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Combined Task-Specific Training and Strengthening Effects On Locomotor Recovery Post-Stroke: A Case Study

Sullivan, Katherine J. PT, PhD1; Klassen, Tara PT, MS, NCS2; Mulroy, Sara PT, PhD3Physical Therapy Clinical Research Network (PT Clin Res Net)

Journal of Neurologic Physical Therapy: September 2006 - Volume 30 - Issue 3 - p 130–141
doi: 10.1097/01.NPT.0000281950.86311.82
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Background and Purpose Task-specific and strength training have demonstrated efficacy as therapeutic interventions post-stroke. The intent of this case study is to describe outcomes associated with a therapy program that combines task-specific and strength training in an individual post-stroke and to discuss some possible mechanisms and modulating factors that may affect post-stroke neurologic recovery and responsiveness to intervention.

Case Description The participant was a 38-year-old female with right middle cerebral artery stroke, evaluated 15 months post-onset. She ambulated independently with an ankle-foot orthosis and straight cane. Her free and fast overground velocity was 0.50 m/s and 0.62 m/s, respectively. Body-weight supported treadmill training and a limb-loaded cycling exercise were alternated over 24 treatments sessions (4 times/wk for 6 wks). Measurements were taken pre-, post-treatment, and at a 6-mo follow-up. Instrumented gait and motion analysis with fine-wire EMG recording of LE muscle activity occurred pre- and post-treatment.

Outcomes Post-treatment, walking speed increased 18% for free- (0.59 m/ s) and 14.4% for fast-velocity (0.71 m/s); 6-min walking distance increased 4% (184.4 m). At 6-mos, continued improvements in all walking outcomes were evident. Gait and motion analysis revealed that functional locomotor recovery was associated with increases in magnitude of paretic leg gluteus maximus and gluteus medius activation during gait. Motion analysis confirmed an increase of hip and knee extension motions throughout stance and swing.

Discussion For the person in this case clinically meaningful changes in walking function were associated with a combined therapeutic program that included both task-specific and LE strength training. Possible mechanisms associated with response to therapy were related to improved motor unit activation associated with increased strength in key muscles used in gait.

1Department of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA (kasulliv@usc.edu)

2Vancouver Coastal Health, BC, Canada

3Pathokinesiology Laboratory, Rancho Los Amigos National Rehabilitation Center, Downey, CA

*Physical Therapy Clinical Research Network (PT Clin Res Net): Network Principal Investigator is Carolee J. Winstein, PhD, PT, FAPTA and the co-Principal Investigator is James Gordon, EdD, PT, FAPTA (both at University of Southern California).

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INTRODUCTION

Stroke is the leading cause of disability in adults. Seventy-five percent of individuals who sustain a stroke each year report limitations in mobility that usually are related to walking.1 While the majority of stroke survivors will regain some ability to walk, 40% will require assistance with walking and of those who are independent, 60% will be limited in community ambulation.2 Perry et al3 have demonstrated that the greatest predictor of community ambulation is walking speed. Unlimited community ambulation is possible if an individual can walk at speeds of 0.8 m/s (1.8 mph) or greater. However, even this level of walking speed only represents 60% of what is normal for most healthy adults.4 Collectively, these observations reflect the importance of therapeutic strategies to improve functional walking ability in order to increase participation and quality of life after stroke.

Walking limitations after stroke are related to several cumulative factors. Decreased muscle activation is one of the primary causes of gait deficits in the early post-stroke phase.5 The magnitude of gait deficits, and hence level of disability, relates to the severity of lower limb involvement.6 The pattern of residual lower extremity paresis can differ between stroke survivors and is one of the reasons that the kinematic and kinetic patterns of gait after stroke are so variable.5,7 Lower limb weakness and power generation are also major contributors to post-stroke walking deficits. Specifically, power generation of the ankle plantarflexors and single joint hip flexors have been shown to be strong determinants of walking velocity.8,9

