | | (paretic/nonparetic) | 3 months | .29,P=.17 | −.16,P=.46 | | | | |
Discussion The main findings of this study were (1) standing balance and QOL (physical component) improved over the 2-month period, (2) the CNS used a variety of ways to increase muscle activation for postural responses following stroke, and (3) subjects recovering from both mild and moderate stroke had significant impairment in muscle activation patterns when compared with healthy subjects and had significantly less postural sway on the paretic than the nonparetic leg. Functional balance and mobility improved over the 2-month period in both groups. The improvement on the COVS in the mild group was small (3 points) yet statistically significant. The moderate group, however, showed an 11-point improvement on the COVS. This improvement was somewhat smaller than that shown in other studies when comparing the change seen between admission and discharge from rehabilitation (17 points2; 22 points3) in subjects poststroke with similar admission scores as the 1-month scores in the current study. This raises the question whether there was a reduction in functional mobility and balance after subjects in the moderate group returned to living in the community for a month or so. It is difficult to interpret the changes in the COVS between the 2 groups because of the ordinal nature of the COVS and the fact that the 2 groups are functioning at different parts of the scale.28 At the top end of the scale (ie, from 84–87/91), the items are much more challenging (walking several blocks), and hence a 3-point improvement may well represent a meaningful change in the mild group. Although the functional balance scores and several of the force platform measures at 1 month were correlated with the physical component of the HRQOL scores, this relation remained significant at 3 months only for the COVS. Furthermore, the extent of improvement of the subject’s perception of QOL was not related to how much his/her mobility changed over the 2 months. At the outset of the study, we hypothesized that improvement in functional mobility would lead to improved QOL. The lack of a significant correlation in the change scores may indicate that the influence of impaired mobility on QOL is strongest in the acute phase poststroke (ie, 1mo) and wanes over time. An alternate explanation is that, given the significance level for the correlation between the change in COVS and that the change in PCS was P equal to 0.1, the study was underpowered to show statistically an important trend. Another important finding is that the physical component of the SF-36 was significantly lower than normative values in both groups and at both tests. This might be expected for those persons with moderate impairments, but it was true even for persons in the mild group, who at 3 months poststroke were functioning at high levels (near maximum BBS scores and COVS scores). Our data are consistent with previous studies in the literature. In Sweden, Jonsson et al29 evaluated 304 subjects 4 months poststroke and found very similar SF-36 scores to the present study: 36.9 and 47.0 for PCS and MCS, respectively. Suenkeler et al30 also compared subjects 3 months poststroke to normative German values and showed a reduced PCS but the same MCS. Hopman and Verner31 showed an improvement in 5 of the 8 domains of the SF-36 in people poststroke between admission and discharge yet equally significant declines in 5 domains between discharge and 6 months poststroke. In our study, only the physical component of QOL was negatively affected by stroke, and, although this improved significantly over time, it remained lower than normative values. The force platform data showed an improvement in the postural stability during quiet stance with a reduction in the COP ellipse area on the paretic and nonparetic sides. An interesting finding was that the postural sway was less in the paretic leg than the nonparetic leg in both quiet stance and during arm-raise perturbation. This has been reported infrequently in the literature. Ustinova et al32 reported that the sway was less on the paretic than the nonparetic leg and suggest that the subjects might be using a stiffening strategy to maintain postural stability. We hypothesized that if the subjects were trying to stiffen the paretic limb, there would be a significant amount of cocontraction of the anterior and posterior muscles. To explore this possibility, we compared the electromyographic areas in quiet stance (see fig 3). In figure 3, the most notable cocontraction at 1 month is in the moderate group in the nonparetic limb. Perhaps the decreased postural sway on the paretic side is resulting from the lower overall level of activation in the paretic muscles. According to Winter et al,33 the ankle plantarflexor muscles are generating about 25% of maximal