Abstract
Background Postural responses are impaired after stroke, with reduced or delayed muscle activity in the paretic leg muscles.
Objective The efficacy of exercises emphasizing speed of movement in modifying postural responses to perturbations that were not practiced was investigated.
Design This was a dual cohort design.
Methods A convenience sample of 32 individuals with hemiparesis poststroke (mean number of weeks poststroke=11.3, SD=4.1) who were recruited upon discharge from an inpatient rehabilitation hospital and a control group of age- and sex-matched individuals who were healthy (n=32) performed a single session of exercise emphasizing speed of movement. To assess postural responses to internal perturbation, unilateral arm raise and load drop tasks were performed before exercises (pre-exercise), immediately after exercises (post-exercise), and 15 minutes after exercises (retention). The time to burst peak and area of the biceps femoris muscle (BF) electromyographic (EMG) activity in the arm raise task was measured with the arm acceleration and velocity of the center of pressure (COP) excursion. For the load drop task, the anticipatory EMG deactivation area of the BF was calculated. In both tasks, the vertical ground reaction forces were recorded for each leg separately.
Results Before exercise, EMG and force platform measures were smaller in the stroke group than in the control group. After exercise, the paretic BF time to burst peak decreased, the paretic BF EMG area increased, and the COP velocity increased in the arm raise task, as did the paretic BF anticipatory EMG deactivation area in the load drop task. The stroke group was weight bearing more symmetrically after exercises. Most changes were retained 15 minutes after the exercises.
Limitations The retention period was short, and there was no control group of individuals with stroke.
Conclusions The results of this efficacy study demonstrated that fast movement exercises improved postural responses to perturbations that were not practiced.
In the last 25 years, the stroke mortality rate has declined and the survival rate has increased,1 with stroke being a leading cause of long-term disability in the United States.2 Thus, more individuals are living with functional limitations that persist for years, including deficits in standing balance resulting from impairments in sensation, motor control, and coordination.3 Balance deficits are common after stroke and are associated with an increased risk of falling.4
Methods of studying standing balance have incorporated internal and external perturbations to postural equilibrium. The reaction to an internal perturbation is a postural response to adjust the center of mass (COM) with respect to the base of support in a feedforward manner to maintain equilibrium.5 An internal perturbation created by a unilateral arm raise in the sagittal plane to horizontal displaces the COM anteriorly and is countered by a postural response preceding the arm raise movement, which produces increased muscle activity in the hamstring, gastrocnemius, and erector spinae muscles. The postural response serves to counteract the destabilizing effects of the arm raise by predicting the size of the perturbation and producing an appropriate centrally programmed response.6
The arm raise internal perturbation has been well characterized in stroke.7,8 The ability to modulate the appropriate responses is impaired, with a delayed onset of muscle activity in the paretic biceps femoris (BF) and paraspinal muscles8,9 and a reduced electromyographic (EMG) BF burst area amplitude,8 suggesting a failure to coordinate the postural muscles with the voluntary movement. Although the acceleration of the arm raise is challenging to standardize across individuals, limbs, or sessions, another internal perturbation, the load drop task, can keep the size of the perturbation constant. This task, in which participants drop a standard load held with the arm extended horizontally, features an anticipatory reduction of EMG activity in the hamstring muscle.10–12
The ability to generate a fast movement with the paretic muscles poststroke is impaired, as evidenced by the inability to increase the EMG amplitude13 or to increase torque14–16 with increasing velocity of movement. There is considerable research to support resistance exercise to strengthen the paretic muscles,17–20 but there is less evidence to demonstrate that strength improvements transfer to functional activities unless the training is task-specific.21,22 In older adults, muscle power (the product of force and velocity) is a predictor of balance and functional mobility23–25; thus, speed of movement may be an important component to train after stroke to improve the postural responses necessary for balance. A systematic review of the impact of physical therapy on functional outcomes concluded that the effects were seen primarily in tasks directly trained26; yet transfer of motor learning to unpracticed tasks is paramount in rehabilitation.
The primary purpose of this study was to determine whether a single session of exercises emphasizing speed of movement improves postural responses associated with internal perturbations in individuals poststroke. A secondary aim was to determine whether there was short-term retention of any improvements. We hypothesized that, after the exercise, there would be faster and larger muscle activation accompanied by an increase in center of pressure (COP) velocity in the arm raise task and more anticipatory EMG deactivation in the load drop task. We further hypothesized that any changes would be retained when tested 15 minutes later.
