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Article

Intentionally Lengthening Nonparetic Step Length Inhibits the Paretic-Side Swing-Phase Ankle Motion More than Knee Motion

by
Yuichi Tsushima
1,2,*,
Kazuki Fujita
3,
Koji Hayashi
4,
Hiroichi Miaki
5 and
Katsuhiro Hayashi
5
1
Department of Physical Therapy Rehabilitation, Fukui General Hospital, Fukui-City 910-8561, Japan
2
Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, Kanazawa-City 920-0934, Japan
3
Graduate School of Health Science, Fukui Health Science University, Fukui-City 910-3190, Japan
4
Department of Rehabilitation Medicine, Fukui General Hospital, Fukui-City 910-8561, Japan
5
Faculty of Health Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa-City 920-0934, Japan
*
Author to whom correspondence should be addressed.
Biomechanics 2024, 4(2), 323-332; https://doi.org/10.3390/biomechanics4020022
Submission received: 16 April 2024 / Revised: 18 May 2024 / Accepted: 21 May 2024 / Published: 29 May 2024
(This article belongs to the Section Gait and Posture Biomechanics)
Browse Figure
Versions Notes

Abstract

:
Gait training to intentionally lengthen the nonparetic step length can increase the propulsive force of the paretic leg but may also induce overactivity of the knee extensor muscles that might limit knee flexion during the swing phase. Herein, we investigated the effects of lengthening the nonparetic step length during gait on the joint motion and muscle activity of the paretic lower limb. Fifteen chronic stroke patients (stroke group) and 15 healthy participants (control group) were evaluated for lower limb joint movements, electromyography, and spatiotemporal gait parameters during walking. Walking conditions were Normal (comfortable walking) and NP-Long/Contralateral-Long (walking with a lengthened step length of the nonmeasured limb). The trailing limb angle, a surrogate for propulsive forces, was increased in both groups by changing the step length, with no significant change in the peak knee flexion angle during the swing phase. However, the stroke group did not increase ankle plantar flexor activity in the stance phase or ankle dorsiflexion angle in the swing phase. Intentionally lengthening the nonparetic step length did not limit knee flexion. However, the effect of increased propulsive force during the stance phase was insufficient, with the possibility of decreased foot clearance.

1. Introduction

Stroke is a leading cause of acquired physical dysfunction in adults worldwide [1], resulting in significant health problems and economic burdens [2]. About 51% of patients are unable to walk after the onset of stroke [3], and subsequent gait disturbances considerably limit their physical functioning. Even if the patient can walk independently, their walking ability is often impaired, especially in terms of gait speed [4] and distance [5], which limits their activities of daily living [6]. Therefore, one of the primary goals of rehabilitation after a stroke is to regain the patient’s walking ability and improve gait speed and continuous gait distance. It is known that propulsive force, which is measured by the anterior component of the ground reaction force, considerably influences the individual’s gait speed and gait distance [7]. Hence, improving the paretic leg propulsive force is an essential factor for improving walking ability in stroke patients.
Biomechanically, propulsive force is composed of the ankle plantar flexion moment and trailing limb angle (TLA), which is the angle between the vertical and a line joining the greater trochanter to the fifth metatarsal head at the terminal stance phase [8]. In particular, the TLA contributes more to propulsive force generation than the ankle plantarflexion moment does [8], and the TLA is a surrogate index of propulsive force of the paretic leg in hemiparetic gait [9]. A recent study has reported that high-speed treadmill gait training combined with electrical stimulation and gait training using a gait-assisted robot can improve propulsive force [10]. However, these methods are not often employed in routine clinical practice as they require expensive external assistive devices. In contrast, gait training that lengthens step length does not require expensive external assistive devices and is considered a gait rehabilitation program that can be easily incorporated into routine clinical practice. Previous studies have stated that propulsive force is related to the contralateral step length, and the paretic leg propulsive force is greater in patients with a larger nonparetic step length [11]. Similarly, lengthening the nonparetic step length in stroke patients increases plantar flexor activity and paretic leg propulsive force [12].
Propulsive force during the stance phase adds mechanical energy to the swing leg and contributes to knee flexion [13], and a positive correlation is observed between the leg extension angle in the late stance phase and knee flexion during the swing phase [14]. However, it is well known that modifying voluntary step symmetry can impair dynamic balance during gait [15], and altering the step length in a self-selected, although asymmetric gait, may be disadvantageous in some cases. Lewek et al. [16] suggested that rapid hip extension during the stance phase may limit knee flexion during the swing phase due to abnormal stretch reflex activity from the hip flexors to the knee extensors. Therefore, walking with an intentionally lengthened nonparetic step length may increase paretic side propulsive force during the stance phase but inhibit knee flexion during the swing phase.
Restricted knee flexion during the swing phase increases the risk of falls and energy costs due to decreased foot clearance [17,18]. Furthermore, paretic side knee flexion during the swing phase is reportedly associated with patient satisfaction and independence in activities of daily living [19]; therefore, any limitation of knee flexion during the swing phase should be avoided. In our previous study [20], we demonstrated that lengthening the nonparetic step length had no effect on knee motion during the swing phase. However, the inclusion criteria in this study did not specify step asymmetry, which is strongly associated with the propulsion force of the paretic leg [21], or the presence or absence of a short leg brace, which affects lower limb motion [22]. Furthermore, determining the changes occurring in normal gait when the step length is lengthened would help in providing a detailed study of the effect of lengthening the nonparetic step length on stroke patients.
Hence, the present study aimed to clarify the effects of intentionally lengthening the nonparetic step length on paretic joint movements and muscle activities during the swing phase. We believe that elucidating this relationship between nonparetic step length and the paretic swing phase will help in planning gait training methods and improving lower limb propulsive force while taking into account the risk of falls and gait disturbances.