voluntary contraction to maintain quiet stance. It is possible that motor unit remodeling in the paretic leg could result in force generation by using fewer higher-threshold motor units. Higher-threshold motor units have larger and faster twitch tensions that would result in a less fused force profile. The lower electromyographic activity in the paretic leg may involve lower-threshold motor units that would result in a smooth force profile, further reflected in the sway measurements. Although speculative, the fact that the paretic leg has a lower burst slope than the nonparetic leg is consistent with the hypothesis of early motor unit remodeling toward slower motor units. Several other studies have shown a reduction in postural sway over time by using posturography (4−8wk poststroke2; 1−52wk poststroke34). A 12-week balance training regimen, which started on average 10 weeks poststroke, resulted in improved lateral weight shift onto the paretic leg35 and reduced root mean square of the COP velocities in the lateral and anteroposterior directions.36 De Haart et al36 also showed that although there was a slight improvement in weight-bearing symmetry (evidenced by more weight bearing through the paretic leg) in the first 4 weeks of training, a residual paretic/nonparetic weight-bearing ratio of .90 persisted, despite continued improvement in the aforementioned variables. Two other studies performed in the acute phase after stroke revealed reduced weight bearing in the paretic leg during quiet stance37 and during translational movements of the force platform, primarily in subjects with left hemiparesis.38 In accordance with de Haart,36 we also showed that although there was a reduction in postural sway, the asymmetrical stance posture in the moderate group remained unchanged with a ratio of .87. A lower ratio of .80 was reported in patients at least 1 year poststroke,39 perhaps showing that this “habit” is very difficult to break. Clinically based functional measures and posturography are not designed to detect the physiologic recovery of the muscle activation required to perform postural tasks. This is particularly evident in figure 6, whereby the subject who scored virtually maximum points on the functional measures had significant impairment in muscle activation. The CNS may increase the effectiveness of muscle activation in a variety of ways. It might increase the speed of muscle activation by activating the postural muscles earlier, as seen by a shift in the burst latency, or it could change the recruitment and firing rate pattern of motor units, which might increase the slope of the muscle burst. It can increase the magnitude of the muscle activity, as seen by increasing burst amplitude and burst area with arm perturbations of increasing speed.27, 40, 41 It is evident from the current study that the CNS can modulate these electromyographic burst parameters independently of each other. Subjects after moderate stroke showed primarily increases in muscle burst area at 3 months poststroke, with little change in slope or latency, suggestive of an inability to recruit motor units quickly enough during postural tasks. Subjects after mild stroke tended to have a better ability to activate muscles quickly, as measured by burst slope, than their counterparts with more severe impairments. Perhaps an inadequate speed of muscle activation during postural tasks is more important in dictating the presence of compensatory weight-bearing strategies (see earlier) than the amount of postural sway. In a previous study, subjects undergoing rehabilitation after stroke showed significant improvements in hamstrings burst latency and burst area at discharge on the paretic and nonparetic sides.2 In the present study, there was no significant change in the burst latency of any muscle tested, with the exception of the nonparetic hamstrings muscle in the mild group. Instead, subjects in the moderate group increased the hamstrings burst area while subjects in the mild group increased the paretic hamstrings burst slope at 3 months poststroke. One possible explanation for the lack of change in burst latency is that the subjects were within normative limits for feed-forward muscle activation at 1 month. To assess this possibility, we compared the hamstrings muscle burst latency associated with unilateral arm raise perturbations (ipsilateral and contralateral) with normative data previously collected.27 The fastest unilateral arm raise perturbations were on average 77.8±25.3m/s2, and 50% movement acceleration was 39.6±13.2m/s2. Subjects in the present study were producing their fastest arm raise perturbations around 50% of fastest movement acceleration in healthy subjects. The mean hamstring latency in healthy subjects for the 50% movement speed was –179.6±31.4ms ipsilaterally and –9.8±25.2ms contralaterally. This