Method
Participants
Thirty-two individuals with hemiparesis were recruited upon discharge from an inpatient rehabilitation hospital from April 2006 until July 2009. Participants were included if they could stand independently for 1 minute and had no other neurological, cardiac, musculoskeletal, or respiratory conditions that interfered with the study protocol. A control group of 32 individuals who were healthy and matching the stroke group for age and sex was recruited from the University of Western Ontario and the Retirement Research Association. A control group was used, as opposed to a stroke group with no intervention, because this was an efficacy study to determine whether changes could be evoked in a single session. As there are limited data in the literature on the motor control of squatting and protective stepping, a control group of individuals who are healthy would provide information on EMG and COP responses. All participants were informed of study procedures and gave written consent according to the policies of the Review Board for Health Sciences Research Involving Human Subjects at the University of Western Ontario.
Procedure
In describing the study sample characteristics, functional balance was assessed in all participants with the Berg Balance Scale (BBS), which comprises 14 tasks scored on a 5-point scale. The tasks include maintaining static position, altering the COM with respect to the base of support, and reducing the base of support. The BBS has been established as a valid and reliable measure of functional balance in people poststroke.27 In the stroke group, motor recovery and sensation were assessed. The Chedoke-McMaster Stroke Assessment (CMSA) impairment inventory for the leg and foot was used to assess motor recovery. The leg and foot items of the CMSA measure motor recovery on a 7-point scale, with 1 representing no recovery and 7 representing complete recovery.28 The scores were combined to give a maximum score of 14. Cutaneous sensations of the plantar aspect of the foot and ankle proprioception were evaluated according to standard clinical procedures.29
Participants performed an exercise protocol of fast movements: 50 squats and 50 steps.30 Briefly, this protocol involved performance of small squats to about 30 degrees of knee flexion, emphasizing a quick downward movement and steps with both legs in which individuals leaned forward until they felt they were going to lose their balance and then took one protective step. The effects of the exercise protocol on remodeling muscle activation patterns have been reported previously.30
The anticipatory postural responses in standing were tested before the exercises (pre-exercise), immediately after the exercises (post-exercise), and 15 minutes after the exercises (retention), using 2 internal perturbation tasks: unilateral arm raise and load drop tasks. Participants performed 10 trials of the arm raise of the nonparetic arm (or dominant arm in the control group) to horizontal as fast as possible. Participants were allowed to sit during the session if required to prevent fatigue. Participants also performed 10 trials in which they dropped a 2.2-kg load that was held in the nonparetic hand (or dominant hand in the control group) with the arm extended horizontally in front of them.
All participants wore a safety harness that did not provide body-weight support and stood with their feet on 2 adjacent AMTI OR6–6–1000 force platforms (Advanced Mechanical Technology, Watertown, Massachusetts). Participants were asked to stand in a comfortable position, and the outlines of the feet were traced on paper taped to the force platform to ensure they assumed the same position on the force platform in each of the 3 testing occasions.
The EMG activity was recorded using differential sensors (DE-2.3, Delsys Inc, Boston, Massachusetts), 1.0- × 0.1-cm strips with a fixed inter-electrode distance of 1 cm equipped with preamplifier (gain=1,000 V/V, bandwidth=20–450 Hz). The sensors were placed bilaterally over the muscle belly of the rectus femoris (RF), BF, tibialis anterior (TA), and soleus muscles. A ground electrode was positioned over the lateral malleolus. The EMG signals were recorded using Myomonitor IV Wireless Transmission and Datalogging System with EMGWorks software (Delsys Inc) at a 2,000-Hz sampling rate.
A linear accelerometer was taped to the dorsal aspect of the web space between the first and second digits of the nonparetic hand (or dominant hand in the control group) for the arm raise task and on the dorsal, distal aspect of the index finger for the load drop task. Force and moment signals from the force platforms (6 from each platform) and the accelerometer signal were recorded simultaneously with the EMG signals using a separate, 16-bit acquisition system (Power 1401 with Spike 2 version 6.03 software, Cambridge Electronic Design, Cambridge, United Kingdom) at a sampling rate of 500 Hz (force platform) and 1,000 Hz (accelerometer). The EMG and force recordings were synchronized and saved for offline analysis.