Evidence is building that strength training leads to improvements in both lower limb muscle strength and gait velocity post-stroke10,11 without increasing spasticity.12,13 In addition, task-specific training appears to be critical to the success of locomotor intervention strategies to improve walking speed after stroke.14–16 Treadmill training with body weight support is an example of a task-specific intervention that has been shown to be effective in increasing post-stroke overground gait velocities especially when more functional walking speeds are used during training.17,18 Since the effects of task-specific and strength training on gait outcomes appear to be beneficial, we were interested in describing some of the underlying biomechanical and neural mechanisms associated with improved walking following a program of muscle strengthening and body weight supported treadmill (BWST) training. Resisted muscle strengthening programs have been shown to increase walking velocity and ankle plantarflexion and knee flexion power, but not hip flexion power or interlimb stance/swing symmetry.19 In contrast, walking on a treadmill with body weight support (short-term, immediate changes compared to overground) has produced symmetrical stance/swing ratios,20–22 increased hip extension in single limb stance, and decreased EMG from gastrocnemius.23 Walking on a treadmill with body weight support at faster velocities (short-term, immediate changes compared to slower treadmill velocities) resulted in increased activation of gastrocnemius, vastus lateralis, biceps femoris, and gluteus medius.24 Together, walking speed, muscle power, and improved spatio-temporal gait characteristics may result from a program that combines muscle strengthening with treadmill training using body weight support.

Recent advances in neuroscience have demonstrated that voluntary exercise, treadmill activity, skills training, and forced limb use can promote brain plasticity and functional changes in both animals and humans.25–29 These findings provide promising evidence in support of the nervous system's potential to recover after stroke-related brain damage. However, there are numerous factors (eg, lesion effects, co-morbidities, behavioral experience) that affect individual neurologic and functional recovery after stroke.30 This case study presents an individual with stroke who participated in the Phase II single-blind, randomized clinical trial (RCT) “Strength Training Effectiveness Post-Stroke (STEPS).” The intent of this case study is to describe outcomes associated with a therapy program that combined task-specific and strength training for an individual post-stroke and to discuss some possible mechanisms and modulating factors that may have affected the post-stroke neurologic recovery and responsiveness to intervention.

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CASE REPORT

JS was a 37-year-old female who sustained a large right middle cerebral artery ischemic stroke on April 21, 2002. She had very supportive family which included a devoted husband and 3 daughters between grade school and junior high school. She reported that one of her greatest functional problems was slow walking. This made her feel that she was a burden to her family and friends who often took her on social outings. At this time, she had been discharged from all outpatient physical and occupational therapy.

Figure 1 is the T2 weighted MRI image in the coronal and axial planes at the level of greatest lesion extent. The MRI images revealed a large right frontal-parietal lesion that included the primary motor and sensory cortices of the hand region. The lesion extended subcortically to include the white matter tracts of the posterior limb of the internal capsule. The stroke resulted in a dense left hemiparesis with no functional use of the left upper extremity.

Figure 1

Figure 1

After providing institutionally approved IRB informed consent, JS received baseline assessments by a blinded evaluator and was randomly assigned to an intervention group that received 12 sessions of body weight supported treadmill (BWST) training alternated with 12 sessions of locomotor-based strength training (LBST). She received 24 sessions over a 6-week period; four 1 hour treatment sessions per week provided by a physical therapist that was standardized on the STEPS intervention protocols. She was enrolled in the STEPS study 15 months post-stroke.

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Clinical Assessments

Body function and structure measures

At baseline assessments (Table 1) her lower extremity Fugl-Meyer motor scores were 21 out of 34 with limited movements out of synergy consistent with a Brunnstrom stage IV motor control. She was able to complete all movements in synergy with minimal ability to flex her knee independent of synergy in the sitting position. Her Berg Balance Score at baseline was 52 out of 56 which is above the range for falls risk. She reported no falls in the past 12 months.