compares with mean values on the ipsilateral (nonparetic) side at 1 month of –101.5±66.5ms and –123.1±57.0ms for the mild and moderate groups, respectively, and 26.8±47.5ms and 26.8±47.5ms on the contralateral (paretic) side for the mild and moderate groups, respectively. We have previously shown that the latencies of the muscle bursts were not significantly different between young and elderly healthy subjects.42 A difference in age between the subjects used for the normative data and the subjects with hemiparesis is not likely a factor mediating the difference in latency. Therefore, the lack of change in the burst latency in the subjects after stroke is not because they were already recovered. The improvement in arm acceleration was in the same range for the 2 studies so this cannot be an explanation for the lack of latency change. Subjects in the present study only had on average 4 days and 24 days of rehabilitation between tests in the mild and moderate groups, respectively. It is tempting to speculate that the rehabilitation process promotes improved activation of postural muscles that is not evident at 3 months when subjects are not receiving intensive rehabilitation. Marigold et al6 showed that community-based exercise training in patients at least 1 year poststroke was effective in producing shorter muscle activation latencies to platform perturbations in paretic ankle and knee muscles. Further research on the influence of rehabilitation on the retraining of muscle activation patterns following stroke is needed. Conclusions This study provides a comprehensive examination of the electromyographic and force platform measurements on the paretic and nonparetic limbs in people between 1 month and 3 months poststroke. Subjects recovering from mild and moderate stroke showed significant improvement in physical HRQOL and functional and physiologic balance, yet the physiologic balance recovery was not complete even in the mild group (relative to healthy age-matched controls). Further research is needed to determine whether interventions can be employed, particularly after mild stroke, to augment the recovery of muscle activation. Decreased postural sway on the paretic side appeared to be a function of decreased muscle activation and not an attempt to stiffen the limb for weight bearing. Suppliers Acknowledgments We gratefully acknowledge the contributions of Deborah Willems and the physiotherapy staff at Parkwood Hospital in participant recruitment. References 1. 1Garraway WM, Akhtar AJ, Smith DL, Smith ME. The triage of stroke rehabilitation. J Epidemiol Community Health. 1981;35:39–44.
CrossRef
2. 2Garland SJ, Willems DA, Ivanova TD, Miller KJ. Recovery of standing balance and functional mobility after stroke. Arch Phys Med Rehabil. 2003;84:1753–1759. Abstract | Full Text |
Full-Text PDF (148 KB)
|
CrossRef
3. 3Eng JJ, Rowe SJ, McLaren LM. Mobility status during inpatient rehabilitation: a comparison of patients with stroke and traumatic brain injury. Arch Phys Med Rehabil. 2002;83:483–490. Abstract | Full Text |
Full-Text PDF (132 KB)
|
CrossRef
4. 4Geurts AC, de Haart M, van Nes IJ, Duysens J. A review of standing balance recovery from stroke. Gait Posture. 2005;22:267–281. Abstract | Full Text |
Full-Text PDF (304 KB)
|
CrossRef
5. 5Kirker SG, Jenner JR, Simpson DS, Wing AM. Changing patterns of postural hip muscle activity during recovery from stroke. Clin Rehabil. 2000;14:618–626. MEDLINE |
CrossRef
6. 6Marigold DS, Eng JJ, Dawson AS, Inglis JT, Harris JE, Gylfadottir S. Exercise leads to faster postural reflexes, improved balance and mobility, and fewer falls in older persons with chronic stroke. J Am Geriatr Soc. 2005;53:416–423. MEDLINE |
CrossRef
7. 7Sharp SA, Brouwer BJ. Isokinetic strength training of the hemiparetic knee: effects on function and spasticity. Arch Phys Med Rehabil. 1997;78:1231–1236. Abstract |
Full-Text PDF (921 KB)
|
CrossRef
8. 8Engardt M, Knutsson E, Jonsson M, Sternhag M. Dynamic muscle strength training in stroke patients: effects on knee extension torque, electromyographic activity, and motor function. Arch Phys Med Rehabil. 1995;76:419–425. Abstract |
Full-Text PDF (788 KB)
|
CrossRef
9. 9McComas AJ, Sica RE, Upton AR, Aguilera N. Functional changes in motoneurones of hemiparetic patients. J Neurol Neurosurg Psychiatry. 1973;36:183–193. MEDLINE |
CrossRef
10. 10Hodges PW, Moseley GL, Gabrielsson A, Gandevia SC. Experimental muscle pain changes feedforward postural responses of the trunk muscles. Exp Brain Res. 2003;151:262–271. MEDLINE |
CrossRef
11. 11Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain (A motor control evaluation of transversus abdominis). Spine. 1996;21:2640–2650. MEDLINE |
CrossRef
12. 12Moseley GL, Nicholas MK, Hodges PW. Does anticipation of back pain predispose to back trouble?. Brain. 2004;127:2339–2347.