2. Materials and Methods

2.1. Participants

We enrolled 15 stroke patients with chronic hemiplegia admitted to the Fukui General Hospital, Japan, for rehabilitation between October 2019 and May 2022 in the experimental group. The sample size was calculated using G* Power 3.1 (effect size (ES): 0.7, significance level: 5%, power: 0.8) with reference to the preliminary study [20]. The inclusion criteria were as follows: (1) hemiplegia due to unilateral stroke; (2) at least 6 months after stroke onset; (3) sufficient paretic knee joint range of motion; and (4) supervised walking ability at least 10 m independently or with a T-cane. Patients were excluded if (1) they required a short leg brace while walking; (2) the nonparetic step length was larger than the paretic side (paretic step length/(paretic step length + nonparetic step length) < 0.465) during comfortable walking [21]; (3) the patient had a history of lower limb joint surgery; (4) they had respiratory or cardiovascular symptoms while walking; or (5) had a Mini-Mental State Examination score of ≤23 with cognitive decline. The control group consisted of 15 age-matched healthy adults without neurological or orthopedic diseases.
This study was approved by the Ethical Review Committee of the Fukui General Hospital, Japan (approval no.: Nittazuka Ethics 2019-42); all participants were provided written and verbal explanations about the study details, following which they gave voluntary consent for participation, and it was conducted in accordance with the Declaration of Helsinki.