Table 1

Table 1

Paretic and nonparetic lower extremity strength was determined with a standardized protocol to measure isometric torque (Nm) using a Biodex dynamometer. Standardized positions were used to determine strength of the hip flexors/extensors, knee flexors/ extensors, and ankle dorsiflexors/plantarflexors, bilaterally. For JS, composite (summed torques of all muscle groups) were 383 Nm for the nonparetic and 201 Nm for the paretic LEs (Fig 2A) which validates the presence of left hemiparesis.

Figure 2

Figure 2

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Activity measures

Walking velocity at free (self-selected) and fast walking speeds were determined using a stopwatch to time the middle 10 meters of a 14 meter walkway. Walking velocity has demonstrated validity, reliability, and sensitivity as an objective measure of functional recovery post-stroke.6 Two trials were timed and averaged to determine walking speed in meters/second. She was tested using the brace and assistive device typically used for community ambulation. For JS, baseline free walking speed was 0.50 m/s and fast walking speed was 0.62 m/s with a fixed joint, plastic, ankle-foot orthosis (AFO), and a straight cane. A free walking velocity of 0.50 m/s represents 37% of normal for a young adult.

Walking endurance was determined by the distance walked in 6 minutes. The 6-minute walk has demonstrated validity and reliability as an indicator of walking endurance post-stroke.31 Two cones were place in a tiled corridor separated at 18 meters distance. She was instructed to walk as quickly as she could in 6 minutes in order to cover as much distance as possible. Chairs were placed every 6 meters if she had to rest. Encouragement was provided in a standardized manner every 1 minute. For JS, the distance walked in 6 minutes was 178.3 meters.

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Participation measure

The Stroke Impact Scale (SIS) was used to determine JS's perception of her stroke-related health status and post-stroke recovery. The SIS is a self-report tool that was developed through interviews with individuals with stroke and their caregivers and has demonstrated reliability and validity in a stroke population as a measure of function and health-related quality of life.32–34 Baseline SIS scores are reported in Table 2. In addition, individuals are asked to rate their perception of their overall post-stroke recovery on a scale for 0 to 100% (fully recovered). JS reported herself as 30% recovered at the time of her enrollment in the STEPS study.

Table 2

Table 2

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Instrumented Gait Analysis

In order to investigate the kinematic, kinetic, and muscle activation characteristics associated with treatment response, JS received a fully instrumented gait assessment including intramuscular dynamic EMG recording prior to and after the first and 24th treatment sessions, respectively. JS ambulated at self-selected speeds for free and fast walking trials conducted with her cane, but without her AFO over a 10m walkway with the middle 6m designated for data collection. Simultaneous recordings were collected of foot-floor contacts, lower extremity kinematics/kinetics, and EMG activity. Gait outcomes included pre- and postmeasurement of spatio-temporal characteristics (cadence, stride length, paretic single-limb stance time) and paretic limb kinematics and kinetics (moments and power) for the ankle, knee, and hip. In addition, EMG timing and intensity across the gait cycle were collected.

Compression closing foot switch insoles with separate switches located under the heel, first and fifth metatarsal heads and toe regions were taped to the bottom of both of the subjects shoes. The foot switches recorded the foot-floor contact patterns which were used to calculate the spatio-temporal characteristics of walking and to provide delineation of stance and swing and single and double limb support phases of the gait cycle. Gait speed without the AFO decreased to 0.33 m/s and 0.42 m/s for free and fast walking, respectively. Spatiotemporal gait characteristics were a cadence of 57 steps/min, a stride length of .69 meters, and a paretic limb single limb stance (SLS) time of 14% of the gait cycle (Table 1).

A VICON motion analysis system was used to define the 3-dimensional motion of the subject's hemiparetic lower limb. Six infrared, 50 Hz cameras, recorded the location of fourteen retro-reflective landmarks taped onto the skin over 14 bony landmarks of the pelvis, thigh, shank, and foot. Intramuscular EMG was recorded with bipolar, fine-wire electrodes inserted into the belly of 8 muscles in the hemiparetic lower extremity (gluteus maximus, vastus intermedius, soleus, gluteus medius, adductor longus, anterior tibialis, semimembranosus, rectus femoris) using a 25 gauge needle as a cannula. EMG activity during walking was normalized by the signal elicited during a maximal voluntary contraction of each muscle performed in supine except for the gluteus medius which was tested in side-lying and soleus which was tested in standing with a single limb heel rise.