CrossRef
13. 13Willems DA, Garland SJ, Ivanova TD. Changes in standing balance during post stroke rehabilitation [abstract]. Physiother Can. 2001;53:S11. 14. 14Simoneau GG, Ulbrecht JS, Derr JA, Becker MB, Cavanagh PR. Postural instability in patients with diabetic sensory neuropathy. Diabetes Care. 1994;17:1411–1421. MEDLINE 15. 15Gowland C, Stratford P, Ward M, et al. Measuring physical impairment and disability with the Chedoke-McMaster Stroke Assessment. Stroke. 1993;24:58–63. MEDLINE 16. 16Berg K, Wood-Dauphinee S, Williams JI. The Balance Scale: reliability assessment with elderly residents and patients with an acute stroke. Scand J Rehabil Med. 1995;27:27–36. MEDLINE 17. 17Seaby L, Torrance G. Reliability of a physiotherapy functional assessment used in a rehabilitation setting. Physiother Can. 1989;41:264–271. 18. 18Ware JE, Sherbourne CD. The MOS 36-Item Short-Form Health Survey (SF-36). I. Conceptual framework and item selection. Med Care. 1992;30:473–483. MEDLINE |
CrossRef
19. 19Ware JE, Kosinski M, Keller SD. SF-36 Physical and Mental Health Summary Scales: a user’s manual. Boston: The Health Institute, New England Medical Center; 1994;. 20. 20Mayo NE, Wood-Dauphinee S, Cote R, Durcan L, Carlton J. Activity, participation, and quality of life 6 months poststroke. Arch Phys Med Rehabil. 2002;83:1035–1042. Abstract | Full Text |
Full-Text PDF (84 KB)
|
CrossRef
21. 21Duncan PW, Samsa GP, Weinberger M, et al. Health status of individuals with mild stroke. Stroke. 1997;28:740–745. MEDLINE 22. 22Hopman WM, Towheed T, Anastassiades T, et al.The Canadian Multicentre Osteoporosis Study Research Group Canadian normative data for the SF-36 health survey. CMAJ. 2000;163:265–271. MEDLINE 23. 23Harburn KL, Hill KM, Kramer JF, Noh S, Vandervoort AA, Matheson JE. An overhead harness and trolly system for balance and ambulation assessment and training. Arch Phys Med Rehabil. 1993;74:220–223. MEDLINE 24. 24Hill KM, Harburn KL, Kramer JF, Noh S, Vandervoort AA, Matheson JE. Comparison of balance responses to an external perturbation test, with and without an overhead harness safety system. Gait Posture. 1994;2:27–31.
CrossRef
25. 25Hodges PW, Bui BH. A comparison of computer-based methods for the determination of onset of muscle contraction using electromyography. Electroencephalogr Clin Neurophysiol. 1996;101:511–519. MEDLINE |
CrossRef
26. 26Klockars AJ, Sax G. Multiple comparisons. Beverly Hills: Sage; 1986;. 27. 27Mochizuki G, Ivanova TD, Garland SJ. Postural muscle activity during bilateral and unilateral arm movements at different speeds. Exp Brain Res. 2004;155:352–361. MEDLINE |
CrossRef
28. 28Merbitz C, Morris J, Grip JC. Ordinal scales and foundations of misinference. Arch Phys Med Rehabil. 1989;70:308–312. MEDLINE 29. 29Jonsson AC, Lindgren I, Hallstrom B, Norrving B, Lindgren A. Determinants of quality of life in stroke survivors and their informal caregivers. Stroke. 2005;36:803–808.