2.2. Evaluation

The paretic limb in the experimental group was evaluated using the Fugl–Meyer assessment for the lower limb (FMA), motricity index (MI), the modified Ashworth scale (MAS) for hip flexors, knee extensors, and ankle plantar flexors, along with the passive range of motion (ROM) for hip extension and ankle dorsiflexion. A 16 m straight line (10 m walking course with a 3 m spare path on both ends) was used as the measurement course for gait analysis. The stroke group was assessed for two walking conditions consecutively: walking at a comfortable speed (Normal) and walking with a lengthened nonparetic step length (NP-Long) (Figure 1). The NP-Long condition was explained as “Please lengthen the nonparetic step length to the extent that you do not lose your balance while walking.” For the NP-Long condition, ten minutes of walking practice were allowed before the actual trial, and no specific target step length was set because it is difficult for stroke patients to conform to a defined step length and they can no longer walk naturally [23], and the gait speed was up to the participant’s discretion. This test was carried out while the participant walked independently or used a T-cane if necessary. For the control group, the measurement limb was selected randomly. Hereafter, the measurement limb is designated as the ipsilateral side and the nonmeasurement limb as the contralateral side in the control group. The control group underwent the same evaluation procedure as the stroke group for two walking conditions: walking at a comfortable speed (Normal) and walking with a lengthened contralateral step length (Contralateral-Long). All participants performed three trials each for the Normal and NP-Long/Contralateral-Long conditions. The primary outcome for gait assessment was paretic knee motion and muscle activity, and secondary outcomes were paretic hip and ankle motion and spatiotemporal gait parameters.
Electromyography (EMG) was performed using the TelemyoDTS (Noraxon Inc., Scottsdale, AZ, USA) equipment, and a three-dimensional motion analysis was performed using Myomotion (Noraxon Inc., Scottsdale, AZ, USA). Myomotion is a device that calculates angles and angular velocities from motion sensors with integrated gyro, acceleration, and magnetic sensors. The reliability of gait analysis using Myomotion has been reported [24]. The sampling frequency for the EMG system was 1500 Hz, and a bandpass filter of 10–500 Hz was used. The following paretic muscles were selected: rectus femoris, biceps femoris, tibialis anterior, and medial head of gastrocnemius. After the skin resistance was lowered to <10 kΩ by skin treatment, silver chloride surface electrodes were applied based on the Surface ElectroMyoGraphy for the Non-Invasive Assessment of Muscle project [25].
For the motion analysis, a sampling frequency of 100 Hz was used. Motion sensors were attached to the sacrum, anterior surfaces of both thighs, shanks, and feet [26]. Zero calibration, which determines the joint angle information, was performed in the upright standing position. Independent of the motion sensor, reflective markers were attached to the greater trochanter and the head of the fifth metatarsal on the paretic limb to measure the TLA [27]. A video camera (sampling frequency: 30 Hz) was placed 5 m to the side of the midpoint of the walking path. MyoSynchro and SynchroLight (Noraxon Inc., Scottsdale, AZ, USA) were used to synchronize all equipment, and the time periods were matched.

2.3. Data Analysis

The MR3 software (Noraxon Inc., Scottsdale, AZ, USA) was used for data analysis. We used the data for three consecutive gait cycles at the midpoint of a 10 m walk for the analysis. The initial contact and toe-off of both lower limbs were determined based on the Myomotion acceleration data, and the three gait cycles were added up and averaged, resulting in one gait cycle of 100%. The gait phase was divided into the loading response phase (paretic initial contact~nonparetic toe-off), single-support phase (nonparetic toe-off~nonparetic initial contact), preswing phase (nonparetic initial contact~paretic toe-off), and swing phase (paretic toe-off~paretic initial contact); the late single-support phase was defined as the second half of the single-support phase [28], and the early swing phase was defined as the period from toe-off to maximum knee flexion [29]. The raw EMG waveforms were full-wave rectified, and the average amplitude of each gait phase was calculated and normalized by dividing them by the average amplitude of the entire gait cycle [28].
For kinematic parameters, joint angles and angular velocities of the hip, knee, and ankle were selected from Myomotion joint angle data—from the late single-support phase to the swing phase [20]. In addition, to evaluate knee joint kinematics during the swing phase, we selected the peak knee flexion angle, knee joint ROM in the early swing phase and during the entire gait cycle, and the duration of the early swing phase [29]. Angular velocity was obtained by differentiating the angular data using MR3. Gait speed was calculated using a stopwatch, and gait cycle rate and cadence were calculated based on acceleration information obtained from MR3 [30]. Step length and stride were calculated from a 1 m calibration scale set at the center of the walking path using ImageJ (NIH) image analysis software [31]. Similarly, the ImageJ (NIH) image analysis software was used to calculate the paretic side TLA (the angle between the vertical axis and a vector created between the greater trochanter and the head of the fifth metatarsal at the toe-off) [27]. The joint kinematics and EMG data were averaged over nine gait cycles (3 gait cycles × 3), and the step length, stride, and TLA were averaged over three gait cycles (1 gait cycle × 3) in the center of the screen to account for marker position error due to distortion at the edge of the screen. Step length asymmetry in the stroke group during comfortable gait was also evaluated by PSR (paretic step length divided by the sum of paretic and nonparetic step length) [21].