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INTERVENTIONS

The BWST training protocol required the participant to walk on a treadmill for four 5-minute training bouts at speeds within the range of 1.5–2.5 mph (.67–1.12 m/s). The participant was allowed to take as many rests as needed throughout each session in addition to the regularly scheduled rest at the 5-minute interval. The unloading on the lower extremities was progressively decreased from 40% to as low as 0% if the participant maintained proper limb kinematics during treadmill walking with or without assistance provided by a physical therapist. [Limb Kinematics During Treadmill Walking symbol.]

Symbol

Symbol

The LBST training protocol required the participant to cycle with the lower extremities on a modified Biodex (Shirley, NY) semi-recumbent isokinetic ergometer that offers resistance during both the flexion and extension phases of pedaling. The speed on the bike was set to 120 rpm. The apparatus includes a releasable seat, such that it is allowed to slide along a linear track similar to a leg press machine; therefore, the limb is loaded during pedaling. Load levels were increased progressively adding preset rubber bands of 10 pound increments up to 100 lbs. Load during the pedaling intervention was determined during a 20-repetition test until the participant was unable to maintain extended leg pedaling for more than 12 out of 20 of the cyclic repetitions. The intervention consisted of 10 sets of 15–20 cyclic repetitions. [Locomotor Based Strength Training symbol.]

Table 3 shows the exercise progression for each training protocol. In each BWST session, she was able to walk the 45-minute bouts for a total walking time of 20 min per session. Over the course of BWST training, JS decreased her percentage of body weight support from 40% in session 1 to 20% in BWST session 12 and decreased the number of trainer assistants from 3 to 2. For LBST, JS was able to cycle with 80 lbs of load for a peak number of 18 repetitions over the 10 sets in session 1. By midway through training, she was using the maximum load available on the resisted cycling bike (100 lbs), therefore, between the middle and end of training the number of repetitions was increased in order to continue to progress the exercise across all 12 training sessions (peak repetitions, 46).

Table 3

Table 3

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OUTCOMES

Clinical measures

After 24 sessions of training (Table 1), hemiparetic lower extremity selective motor control improved as noted by a modest increase in the Fugl-Meyer motor score from 21/34 to 24/34. JS could now perform selective movement of knee flexion and dorsiflexion in sitting. The Berg Balance score decreased from 52/56 to 49/56. Free walking speed increased by 18% (0.59 m/s) and fast walking speed increased by 15% (0.71 m/s) after training. Distance walked in 6 minutes increased by 4% to 184.4 meters. JS continued to make motor and functional improvements between the last training session and the 6-month follow-up. Compared to baseline, at 6 months there was a 20% increase in free walking speed, 21% increase in fast walking speed, and 13% increase in distance walked in 6 minutes. LE Fugl-Meyer motor scores were maintained and the Berg Balance score increased to 54/56 from 52/56.

There were no changes in the nonparetic LE composite strength between the baseline and post-24 session measurements. However, nonparetic LE composite strength increased 14% between the end of training and the 6-month follow-up (Figure 2A).

In contrast, paretic LE composite strength increased 30% from baseline to the post-24 session measurement and continued to show an additional 19% increase between post-training and the 6-month follow-up (composite torque: baseline, 208.5 Nm; post-24, 271 Nm, 6-mo, 310.1 Nm). In order to determine if the composite value was a reflection of increased strength across all or select muscle groups, individual torque values for the baseline, post-24, and 6-mo follow-up are shown in Figure 2B. This figure demonstrates that between baseline and post-training the greatest torque gains (in ascending order) were present in the plantarflexors, hip flexors, knee extensors, and hip extensors. At 6 months, torque increases were evident in paretic plantarflexors and, most notably, hip extensors while the other muscle groups either decreased or maintained strength. Isometric toques increased 28% for plantarflexor and 45% for hip extensors.