The linear accelerometer measured the peak tangential acceleration in the arm raise task and was used to detect the onset of movement in the arm raise and load drop tasks. Accelerometry has been used to detect phases of gait in individuals who were healthy and in individuals with hemiparesis, with few errors.31
All analyses were performed using Spike 2 software. The recorded signals were converted to physiological units before analysis. The onset of movement was detected on the acceleration trace when the first derivative of the signal was greater than 0. The EMG, COP, and accelerometer signals for the 10 trials of each task were averaged for 2 seconds starting 0.7 seconds before the onset of movement.
In the arm raise task, the dependent variables examined were the time to burst peak, EMG peak area, COP velocity, arm acceleration, and vertical ground reaction force (VGRF). In the load drop task, the dependent variables were the anticipatory EMG deactivation area and VGRF. The time to burst peak was calculated as the time from the onset of the EMG burst to the time of the maximum amplitude of the EMG burst. Thus, a smaller time means the peak EMG burst amplitude is achieved more quickly. The EMG peak area was measured for 75 milliseconds before and after the peak of the EMG burst (150 milliseconds total), an area comprising more than 95% of the EMG burst. A baseline area of the same duration, measured starting 500 milliseconds before the arm raise, was subtracted. The resultant EMG peak area was normalized to quiet stance by dividing by the baseline area. For the load drop task, the anticipatory EMG deactivation area was measured for 100 milliseconds immediately preceding the load drop.11 This area was subtracted from a preload drop EMG area of the same duration, measured starting 500 milliseconds before the load drop, and the resultant anticipatory EMG deactivation area was normalized by dividing by the preload drop EMG area. Thus, larger values reflect more anticipatory deactivation of the EMG activity. The average COP velocity (V) was calculated as,
where N is the number of data sets, dt is the sampling interval, and L is the COP length of path, calculated as,
where x and y are the coordinates of the COP.
In both the arm raise and the load drop tasks, the stroke group was subdivided based on the VGRF on the paretic side, expressed as a percentage of the combined VGRF, which is an indication of the weight-bearing symmetry during the tasks. The VGRF on the paretic side was <45% for the asymmetrical group and ≥45% for the symmetrical group. The purpose was to determine whether individuals bearing less weight on the paretic leg showed improved symmetry after exercise.
Data Analysis
Statistical analysis was performed using SPSS for Windows version 17.0 (SPSS Inc, Chicago, Illinois). Missing data from equipment failure were coded as missing data. Two-way, mixed-model, repeated-measures analyses of variance were used, with factors of group (stroke, control) and time (pre-exercise, post-exercise, retention) as the repeated measures to assess differences in the dependent variables for the paretic and nonparetic legs, separately. For the group comparisons, the paretic leg was compared with the nondominant leg of the control group participants and the nonparetic leg was compared with the dominant leg of control group participants because the unilateral arm raise and load drop tasks resulted in different muscle activity in the 2 legs. Newman-Keuls post hoc comparisons were used to detect any significant differences between the mean values. For the dependent variables not normally distributed, a nonparametric repeated-measures comparison was performed (Friedman test), and significant differences were examined further with the Wilcoxon signed-rank test. For the between-group differences, the Mann-Whitney U test was used.
Several secondary statistical analyses were performed. Student t tests were used for differences in the VGRF of the symmetrical and asymmetrical stroke subgroups. To determine whether the side of the paresis (dominant or nondominant) influenced the postural responses, a subanalysis using a 2-way, mixed-model, repeated-measures analysis of variance with factors of paresis (dominant, nondominant side) and time (pre-exercise, post-exercise, retention) as the repeated measures was performed. Nonparametric tests were used as stated above when the data were not normally distributed. Student t tests were used to detect differences in the CMSA and BBS scores when the paretic limb was dominant versus nondominant.
The level of significance was set at P<.05 for all analyses. Normally distributed data are presented as means and standard deviations, and data not normally distributed are presented as medians and ranges from the 25th to the 75th percentile. Statistical analysis was run on the raw data, and the data are expressed as percentages in the text. The percent difference between groups was calculated as (stroke group value/control group value) − 1 × 100%, and difference in pre-exercise and post-exercise values and pre-exercise and retention values is expressed as percent change ([post-exercise − pre-exercise]/pre-exercise × 100% or [retention − pre-exercise]/pre-exercise × 100%).