2.4. Statistical Analysis

All statistical analyses were performed using BellCurve for Excel (Social Survey Research Information Co., Ltd., Tokyo, Japan). The subject characteristics were compared using the chi-square test, t-test, and Mann–Whitney U-test. The Normal and NP-Long or Contralateral-Long gait parameters were compared using the paired t-test or Wilcoxon’s signed-rank sum test, according to normality distribution. The change in gait parameters (NP-Long or Contralateral-Long data–Normal data) for each group was compared using the t-test or Mann–Whitney U-test. The significance level was set at 5% for all analyses. Cohen’s d was calculated as the ES for each data set; d = 0.2 was defined as a small ES, 0.5 as a medium ES, and 0.8 as a large ES [32].

3. Results

Table 1 shows the characteristics of the patients. There were no significant differences in age, height, or weight between the stroke and control groups. The stroke group had significantly lower strength in the paretic leg muscles in terms of MI, a significantly higher MAS score, and a greater ankle dorsiflexion restriction.

3.1. Spatiotemporal Parameters

There was a significant between-group difference in the change in cadence (p = 0.006; ES = 1.047) and paretic or ipsilateral step length (p = 0.007; ES = 1.027) when comparing Normal and NP-Long or Contralateral-Long conditions. There was no significant between-group difference in the change in nonparetic or contralateral step length (p = 0.229; ES = 0.311) (Table 2).

3.2. Kinematics

With regard to hip motion, both groups showed a significant increase in peak hip extension angle during the late single-support phase (stroke: p < 0.001; ES = 0.570, control: p < 0.001; ES = 0.748) and TLA at toe-off (stroke: p < 0.001; ES = 0.791, control: p < 0.001; ES = 2.658) in the NP-Long or Contralateral-Long compared to Normal conditions, with no significant between-group difference in the amounts of change. The peak hip extension angular velocity was significantly increased only in the stroke group (p < 0.001; ES = 0.324). Both groups exhibited an increase in the range of hip motion during the swing phase (stroke: p < 0.001; ES = 0.761, control: p < 0.001; ES = 2.106) (Table 3).
With regard to knee motion, both groups showed a significant decrease in the knee flexion angle at the toe-off (stroke: p = 0.027; ES = 0.391, control: p < 0.001; ES = 1.357) in the NP-Long and Contralateral-Long conditions, and there was a significant between-group difference in the change in the knee flexion angle at the toe-off (p = 0.005; ES = 1.07). However, no change was observed in the peak knee flexion angle during the swing phase (stroke: p = 0.82; ES = 0.015, control: p = 0.112; ES = 0.346), total ROM during the gait (stroke: p = 0.363; ES = 0.10), or duration of the early swing (stroke: p = 0.125; ES = 0.40). ROM during early swing was significantly increased in both groups (stroke: p = 0.011; ES = 0.359, control: p < 0.001; ES = 1.665), and there was a significant between-group difference in the change in the ROM during early swing (p = 0.016; ES = 0.751).
Finally, for ankle motion, the ankle plantarflexion velocity at toe-off was significantly increased (p = 0.017; ES = 0.510) with NP-Long in the stroke group, and the ankle plantarflexion angle at toe-off was also significantly increased (p = 0.009; ES = 0.395) with Contralateral-Long in the control group. A significant increase in peak dorsiflexion angle during the swing phase was observed only in the control group (p < 0.001; ES = 0.775) but not in the stroke group (p = 0.427; ES = 0.09).