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Biomechanical gait measures

Table 1 shows the spatiotemporal gait characteristics at baseline and post-treatment. Gait speed without the AFO increased 9% from 0.33.m/s to 0.36 m/s. This post-treatment improvement was only half as much as when she ambulated with the AFO. Te improvement in velocity resulted primarily from increases in stride length (from 0.69 to 0.74 meters) as opposed to cadence (from 57 to 58 steps/minute). Paretic limb single limb stance time increased from 14% to 18% of the gait cycle; an improvement from 33% to 44% of normal.

The primary changes in the biomechanical parameters of walking occurred in the kinematics of the hip and knee (Figure 3). Hip extension motion in single limb stance was incomplete with 15° of residual flexion at baseline, and improved to 3° of residual flexion at the postintervention assessment. Similarly, peak knee extension in stance improved from 10° flexion to 2° hyperextension. At the ankle, dorsiflexion during swing was absent at baseline and the ankle moved to 12° of plantarflexion from mid swing through initial contact. Te rapid plantarflexion of push-of was reduced. Ankle motion was not improved at the postintervention test and in fact, demonstrated a further reduction in dorsiflexion in swing. Te joint moments and powers were reduced at all joints (ankle, hip, and knee) and did not change significantly after the intervention; and therefore, are not presented.

Figure 3

Figure 3

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EMG measures

Dynamic EMG recording demonstrated changes in muscle activation primarily in the muscles of the hip and knee of the paretic leg with increased activation of gluteus maximus and gluteus medius in single limb stance and decreased inappropriate activity of semimembranosus in initial swing when it would impede thigh flexion (Figure 4). Post-treatment, gluteus maximus EMG intensity increased 3-fold as a percentage of the within session maximal effort manual muscle test intensity (pre 10.3 % MMT; post 30.7 %MMT) with normal onset at terminal swing that continued throughout stance. Gluteus medius intensity also increased from 14.9% MMT before the intervention to 22.2% MMT post training, evident primarily in the increased peak activity in early stance. Vastus intermedius demonstrated reduced intensity and duration in the post-training gait assessment (pre 15.1% MMT to post 9.7% MMT). At the ankle no improvements were seen in muscle timing or intensity during walking. Very low activation of anterior tibialis did not change and intensity of soleus activity decreased from 30.7% MAX to 23.9 % MAX following the intervention.

Figure 4

Figure 4

Figure 4

Figure 4

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Participation measure

A 10 point or greater change in a SIS domain score was identified a priori as a meaningful change. Te SIS questionnaire was administered to JS at baseline and at the 6-month follow-up. Te SIS domains that had a 10-point or greater change from baseline included: strength, mobility, emotion, and social participation (Table 3). These improvements in the strength and mobility domains lend validity to the appropriateness of interventions that JS participated in (the BWST and LBST protocols that were designed to increase walking mobility and LE strength). In addition, JS self-reported a 14-point increase in the emotional items (eg, feelings of sadness, burden to others, nothing to look forward to) and a 15-point increase in the social participation items (eg, participation in social, recreational, family, and spiritual activities). Finally, her assessment of her recovery on a scale of 0 (no recovery) to 100 (full recovery) changed from 30 at baseline to 50 at 6 months postintervention.

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DISCUSSION

Evidence for functional recovery

We report the results of a therapeutic program that included task-specific and locomotor-based strength training using a LE cycle ergometer to improve functional walking ability for an individual with chronic stroke. Functional recovery reflects an individual's ability to perform the tasks and activities of everyday life. Functional walking recovery includes the walking skills needed to walk at adequate speeds and distance to participate in community mobility. Perry et al3 have demonstrated that walking velocity is a significant predictor of community ambulation ability. In this case, JS demonstrated clinically meaningful changes in walking speed. Free walking velocity with her AFO and assistive device increased from 0.50 ms at baseline to .60 m/s at 6-months (20% increase); fast velocity increased 21%. According to the Perry's functional ambulation classification, this would indicate that JS improved from an initial classification as a most-limited community ambulator to classification as a least-limited community ambulator 6 months postintervention. In contrast, less change was noted in baseline to post-treatment gait lab measures of walking speed when the AFO was not worn (increase: free velocity, 9%; fast velocity, 17%). This would suggest that proper orthotic prescription is a critical element in functional walking ability post-stroke.