Sample Size Calculation
The sample size was calculated based on the time to burst peak derived from the normalized slope data from 2 previous studies.8,32 The EMG parameters were not expected to change after exercise in the control group, so calculations were based on the expected change in the time to burst peak of the paretic side of individuals poststroke. The expected mean change during the short-term practice was estimated from the change found in a single bout of practice in individuals poststroke.33 Cirstea et al33 found a statistically significant increase of between 30% and 50% in performance variables; thus, the sample size was estimated based on a 30% decrease in the BF time to burst peak in the paretic leg calculated from the aforementioned studies. For the paretic BF time to burst peak, the expected mean change was 0.05 seconds (SD=0.1); thus, the sample size is 32.34
Role of the Funding Source
The Heart and Stroke Foundation of Ontario (Grant No. HSFO NA5585) provided financial support.
Results
The stroke group comprised 21 men and 11 women; 5 participants were left-hand dominant, and 27 were right-hand dominant. Ten participants poststroke had hemiparesis on the right side, and 22 had hemiparesis on the left side. In 13 participants poststroke, the dominant limb was the paretic limb, and in 19 participants, the nondominant limb was the paretic limb. Four of the participants sustained a hemorrhagic stroke, and 28 had an ischemic stroke. The mean age of the participants in the stroke group was 55.6 years (SD=13.5), and the mean time poststroke was 11.3 weeks (SD=4.1, range=3–13). The mean BBS score for the participants poststroke was 52.1 out of 56 (SD=4.5, range=40–56), and the mean CMSA score was 10.2 out of 14 (SD=3.1, range=6–14). Sensation was intact in all individuals. The mean age of the individuals in the control group was 56.1 years (SD=14.0), and the mean BBS score was 55.9 (SD=0.2). Two of the control group participants were left-hand dominant, and 30 were right-hand dominant.
Arm Raise Task
A soleus muscle burst was evident in fewer than a quarter of the participants in both groups. Similarly, the TA and RF muscles were not activated consistently, with only half of participants in both groups having an EMG burst. All participants in the control group activated the BF consistently in both legs, and all participants in the stroke group had a burst in the nonparetic BF (30 participants activated the paretic BF). Thus, the remainder of the article will focus on the BF.
The arm acceleration of the stroke group before exercise was significantly less (36.2%) compared with that of the control group (P<.001). Post-exercise increases in arm acceleration for the stroke group (6.5%) and the control group (5.2%) were not statistically significant and returned to pre-exercise values at the time of retention testing (Tab. 1).
Unilateral Arm Raise: Biceps Femoris Muscle Electromyographic Time to Burst Peak, Peak Area, Acceleration, and Center of Pressure (COP) Velocity
Before exercise, the BF time to burst peak in the stroke group compared with the control group was 28.3% less (P<.006) on the paretic side. After exercise, the BF time to burst peak decreased by 10.8% (P<.048) in the paretic leg, and this decrease in time to burst peak was maintained at the time of retention testing in the paretic leg (12.9%, P<.027) (Tab. 1).
The pre-exercise value for the EMG peak area was 72.3% (P<.001) and 35.5% (P=.15) less than in the control group in the paretic BF and nonparetic BF, respectively. Post-exercise, the EMG peak area increased in the paretic BF by 39.3% (P=.004). These increases in the paretic BF were maintained at retention testing (48.5%, P=.003). There was no difference in time to burst peak or peak area in the control group across pre-exercise, post-exercise, and retention testing (Tab. 1). Figure 1 depicts the arm acceleration and BF EMG signals for a representative participant in the stroke group (A) and the control group (B).
Arm acceleration and biceps femoris muscle electromyographic (EMG) signals during the arm raise task for a representative participant from the stroke group (A) and a representative participant from the control group (B). Traces are an average of the 10 arm raise trials: pre-exercise data represented by thin black line with gray shading, post-exercise data represented by thick black line, and retention data represented by dashed line. The vertical line represents the onset of movement.