3.3. Muscle Activity

In the late single-support phase, the control group showed significantly increased rectus femoris (p < 0.001; ES = 1.860), biceps femoris (p = 0.015; ES = 0.768), tibialis anterior (p < 0.001; ES = 0.633), and medial head of gastrocnemius (p = 0.036; ES = 0.503) muscle activity, whereas the stroke group showed no change in activity of these muscles. There was a significant between-group difference in the change in activity of the rectus femoris (p = 0.001; ES = 1.23) or medial head of the gastrocnemius (p = 0.019; ES = 0.88). In the preswing phase, the stroke group showed significantly increased rectus femoris muscle activity (p < 0.001; ES = 0.594), whereas the control group showed significantly decreased rectus femoris muscle activity (p = 0.031; ES = 0.1) and significantly increased biceps femoris muscle activity (p < 0.001; ES = 1.856). In the early swing phase, the stroke group showed no change in tibialis anterior muscle activity (p = 0.78; ES = 0.07), whereas the control group showed a significant increase in tibialis anterior muscle activity (p = 0.027; ES = 0.592) (Table 4).

4. Discussion

There was no significant difference in changes in the TLA, or nonparetic and contralateral step length, between the stroke and control groups, and the gait conditions were similar in both groups. Lengthening the nonparetic step length increased the paretic-side TLA by about 5°, which was accompanied by a large ES. In chronic stroke patients, the minimum detectable change in TLA within a session has been reported to be 1° [33], and the fast-speed gait increased the TLA by 4.8° as compared with the comfortable gait [27]. This indicates that lengthening the nonparetic step had a significant effect on the paretic-side TLA. There was an increase in knee extensor and ankle plantar flexor activity (the antigravity muscles) in the control groups during the late single-support phase. However, there was no change in paretic lower limb muscle activity in the stroke groups. Lewek et al. [16] reported increased rectus femoris muscle activity at 90°/s and 120°/s as compared to 60°/s hip extension angular velocity. In this study, the peak hip extension angular velocity in the NP-Long was 62.2 ± 30.9°/s, which was less than the angular velocity at which the abnormal stretch reflex was elicited; thus, it is likely that rectus femoris activity was unchanged. Stroke patients already showed >100% knee flexor and extensor muscle activity during normal walking and might not have been able to further increase muscle activity due to impaired recruitment of the paretic muscles [34,35]. Clark et al. [12] reported an increase in paretic ankle plantar flexor activity by lengthening the nonparetic step length, which we did not observe in the stroke groups in the present study. This difference might have occurred due to the difference in the processing technique used for the normalization of the EMG waveform. In addition, it is known that passive stiffness of the paretic ankle plantar flexor muscle compensates for limited ankle plantar flexor muscle activity [36]. Unlike control groups, stroke participants had limited ankle dorsiflexion, and possibly the effect of passive stiffness compensation for plantar flexor activity resulted in no significant change in muscle activity.
Although overactivity of the rectus femoris during the preswing phase has long been reported as a factor that limits knee flexion during the swing phase [37,38], no change was observed in the peak knee flexion angle during the swing phase, total ROM during the gait, or duration of the early swing. It has been suggested that activity of the rectus femoris muscle during the preswing phase contributes to leg progression in stroke patients [28]. A recent study conducted on stroke patients reported that rectus femoris muscle activity during the preswing phase is more likely to play a role in hip flexion than in knee flexion limitation [39]. During the swing phase, the hip joint flexion moment contributes to the knee joint flexion angle [40]. Therefore, rectus femoris activity may contribute to leg progression and increased hip flexion ROM after toe-off, thereby maintaining the knee motion during the swing phase. In contrast to the stroke groups, the control groups showed lower rectus femoris muscle activity and higher biceps femoris muscle activity during the preswing phase. Moreover, they demonstrated a markedly smaller knee flexion angle at toe-off, which suggests increased knee flexor muscle activity to increase knee flexion after toe-off. In addition, both groups showed an increased ankle plantarflexion angle or plantarflexion angular velocity at toe-off. Ankle plantarflexion at toe-off is associated with reduced foot clearance during the swing phase [41]. The control groups showed an increase in ankle dorsiflexion angle, which was brought about by the tibialis anterior muscle to ensure foot clearance during the swing phase. However, in the stroke groups, the ankle dorsiflexion angle likely did not increase during the swing phase due to weakness of the ankle dorsiflexion muscle caused by motor paralysis [42].
There were certain limitations in this study. First, this study included chronic stroke patients, and it therefore cannot be stated whether similar results could be obtained in patients with acute or subacute stroke. Second, this study estimated propulsive forces using TLA. As ground reaction forces were not measured, it is not possible to accurately assess changes in propulsive forces during gait, which limits the interpretation of the results.