Changes in the distance walked in 6-minutes were not as impressive as the gains in walking speed. However, her 6-minute walking distance from baseline to 6 months increased 23 meters. This change is within the 95% confidence interval reported by Salbach and colleagues16 for a 1-yr post-stroke group who received functional task training and was of similar severity as JS. Walking 28 m is the distance needed to cross an intersection in a typical commercial district and has been used as a marker of clinically meaningful distance change in a 1-yr post-stroke population.16

An important finding is JS's perspective that her mobility skills improved and were less difficult to perform. Mobility items on the SIS ask the individual to report how difficult it is, from their perspective, to complete mobility tasks such as walking without losing balance, walking fast, or climbing fights of stairs. JS reported a 14 point increase in the SIS mobility and 19 point increase in the SIS strength domain at 6 months. Further work is needed to validate clinically meaningful changes within the SIS domains35 however, the SIS appears to be an effective measurement tool to assess an individual's perception of their health-status as it relates to functional mobility and strength. Evidence for functional recovery as a result of a combined task-specific and strengthening program is evident in both this patient's perspective and in clinically meaningful increases in objective measures of walking speed. In addition, the SIS results lend validity to the interventions that JS participated in since the BWST and LBST protocols were designed to increase walking mobility and LE strength.

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Potential mechanisms for response to treatment

One of the purposes of this case study was to probe potential mechanisms associated with the response to an intervention that incorporates task-specific and strength training to improve walking ability after stroke. We were particularly interested in understanding if the intervention was effective, was it due to compensation (ie, movement strategies that are primarily reliant on the less affected extremities with little evidence of increased use or change in movement patterns of the hemiparetic extremities) or functional neurorecovery (ie, the neural systems affected by the brain damage are engaged in order to promote neural adaptation).36 In the literature, this differentiation is sometimes referred to as the distinction between compensation versus restitution.37 We would argue that changes in strength that occur as a result of a relatively short activity or exercise bout such as the 6-week program provided in this case would be an example of neural adaptation. Whether these changes are peripheral or central cannot be unequivocally determined from this case report.

After stroke, the primary motor control impairments are loss of movement selectivity38 and decrease force production.13 For JS, the Fugl-Meyer motor score increased from 21 at baseline to 24 post-treatment which was maintained at the 6-month follow-up. With training, JS was able to perform movements with greater selectivity at the knee and ankle movements while sitting. Te Fugl-Meyer motor score has established reliability and validity that quantitatively measures stages of movement patterns during motor recovery post-stroke.39 An increase in the LE Fugl-Meyer score would provide some clinical evidence of motor recovery in JS's ability to selectively recruit motor unit pools in movements deviating from synergy. We are not aware of any literature that reports the clinical or functional significance of changes in the LE motor component of the Fugl-Meyer. Therefore it is difficult to interpret the meaningfulness of a 3 point increase.

Changes in central drive that impact motor unit recruitment and firing patterns as well as muscular factors such as fiber and motor unit properties can contribute to post-stroke weakness.13 With 6 weeks of combined task-specific and resistive cycling training, JS demonstrated an increase in composite paretic limb force production of 30%. Furthermore, by 6 months post-training there was a 49% increase in composite paretic limb and 14% increase in nonparetic limb strength, compared to baseline. It is well-established that short-term gains in muscle strength (eg, like those seen at the 6-week post-test in this case study) are most likely attributed to changes in neural adaptation (ie, more effective motor unit recruitment) than peripheral adaptation within the muscle.40 JS's EMG findings provide further evidence of neural adaptation as a result of training. Increased activation of the single joint hip extensor, gluteus maximus, was consistent with improvements in extension motion at both the hip and knee joints and the increased hip extension moment during terminal stance. This increased EMG intensity and more appropriate timing during gait, most likely, were due to changes in volitional drive. Additionally, the reduction in vastus intermedius activity reflected the reduced requirement for quadriceps support with the decreased residual knee flexion. It is interesting to note, however, that there was little change at the ankle particularly in ankle dorsiflexion kinematic and kinetics and in EMG for tibialis anterior. We have no neurophsysiologic measures to explain the 6-month increase in paretic and nonparetic lower limb strength. However, it is likely that increased use in functional mobility and peripheral muscular adaptations could explain continued increases in strength during the post-training period.