Compared with the control group, the pre-exercise COP velocity in the stroke group was 23.6% (P=.19) less on the paretic side and 22.6% less on the nonparetic side (P=.022). Post-exercise COP velocity increased on the paretic side by 25.9% (P=.001) and the nonparetic side by 13.7% (P<.001). The COP velocity remained higher at the time of retention testing compared with pre-exercise values (34.0% on the paretic side, P<.001; 20.9% on the nonparetic side, P<.001). There was no significant change in the COP velocity over time in the control group.
The control group bore weight symmetrically (pre-exercise mean of 48.5% on the nondominant [mostly left] leg), and this finding did not change with exercise (Fig. 2). The stroke group was not significantly different from the control group, but had a high degree of heterogeneity. Consequently, the stroke group was divided into 2 subgroups: an asymmetrical subgroup (n=17) and a symmetrical subgroup (n=13). Data were missing from 2 participants as a result of technical issues. The asymmetrical subgroup had a mean CMSA score of 9.9 (SD=2.6), and the symmetrical subgroup had a mean CMSA score of 11.6 (SD=2.2). Post-exercise, there was an 8.3% shift in weight to the paretic leg in the asymmetrical group (P=.002), which was maintained at the time of retention testing (9.6%, P=.001). Figure 2A shows the substantial improvement in symmetry in the asymmetrical subgroup (triangles and dashed line), whereas there was no difference in the control group or symmetrical stroke subgroup.
The group means of the vertical ground reaction forces of the stroke group (squares) and the control group (circles) with standard error bars. The stroke group was divided into the symmetrical (Symm) subgroup with ≥45% weight on the paretic leg (diamonds) and the asymmetrical (Asymm) subgroup with <45% weight distribution on the paretic leg (triangles) for the arm raise (A) and load drop tasks (B) for pre-exercise, post-exercise and retention measurements. * Between-group differences, symmetrical and asymmetrical, P<.05; † within-group differences (pre-exercise to post-exercise; pre-exercise to retention), P<.05
Load Drop Task
Figure 3 depicts the anticipatory EMG deactivation area of the BF for a representative control group participant and 2 individuals in the stroke group. The 2 individuals poststroke demonstrate 2 different ways of improving the anticipatory EMG deactivation area: by increasing the EMG modulation (Stroke A) or by shifting the onset of the anticipatory EMG deactivation (Stroke B). The BF anticipatory EMG deactivation area was significantly smaller, by 67.3%, in the paretic leg (P=.004) compared with the control group before exercise (Tab. 2). There was an increase in the anticipatory EMG deactivation area of the paretic BF of 59.9% post-exercise (P=.029) and a tendency for this improvement to be retained (51.0%, P=.080). There was no difference between the nonparetic leg and control group, and no changes with exercise.
Biceps femoris muscle electromyographic (EMG) signals from a representative participant from the control group and 2 representative participants from the stroke group of the paretic/nondominant side (A) and nonparetic/dominant side (B). Traces are an average of 10 load drop trials: pre-exercise data represented by thin black line with gray shading, post-exercise data represented by thick black line, and retention data represented by dashed line. The vertical line represents the onset of movement.
Load Drop: Anticipatory Electromyographic Deactivation Area (au) in the Biceps Femoris Muscle
As in the arm raise task, there was no difference in weight bearing between the stroke group and the control group in the load drop task before exercise (Fig. 2B). However, when the stroke group was divided into asymmetrical and symmetrical subgroups, a significant reduction in weight bearing on the paretic side before exercise was observed in the asymmetrical subgroup (n=12) compared with the symmetrical subgroup (P=.002), as shown in Figure 2B. The mean CMSA score was 9.9 (SD=2.6) in the asymmetrical subgroup and 11.6 (SD=2.2) in the symmetrical subgroup. The asymmetrical subgroup showed improvements in weight bearing after exercise of 7.2% (P<.001) on the paretic leg, which continued to be significant at the time of retention testing (11.2%, P=.001).
Side of Paresis: Dominant Versus Nondominant
In the stroke group, the paresis was on the dominant side for 13 individuals and on the nondominant side for 19 individuals; thus, the arm raise task was performed with the nondominant and dominant arms in the stroke group. There was no statistical difference in the magnitude of the arm acceleration between the nondominant arm (X̅=50.8 m/s2, SD=25.4) and the dominant arm (X̅=44.0 m/s2, SD=17.0). From a functional perspective, individuals with paresis on the dominant side had significantly higher BBS scores (X̅=54.8, SD=2.0) than when the nondominant side was paretic (X̅=50.1, SD=5.1) (P<.001).