5. Conclusions

In conclusion, in chronic stroke patients, intentionally lengthening the nonparetic step length increased the paretic-side TLA, a surrogate for propulsive forces, but did not limit knee motion during the swing phase. However, compared with healthy participants, the ankle plantar flexor activity during the stance phase and the ankle dorsiflexor activity and ROM during the swing phase were insufficient. Therefore, the effect of increased propulsive force during the stance phase was insufficient, and combination therapy, such as electrical stimulation therapy of the ankle plantar flexor muscles, may be required. In addition, reduced foot clearance associated with insufficient ankle dorsiflexion during the swing phase may require the use of short leg braces to prevent falls. The effectiveness of long-term interventions to intentionally lengthen the nonparetic step length should be confirmed through future longitudinal studies.

Author Contributions

Conceptualization, Y.T., K.F. and H.M.; methodology, Y.T., K.F. and H.M.; software, K.F. and K.H. (Katsuhiro Hayashi); validation, Y.T. and K.F.; investigation, Y.T.; resources, K.H. (Katsuhiro Hayashi); data curation, Y.T. and K.F.; writing—original draft preparation, Y.T., K.F., K.H. (Koji Hayashi) and H.M.; writing—review and editing, Y.T., K.F., K.H. (Koji Hayashi) and H.M.; supervision, H.M. and K.H. (Katsuhiro Hayashi); project administration, Y.T.; funding acquisition, K.F. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of Fukui General Hospital (protocol code Nittazuka Ethics 2019-42).

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study. Written informed consent has been obtained from the patient(s) to publish this paper.

Data Availability Statement

The data are available upon reasonable request.

Conflicts of Interest

The authors declare no conflicts of interest.

