Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, April 1, 2023

Immediate improvements in post-stroke gait biomechanics are induced with both real-time limb position and propulsive force biofeedback

I see nothing here that suggests they are solving the spasticity problem in walking.

Since 30% of survivors that have spasticity, they are screwed in walking recovery.

 Right now I have zero propulsion, the whole leg is swung from the hip

Immediate improvements in post-stroke gait biomechanics are induced with both real-time limb position and propulsive force biofeedback

Abstract

Background

Paretic propulsion [measured as anteriorly-directed ground reaction forces (AGRF)] and trailing limb angle (TLA) show robust inter-relationships, and represent two key modifiable post-stroke gait variables that have biomechanical and clinical relevance. Our recent work demonstrated that real-time biofeedback is a feasible paradigm for modulating AGRF and TLA in able-bodied participants. However, the effects of TLA biofeedback on gait biomechanics of post-stroke individuals are poorly understood. Thus, our objective was to investigate the effects of unilateral, real-time, audiovisual TLA versus AGRF biofeedback on gait biomechanics in post-stroke individuals.

Methods

Nine post-stroke individuals (6 males, age 63 ± 9.8 years, 44.9 months post-stroke) participated in a single session of gait analysis comprised of three types of walking trials: no biofeedback, AGRF biofeedback, and TLA biofeedback. Biofeedback unilaterally targeted deficits on the paretic limb. Dependent variables included peak AGRF, TLA, and ankle plantarflexor moment. One-way repeated measures ANOVA with Bonferroni-corrected post-hoc comparisons were conducted to detect the effect of biofeedback on gait biomechanics variables.

Results

Compared to no-biofeedback, both AGRF and TLA biofeedback induced unilateral increases in paretic AGRF. TLA biofeedback induced significantly larger increases in paretic TLA than AGRF biofeedback. AGRF biofeedback increased ankle moment, and both feedback conditions increased non-paretic step length. Both types of biofeedback specifically targeted the paretic limb without inducing changes in the non-paretic limb.

Conclusions

By showing comparable increases in paretic limb gait biomechanics in response to both TLA and AGRF biofeedback, our novel findings provide the rationale and feasibility of paretic TLA as a gait biofeedback target for post-stroke individuals. Additionally, our results provide preliminary insights into divergent biomechanical mechanisms underlying improvements in post-stroke gait induced by these two biofeedback targets. We lay the groundwork for future investigations incorporating greater dosages and longer-term therapeutic effects of TLA biofeedback as a stroke gait rehabilitation strategy.

Trial registration NCT03466372

Introduction

Hemiparesis following stroke causes unilateral deficits in gait kinematics and kinetics, contributing to slowed gait speed, gait asymmetries, and increased fall risk [1,2,3]. While increasing gait speed is a major goal of stroke rehabilitation [4, 5], improvements in speed can be achieved either through restoration of paretic limb function or compensatory strategies [6]. Measurement of kinematic and kinetic gait biomechanics variables can parse out restoration versus compensation as sources of gait recovery or training-induced improvements [7]. Reduced paretic propulsion, measured as the anterior component of the ground reaction force (AGRF) generated during late stance, is an important biomechanical deficit closely associated with gait speed and walking function post-stroke [8,9,10,11]. Importantly, individuals post-stroke demonstrate a paretic propulsive reserve [12] that can be exploited using gait training interventions [13, 14], with improvements in propulsion correlating to improvements in gait speed [8]. Thus, propulsion has emerged as a key modifiable post-stroke gait variable that is biomechanically and clinically relevant.

Previous studies have demonstrated two major biomechanical gait variables that contribute to overall propulsion, ankle plantarflexor moment, and trailing limb angle [15]. Ankle plantarflexors generate most of the force required to facilitate a smooth stance-to-swing transition [16]. Trailing limb angle (TLA), a measure of the overall limb angle or position with respect to the center of mass, places the leg in a better orientation to direct ground reaction forces more anteriorly [17]. Individuals post-stroke demonstrate deficits in both paretic plantarflexor moment and TLA [15], yet increases in paretic propulsion appear to originate mainly from improvements in paretic TLA [12, 18]. Post-stroke AGRF and TLA show robust inter-relationships, indicating that TLA can be used as a surrogate for paretic AGRF measurements [19]. Taken together, these studies suggest that targeting post-stroke TLA deficits may be a feasible and effective way of improving paretic propulsion.

Real-time biofeedback has emerged as a promising post-stroke gait training strategy that can target specific gait deficits on the paretic limb [20,21,22,23]. Previously, unilateral biofeedback targeting paretic propulsion was shown to induce significant increases in paretic limb propulsion without concomitant compensatory changes in the non-paretic limb [20]. However, translation of propulsion biofeedback from laboratory to clinic remains difficult because laboratory-based instrumented walkways or treadmills needed to measure AGRF may not be clinically accessible. The use of portable and wearable AGRF sensors for gait assessment is under study and not yet clinically available [24]. Moreover, estimation of propulsion through observational gait analysis is challenging even for movement experts with considerable clinical experience [25]. In contrast, measurements of TLA do not require the use of force platforms, and can be more easily subjectively estimated by clinicians based on the relationship of the forefoot to the pelvis or greater trochanter during observational gait analysis [19]. Recently, we demonstrated that able-bodied individuals are able to modulate TLA and AGRF unilaterally in response to real-time unilateral TLA biofeedback [26]. Thus, TLA biofeedback holds promise as a clinically applicable intervention that could preferentially increase paretic AGRF and reduce post-stroke propulsion deficits. While AGRF and TLA have been studied together as outcome variables in previous research, to our knowledge, biofeedback for these 2 biomechanical targets has not been directly compared in people post-stroke. Thus, an initial assessment of the feasibility and immediate biomechanical effects of TLA biofeedback on post-stroke individuals is needed.

Here, we studied the effects of TLA biofeedback on post-stroke gait biomechanics. Moreover, to assess its use as a suitable and clinically applicable alternative to AGRF biofeedback, we compared the immediate biomechanical effects of TLA biofeedback to AGRF biofeedback. We hypothesized that a biofeedback paradigm targeting paretic TLA would elicit favorable improvements in paretic propulsion and other post-stroke gait biomechanics impairments that are comparable in magnitude to AGRF biofeedback.

More at link.

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