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Factors that modulate recovery and responsiveness to therapy

There are numerous covariates associated with stroke-related brain damage that can modify brain function, and hence, motor recovery and responsiveness to therapy. Cramer30 discussed the impact that clinical variables such as stroke characteristics (eg, location, volume, hemorrhagic, or ischemic injury), time post-stroke, age, and depression (to name a few) have on recovery potential. Lesion characteristics, particularly the degree of pyramidal tract damage, is associated with both stroke severity and recovery potential.41,42 In particular, stroke severity as determined by motor recovery measures such as the Fugl-Meyer motor assessment is directly correlated with the degree of pyramidal tract damage. In other words, lower Fugl-Meyer motor scores indicate more synergistic movement patterns that are associated with a greater degree of pyramidal tract damage and less motor recovery potential. From the MRI (Figure 1), the stroke-related brain damage in this subject's case was extensive and involved substantial damage to the pyramidal tracts. This degree of brain damage is most likely a modulating factor that limits the potential change of movement selectivity as measured by the Fugl-Meyer motor assessment and it is a poor prognostic indicator of more substantial improvements in neurologic recovery.

In addition to the individual and stroke-related factors that impact cortical reorganization and recovery, post-stroke therapy also can influence the restitution of neurological function. There is strong evidence that task-specific training performed at high intensity is associated with improvements in gait.43–45 With task-specific gait therapies such as BWST training, responsiveness to this particular intervention is related to the training parameters used. Recent evidence consistently demonstrates that treadmill training at higher speeds (ie, higher intensity), with or without body weight support, is more effective for improving gait speed post-stroke then training at slower speeds.17,18,46 These reports of differences in therapeutic effectiveness related to the type and dosing of the exercise program illustrate the modulation that therapy itself has on individual recovery. Te interventions protocols selected for the STEPS study were specifically designed to ensure that the exercise programs were of high intensity and adequately progressed from session to session. In this subject's case, the improvements in strength and functional performance that occurred provide validity for the intervention protocol and an opportunity to explore the mechanisms of response to treatment.

Careful examination of an individual case such as JS can be informative since the specific individual characteristics she brings to a structured and standardized exercise protocol can reveal important attributes that may affect response to therapy. JS made clinically meaningful changes in her functional gait speed and paretic limb strength after participating in a therapy regimen that combined task-specific and strength training. Te biomechanical and EMG gait analysis suggest that changes in proximal strength and activation of the hip musculature resulted in improvements in trailing limb posture during terminal stance and greater single limb stance time on the paretic limb with less need for quadriceps activation. In contrast, there was little evidence of change in the ankle musculature or ankle kinematics/kinetics. In fact, ambulation with an AFO contributed to significantly increased overground walking speeds both before and after the intervention.

Why were changes realized at the hip and knee but not at the ankle? Te MRI scan of the stroke lesion (Figure 1) shows extensive damage to white matter tracts that extend from both UE and LE motor cortical areas. LE motor cortical areas contribute to walking particularly as it relates to the modulation of both tibialis anterior and gastroc/soleus during volitional ankle movements and of tibialis anterior during the swing phase of gait.47–49 For JS, the extensive damage to these pyramidal tract neurons could be a modulating factor that interferes with central drive from these cortical areas, and hence, significant motor unit recruitment to the ankle. JS's moderate stroke severity and LE Fugl-Meyer scores provide validating evidence for this interpretation. While there is some literature that has examined the relationship between UE recovery and lesion location/size,41,42 there is no literature to date that has specifically examined this relationship as it relates to lower limb and walking recovery. Clearly, more work is needed to better understand the effects of brain lesion effects on walking recovery.