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Biomechanics 04 00022 g001
Figure 1. Gait measurement process.
Figure 1. Gait measurement process.
Biomechanics 04 00022 g001
Table 1. Baseline characteristics for all study participants.
Table 1. Baseline characteristics for all study participants.
ProfileStroke
(n = 15)		Control
(n = 15)		p-Value
Age(years)61.8 ± 12.462.0 ± 4.4NS
Height(cm)163.6 ± 12.2164.7 ± 10.6NS
Weight(kg)65.9 ± 15.263.9 ± 11.2NS
Gender(Female/male)3/125/10NS
Months of onset58.6 ± 52.3N/AN/A
Type of stroke(CI/ICH)4/11N/AN/A
Paretic side (Right/left)11/4N/AN/A
Fugl–Meyer assessment LE22.6 ± 4.5N/AN/A
Motricity IndexHip25 (0)33 (0)<0.05
Knee25 (8)33 (0)<0.05
Ankle19 (6)33 (0)<0.05
MASHip flexors1 (0.5)N/AN/A
Knee extensors2 (2.5)N/AN/A
Ankle plantar flexors2 (1.5)N/AN/A
ROMHip extension (°)12.5 ± 7.1N/AN/A
Ankle dorsiflexion (°)6.7 ± 7.5N/AN/A
Step length asymmetry
(low/symmetric/high PSR)		0/8/7N/AN/A
Assistive device(None/T-cane/AFO)6/9/0N/AN/A
Values are presented as the mean ± standard deviation or median (quartile deviation). p-value: comparison between the stroke and control groups (chi-squared test, t-test, or Mann–Whitney U-test). A score of 1+ on the modified Ashworth scale was assigned as 2, and scores of 2 and higher were revised upward by 1. Step length asymmetry is indicated by low, PSR < 0.465; symmetric, 0.535 > PSR > 0.465; and high, 0.535 > PSR. CI, cerebral infarction; ICH, intracerebral hemorrhage; LE, lower extremity; MAS, modified Ashworth scale; ROM, range of motion; AFO, ankle–foot orthosis; NS, no significant difference.
Table 2. Comparison of the spatiotemporal gait parameters between the stroke and control group participants.
Table 2. Comparison of the spatiotemporal gait parameters between the stroke and control group participants.
Stroke (n = 15)Control (n = 15)p-Value
NormalNP-LongNormalContralateral-Long
LR period%12.9 ± 3.010.7 ± 3.1*12.9 ± 1.712.0 ± 2.0**NS
SS period%31.0 ± 4.533.6 ± 5.0**37.0 ± 1.939.1 ± 1.9**NS
PSw period%15.0 ± 4.312.8 ± 5.4**13.0 ± 2.011.2 ± 1.5**NS
Sw period%41.2 ± 3.842.9 ± 3.5**37.1 ± 1.837.8 ± 1.4**NS
Cadencesteps/min84.8 ± 15.783.0 ± 16.1 113.1 ± 8.3105.2 ± 10.8**0.006
Gait cycle times1.44 ± 0.41.48 ± 0.4 1.07 ± 0.081.15 ± 0.13**NS
Gait velocitym/s0.58 ± 0.30.69 ± 0.4**1.30 ± 0.11.34 ± 0.1 NS
Stridecm97.4 ± 24.7117.0 ± 30.5**139.2 ± 13.4155.2 ± 10.9**NS
Step length paretic/ipsilateralcm51.0 ± 12.153.3 ± 14.9 69.2 ± 8.464.1 ± 8.4**0.007
Step length nonparetic/contralateralcm46.4 ± 13.463.7 ± 18.6**70.0 ± 6.891.0 ± 6.8**NS
All values are presented as the mean ± standard deviation. * p < 0.05, ** p < 0.01 (Normal vs. NP-Long or Contralateral-Long, paired t-test or Wilcoxon signed-rank test). p-value: comparison of the change (NP-Long or Contralateral-Long data–Normal data) between the stroke and control groups (t-test or Mann–Whitney U-test). Normal, comfortable gait; NP-Long, gait with lengthened nonparetic step length; Contralateral-Long, gait with lengthened contralateral step length; LR, loading response phase; SS, single-support phase; PSw, preswing phase; Sw, swing phase; NS, no significant difference.
Table 3. Comparison of the kinematic data between the stroke and control group participants.
Table 3. Comparison of the kinematic data between the stroke and control group participants.
Stroke (n = 15)Control (n = 15)p-Value
NormalNP-LongNormalContralateral-Long
HipPeak extension angle during late single support°7.2 ± 5.110.2 ± 5.4**15.0 ± 5.419.2 ± 6.2**NS
Peak extension angular velocity during late single support°/s53.3 ± 25.862.2 ± 30.9**120.0 ± 22.0110.6 ± 32.1 0.004
Peak flexion angle during swing°22.2 ± 7.624.0 ± 8.0 31.7 ± 3.833.5 ± 4.5 NS
Range of motion during swing°21.6 ± 8.828.5 ± 9.8**36.2 ± 5.245.8 ± 4.3**NS