CrossRef
30. 30Suenkeler IH, Nowak M, Misselwitz B, et al. Timecourse of health-related quality of life as determined 3, 6 and 12 months after stroke (Relationship to neurological deficit, disability and depression). J Neurol. 2002;249:1160–1167. MEDLINE |
CrossRef
31. 31Hopman WM, Verner J. Quality of life during and after inpatient stroke rehabilitation. Stroke. 2003;34:801–805.
CrossRef
32. 32Ustinova KI, Goussev VM, Balasubramaniam R, Leven MF. Disruption of coordination between arm, trunk, and center of pressure displacement in patients with hemiparesis. Motor Control. 2004;8:139–159. MEDLINE 33. 33Winter DA, Patla AE, Rietdyk S, Ishac MG. Ankle muscle stiffness in the control of balance during quiet standing. J Neurophysiol. 2001;85:2630–2633. MEDLINE 34. 34Rogind H, Christensen J, Danneskiold-Samsoe B, Bliddal H. Posturographic description of the regaining of postural stability following stroke. Clin Physiol Funct Imaging. 2005;25:1–9. MEDLINE 35. 35de Haart M, Geurts AC, Dault MC, Nienhuis B, Duysens J. Restoration of weight-shifting capacity in patients with postacute stroke: a rehabilitation cohort study. Arch Phys Med Rehabil. 2005;86:755–762. Abstract | Full Text |
Full-Text PDF (227 KB)
|
CrossRef
36. 36de Haart M, Geurts AC, Huidekoper SC, Fasotti L, van Limbeek J. Recovery of standing balance in postacute stroke patients: a rehabilitation cohort study. Arch Phys Med Rehabil. 2004;85:886–895. Abstract | Full Text |
Full-Text PDF (139 KB)
|
CrossRef
37. 37Laufer Y, Sivan D, Schwarzmann R, Sprecher E. Standing balance and functional recovery of patients with right and left hemiparesis in the early stages of rehabilitation. Neurorehabil Neural Repair. 2003;17:207–213. MEDLINE 38. 38Ikai T, Kamikubo T, Takehara I, Nishi M, Miyano S. Dynamic postural control in patients with hemiparesis. Am J Phys Med Rehabil. 2003;82:463–469. MEDLINE |
CrossRef
39. 39Eng JJ, Chu KS. Reliability and comparison of weight-bearing ability during standing tasks for individuals with chronic stroke. Arch Phys Med Rehabil. 2002;83:1138–1144. Abstract | Full Text |
Full-Text PDF (119 KB)
|
CrossRef
40. 40Horak FB, Esselman P, Anderson ME, Lynch MK. The effects of movement velocity, mass displaced, and task certainty on associated postural adjustments made by normal and hemiplegic individuals. J Neurol Neurosurg Psychiatry. 1984;47:1020–1028. MEDLINE |
CrossRef
41. 41Lee WA, Buchanan TS, Rogers MW. Effects of arm acceleration and behavioral conditions on the organization of postural adjustments during arm flexion. Exp Brain Res. 1987;66:257–270. MEDLINE 42. 42Garland SJ, Stevenson TJ, Ivanova T. Postural responses to unilateral arm perturbation in young, elderly, and hemiplegic subjects. Arch Phys Med Rehabil. 1997;78:1072–1077. Abstract |
Full-Text PDF (769 KB)
|
CrossRef
a School of Physical Therapy, University of Western Ontario, London, ON, Canada b Department of Physiology and Pharmacology, University of Western Ontario, London, ON, Canada c Centre for Stroke Recovery, Sunnybrook Health Sciences Centre and the Toronto Rehabilitation Institute, Toronto, ON, Canada.  Reprint requests to S. Jayne Garland, PhD, Sch of Physical Therapy, Elborn College, University of Western Ontario, London, ON N6G 1H1, Canada.
Supported by the Heart and Stroke Foundation of Ontario (grant nos. NA4838, T5131) and the Canadian Stroke Network. 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. PII: S0003-9993(06)01531-0 doi:10.1016/j.apmr.2006.11.023 © 2007 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved. | |
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