The force platform measures were influenced by the side of paresis. In the pre-exercise arm raise task, the VGRF was symmetrical when the dominant side was paretic (47.6%) but asymmetrical when the nondominant side was paretic (43.7%, P=.023). The pre-exercise to post-exercise and the pre-exercise to retention differences were not significant after post hoc tests. Before exercise, there were no group differences in COP velocity, but after exercise, when paresis was on the nondominant side, the COP velocity increased in the paretic leg by 32.7% (P=.006), which was maintained at the time of retention testing (44.6%, P<.001). The increase in COP velocity when the dominant side was the paretic side was not significant (P=.29). There was no effect of side of paresis on any EMG parameters in either task or on VGRF in the load drop task.
Discussion
The purpose of this study was to determine whether postural responses can be modified poststroke by a single session of exercise emphasizing speed of movement and whether these changes show any short-term retention. The main findings of this study were that after exercise: (1) improvements in paretic muscle activation were evident from the decrease in the BF time to burst peak and the increased EMG area during the arm raise task and improved anticipatory BF EMG deactivation in the load drop task, and (2) individuals with weight-bearing asymmetry after stroke accepted more weight on the paretic leg. In addition, the vast majority of the changes were retained 15 minutes after the end of the exercises.
Time to Burst Peak
This study demonstrated that exercises focusing on speed produced faster muscle activation (shorter time to burst peak) in a nonpracticed balance task. It is possible that the decrease in time to burst peak during the arm raise task was related to the small (and nonsignificant) increase in the arm acceleration after exercises that occurred in the control and stroke groups because it is known that as the velocity of movement increases, the slope of the EMG signal increases.35 The increase in time to burst peak in the stroke group cannot be attributed solely to this explanation for 4 reasons. First, in the control group, there was no significant decrease in time to burst peak, despite similar increases in arm acceleration. Second, the arm acceleration values in both groups returned to pre-exercise levels at the time of retention testing, yet the decrease in time to burst peak was maintained in the stroke group. Third, there was a small (and nonsignificant) difference in the arm acceleration between the dominant and nondominant arms in the stroke group, yet there were no differences in the EMG parameters between these 2 subgroups. Fourth, the velocity changes in the study by Corcos et al35 were large compared with the modest (and nonsignificant) change in arm acceleration observed in the current study. It is more likely that the decrease in time to burst peak can be attributed to neuromuscular mechanisms resulting from the exercise. It has been shown previously in individuals who were healthy that velocity-specific training leads to selective recruitment of fast motor units36 and increased instantaneous discharge frequency,37 both of which would decrease the time to burst peak.
EMG Area
The EMG area also increased in the arm raise task after exercise, emphasizing speed of movement. The EMG area also increases in the presence of muscle fatigue,38 and the exercise protocol conceivably could have been fatiguing for the stroke group. It is important to note that the increase in EMG area was maintained in the retention period, when participants rested for 15 minutes and engaged in conversation with the investigators. The effects of fatigue recover quickly upon rest.39,40 Furthermore, Boyas et al41 fatigued the ankle plantar-flexor muscles and examined the effects on postural control, and any fatigue-related effects recovered within 10 minutes. The increase in EMG area is unlikely to be strictly a function of muscle fatigue and can be attributed to the improved neuromuscular activation evoked by the exercise.