KneeFlexion angle at toe-off°26.5 ± 9.323.1 ± 8.7*48.7 ± 6.139.7 ± 7.2**0.005
Flexion velocity at toe-off°/s147.8 ± 93.7158.3 ± 92.5 382.3 ± 50.3358.2 ± 92.1 NS
Peak flexion angle during swing°34.9 ± 12.735.1 ± 12.5 68.5 ± 5.266.4 ± 6.9 NS
ROM during early swing°8.43 ± 10.012.0 ± 10.0*19.8 ± 3.826.8 ± 4.8**0.016
Total ROM during gait cycle°36.0 ± 11.734.9 ± 12.5 66.5 ± 5.163.6 ± 6.3**NS
Duration of early swing%GC9.9 ± 8.414.3 ± 8.9 9.9 ± 0.811.9 ± 1.0**NS
AnklePlantar flexion angle at toe-off°7.4 ± 7.38.5 ± 8.8 8.6 ± 9.712.6 ± 10.7**NS
Plantar flexion velocity at toe-off°/s78.9 ± 81.6124.9 ± 98.4*154.7 ± 88.9178.5 ± 91.6 NS
Peak dorsiflexion angle during swing°−2.9 ± 8.1−2.1 ± 9.4 3.1 ± 5.97.9 ± 6.4**<0.01
Trailing limb angle (TLA) at toe-off°13.8 ± 5.919.0 ± 7.7**26.3 ± 2.233.6 ± 3.1**NS
Mean ± standard deviation. * p < 0.05, ** p < 0.01 (Normal vs. NP-Long or Contralateral-Long, paired t-test or Wilcoxon signed-rank test) p-value: comparison of the change (NP-Long or Contralateral-Long data–Normal data) between the stroke and control groups (t-test or Mann–Whitney U-test). Normal, comfortable gait; NP-Long, gait with lengthened nonparetic step length; Contralateral-Long, gait with lengthened contralateral step length; NS, no significant difference.
Table 4. Comparison of the electromyography data between the stroke and control group participants.
Table 4. Comparison of the electromyography data between the stroke and control group participants.
MusclesGait PhaseStroke (n = 15)Control (n = 15)p-Value
NormalNP-LongNormalContralateral-Long
RFLate SS%107.5 ± 39.5116.4 ± 41.9 64.7 ± 30.5120.4 ± 31.5**0.001
PSw%91.6 ± 34.0115.0 ± 46.4**90.2 ± 47.681.8 ± 105.0*<0.001
ESw%109.4 ± 85.392.5 ± 60.2 79.4 ± 58.467.5 ± 57.6**NS
BFLate SS%115.3 ± 54.1119.4 ± 49.4 28.7 ± 17.855.1 ± 45.3*NS
PSw%63.9 ± 47.272.0 ± 55.5 24.5 ± 13.290.7 ± 50.5**<0.001
ESw%43.2 ± 32.141.4 ± 28.8 36.0 ± 38.239.4 ± 20.8 NS
TALate SS%87.3 ± 54.890.2 ± 44.3 51.3 ± 18.364.5 ± 24.4**NS
PSw%114.6 ± 39.6119.1 ± 50.7 99.1 ± 28.4110.2 ± 29.9*NS
ESw%134.6 ± 62.5122.9 ± 46.5 114.9 ± 32.4136.3 ± 39.6*0.013
MGLate SS%145.6 ± 44.0143.1 ± 48.0 208.0 ± 70.3240.4 ± 58.0*0.019
PSw%98.0 ± 49.9108.2 ± 49.4 54.8 ± 29.464.9 ± 30.6 NS
ESw%61.4 ± 52.168.7 ± 69.7 45.9 ± 33.545.9 ± 29.4 NS
Mean ± standard deviation. * p < 0.05, ** p < 0.01 (Normal vs. NP-Long or Opposite-Long, paired t-test or Wilcoxon signed-rank test). p-value: comparison of the change (NP-Long or Contralateral-Long data–Normal data) between the stroke and control groups (t-test or Mann–Whitney U-test). Normal, comfortable gait; NP-Long, gait with lengthened nonparetic step length; Contralateral-Long, gait with lengthened contralateral step length. RF, rectus femoris; BF, biceps femoris; TA, tibialis anterior; MG, medial gastrocnemius; SS, single-support phase; PSw, preswing phase; ESw, early swing phase; NS, no significant difference.
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Tsushima, Y.; Fujita, K.; Hayashi, K.; Miaki, H.; Hayashi, K. Intentionally Lengthening Nonparetic Step Length Inhibits the Paretic-Side Swing-Phase Ankle Motion More than Knee Motion. Biomechanics 2024, 4, 323-332. https://doi.org/10.3390/biomechanics4020022

AMA Style

Tsushima Y, Fujita K, Hayashi K, Miaki H, Hayashi K. Intentionally Lengthening Nonparetic Step Length Inhibits the Paretic-Side Swing-Phase Ankle Motion More than Knee Motion. Biomechanics. 2024; 4(2):323-332. https://doi.org/10.3390/biomechanics4020022

Chicago/Turabian Style

Tsushima, Yuichi, Kazuki Fujita, Koji Hayashi, Hiroichi Miaki, and Katsuhiro Hayashi. 2024. "Intentionally Lengthening Nonparetic Step Length Inhibits the Paretic-Side Swing-Phase Ankle Motion More than Knee Motion" Biomechanics 4, no. 2: 323-332. https://doi.org/10.3390/biomechanics4020022

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