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IMPLICATIONS FOR CLINICAL PRACTICE

This case report describes how a combined therapeutic program that includes both task-specific and strength training can be associated with clinically meaningful changes in walking function. Te mechanisms associated with response to therapy are multifaceted and driven by factors that are directly associated with the individual and the therapeutic intervention. In this case, a carefully implemented and standardized program was developed based upon the literature on task-specific and strength training that used training parameters and exercise progression designed to maximize response to therapy and promote walking recovery after stroke. We report findings from neurophysiologic and biomechanical measures and propose that response to therapy was related to neural adaptation and not solely compensation. The immediate post-treatment and longer-term gains in LE strength most likely contributed to JS's changes in walking speed and functional mobility that were noted at the 6-month follow-up. We cannot exclude the possibility that compensatory strategies are a component of the functional gains that this individual made since JS still presents with moderate stroke severity and limitations in volitional control of the paretic limbs. One of the major limiting factors for JS is the extensive nature of the stroke-related brain damage. Given this limitation, it appears that the neural systems related to proximal hip control during walking were more responsive to our intervention than the ankle where little change was observed. In addition, an appropriately prescribed AFO was a critical element of functional walking and community mobility for this individual.

Based upon this case, we propose the following clinical implications for patient management. Functional recovery that results in clinically meaningful gains can occur with a multifaceted and comprehensive rehabilitation program for walking recovery after stroke. A therapeutic program that included intense, task-specific, repetitive walking practice (such as BWST), exercise to increase muscle strength and endurance in muscles that support locomotion (such as BLST), and proper LE orthotic and assistive device prescription produced positive outcomes related to walking recovery in the case of chronic stroke. This suggests that home exercise programs could be designed that specifically target the muscle groups that can respond to strength training. For individuals with moderate to severe stroke and little distal control at the ankle such as the one presented in this case report, a program that emphasizes proximal muscle strength may be more effective in contributing to functional walking gains than exercises that focus on distal muscle strength.

Regardless of the mechanism underlying recovery, an individual's perception of health-status, participation, and quality of life can be positively impacted by therapeutic interventions. Interventions that can improve walking speed and endurance can result in self-reported changes in mobility, lead to improvements in emotional well-being, and increase participation in meaningful social, recreational, and family activities. Despite the mobility and participation gains reported by the individual in this case report; there was little evidence for improvements in instrumental activities of daily living, which underscores the importance of a multidisciplinary effort to address more areas of health and well-being after stroke.

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ACKNOWLEDGEMENTS

This study was supported by a grant from the Foundation for Physical Therapy to establish PTClinResNet: A clinical research network to evaluate the efficacy of physical therapist practice. We would like to acknowledge JS for her commitment throughout the study and her willingness to share her experiences. In addition, we acknowledge the efforts of our fellow investigator David Brown, PT, PhD, Northwestern University and the STEPS Evaluation and Intervention Therapists who were the clinicians of this multi-site clinical trial:

University of Southern California: Robbin Howard, Didi Matthews, Bernadette Currier, Arlene Yang, Barbara Lopetinsky, Maria Caro; Northwestern University: Nicole Furno, Nicole Korda, Carolina Carmona, Allie Hyngstrom, Sheila Schindler-Ivens, Lynn Rogers; Rancho Los Amigos National Rehabilitation Center: Craig Newsam, Valerie Eberly, JoAnne Gronley, Jennifer Whitney, Betsy King, Louis Iberra

This case study was presented as a platform presentation at the IIISTEP Conference, July 19, 2005 in Salt Lake City, UT.

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REFERENCES

1 Duncan PW, Zorowitz R, Bates B, et al. Management of Adult Stroke Rehabilitation Care: a clinical practice guideline. Stroke. 2005;36:e100–143.
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