Anticipatory EMG Deactivation
The advantage of the load drop task was a standardization of the internal perturbation because of the aforementioned effects of the amplitude of the arm acceleration in the arm raise task on the magnitude of the postural sway and the EMG burst area.32 This load drop task has been used previously to show clear anticipatory postural adjustments in controls and reduced anticipatory postural adjustments after stroke, with an inability to modulate the deactivation of the BF with changes in load drop direction.12 In the present study, we found a significantly reduced anticipatory EMG deactivation area of the BF preceding the movement, indicating an improved anticipatory postural response to the internal perturbation. Because the stepping exercise required an initial lean, the hamstring muscle activity was larger than in quiet stance and showed a clear pattern of deactivation during the step. Although speculative, it is possible that exercises need to be designed to promote the fast modulation of hamstring muscle activity that is necessary for postural tasks.7
COP
Center of pressure velocity has been shown to play a major role in control of balance.42 In static standing, COP velocity was found to be a useful measure to classify elderly fallers and nonfallers, with the fallers having larger velocity values.43 This finding suggests that increases in COP velocity during quiet stance may reflect poorer standing balance. The current study, however, investigated dynamic balance, and the increase in COP velocity does not necessarily reflect deterioration in balance. That is, the COP velocity was smaller in the stroke group than in the control group. McCrory et al44 also found COP velocity was smaller in pregnant fallers compared with pregnant nonfallers in platform translations. Postural sway incorporates sensory information to explore the limits of stability; thus, increases in postural sway are not necessarily an indication of balance deficits, but rather an exploratory mechanism to maintain balance.45
Previous research by Anker et al46 showed that COP velocity was greater on the loaded limb when in asymmetrical stance. In the current study, the increase in COP velocity was greater in the stroke group when the paresis was on the nondominant side. Those participants with paresis on the dominant side had less impairment to balance (higher BBS scores) and symmetrical weight bearing compared with participants with paresis on the nondominant side. This finding is similar to that reported by Harris and Eng47 in which individuals with paresis on the dominant side had fewer impairments in the upper extremity than those with paresis on the nondominant side. The finding that participants with paresis on the dominant side were less impaired than those with paresis on the nondominant side may be related to asymmetries in the brain, with the dominant side having a larger representation.48 Alternatively, individuals may be more motivated to use the paretic side when it is the dominant side than when it is the nondominant side.
One limitation in this study was the short retention period, although we speculate that multiple sessions would be required for long-term retention or functional gains. In this efficacy study, we also used a control group of individuals who were healthy to provide information on muscle activation patterns and COP, which have not been examined previously.
Conclusion
Before the exercises, participants poststroke had smaller arm acceleration and longer time to burst peak, EMG peak area, and COP velocity during the arm raise task. There also was a subgroup of participants with stroke who demonstrated less symmetry with increased weight bearing on the nonparetic leg. The load drop task reaffirms an asymmetrical weight-bearing pattern and impairment in the BF burst deactivation before exercise. After the fast functional exercises that emphasized speed of movement, the stroke group improved their BF EMG activity in both the arm raise and load drop tasks, which was maintained in the retention testing. Those participants who were initially asymmetrical in their weight bearing shifted the weight to the paretic leg to become more symmetrical. Thus, exercises emphasizing speed of movement were efficacious in improving the postural responses to internal perturbations poststroke. Importantly, the observed improvements transferred to a task that was not practiced.
The Bottom Line
What do we already know about this topic?
Postural responses required for standing balance are compromised after stroke and lead to an increased risk for falls.
What new information does this study offer?
After a single session of exercises emphasizing speed of movement, people with stroke demonstrated an improvement in postural muscle responses during 2 balance perturbation tasks.
If you're a patient, what might these findings mean for you?
This study demonstrates that the muscle activation necessary for postural responses can be modified with exercise after stroke. This study is a first step in the development of exercise programs to improve functional mobility and dynamic balance after stroke.
Footnotes
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Dr Garland provided concept/idea/research design, fund procurement, facilities/equipment, and institutional liaisons. Dr Gray and Dr Garland provided writing. Dr Gray, Dr Ivanova, and Dr Garland provided data collection. Dr Gray, Dr Juren, and Dr Ivanova provided data analysis. Dr Ivanova provided project management. Dr Juren provided consultation (including review of manuscript before submission.
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Data from this study were presented at the following meetings: the Annual Meeting of the Society for Neuroscience, November 12–16, 2011, Washington, DC; the Canadian Stroke Congress, June 7–8, 2010, Quebec City, Quebec, Canada; the Annual Meeting of the Canadian Physiotherapy Association, May 29–June 1, 2008, Ottawa, Ontario, Canada; the International Brain Research Organization World Congress of Neuroscience Satellite Motor Control Meeting, July 12–17, 2007, Melbourne, Victoria, Australia; and the XVIIth Congress of the International Society of Electrophysiology & Kinesiology, Niagara Falls, Ontario, Canada, June 18–21, 2008.
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The Heart and Stroke Foundation of Ontario (grant no. HSFO NA5585) provided financial support.
- Received November 24, 2011.
- Accepted March 4, 2012.
- © 2012 American Physical Therapy Association
References
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