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.

Wednesday, October 28, 2020

Biomechanical control of paretic lower limb during imposed weight transfer in individuals post-stroke

So fucking what, you described a problem but offered NO SOLUTION.

Biomechanical control of paretic lower limb during imposed weight transfer in individuals post-stroke

Abstract

Background

Stroke is a leading cause of disability with associated hemiparesis resulting in difficulty bearing and transferring weight on to the paretic limb. Difficulties in weight bearing and weight transfer may result in impaired mobility and balance, increased fall risk, and decreased community engagement. Despite considerable efforts aimed at improving weight transfer after stroke, impairments in its neuromotor and biomechanical control remain poorly understood. In the present study, a novel experimental paradigm was used to characterize differences in weight transfer biomechanics in individuals with chronic stroke versus able-bodied controls

Methods

Fifteen participants with stroke and fifteen age-matched able-bodied controls participated in the study. Participants stood with one foot on each of two custom built platforms. One of the platforms dropped 4.3 cm vertically to induce lateral weight transfer and weight bearing. Trials involving a drop of the platform beneath the paretic lower extremity (non-dominant limb for control) were included in the analyses. Paretic lower extremity joint kinematics, vertical ground reaction forces, and center of pressure velocity were measured. All participants completed the clinical Step Test and Four-Square Step Test.

Results

Reduced paretic ankle, knee, and hip joint angular displacement and velocity, delayed ankle and knee inter-joint timing, increased downward displacement of center of mass, and increased center of pressure (COP) velocity stabilization time were exhibited in the stroke group compared to the control group. In addition, paretic COP velocity stabilization time during induced weight transfer predicted Four-Square Step Test scores in individuals post-stroke.

Conclusions

The induced weight transfer approach identified stroke-related abnormalities in the control of weight transfer towards the paretic limb side compared to controls. Decreased joint flexion of the paretic ankle and knee, altered inter-joint timing, and increased COP stabilization times may reflect difficulties in neuromuscular control during weight transfer following stroke. Future work will investigate the potential of improving functional weight transfer through induced weight transfer training exercise.

Background

Stroke is a leading cause of death and serious long-term disability in the United States [1, 2]. Individuals with hemiparesis due to stroke commonly demonstrate difficulty bearing weight on the paretic lower extremity and transferring weight from one leg to the other [3,4,5]. Reduced paretic limb weight bearing has been associated with functional deficits when rising from a chair [6], standing [7], and walking [8, 9]. The ability to transfer bodyweight between the lower limbs is related to impaired standing and stepping balance [10, 11] and gait performance [3, 12]. In particular, diminished weight transfer to the paretic limb contributes to gait asymmetries, which commonly lead to greater energy expenditure [13]. Previously we reported the ability to transfer weight laterally to the paretic leg during single stance was associated with self-selected walking speed and the capacity to increase walking speed [14]. This may indicate that weight transfer deficits negatively affect forward progression. Indeed, forceful weight shift towards the paretic limb enhanced paretic lower extremity kinetics and muscle activities that contribute to forward progression [15]. Moreover, deficits in paretic limb weight-bearing contribute to lateral and vertical balance instability and are associated with risk of falling in individuals with chronic stroke [16]. These functional limitations can affect community participation and quality of life. Consequently, restoring the capacity to load the paretic limb is an important goal for rehabilitation post-stroke [17,18,19].

Despite considerable rehabilitation efforts aimed at improving weight transfer following a stroke [10, 20], the impairments in neuromotor and biomechanical control underlying weight transfer dysfunction remain poorly understood. Functional weight transfer requires the coordination of multi-joint actions to absorb the impact force and provide support to the body. In particular, the ankle and knee joints are key contributors to shock absorption [21,22,23,24] and body weight support [25]. Increased stiffness in the paretic limb knee and ankle joints has been reported in persons with stroke [26, 27]. Inadequate lower limb joint flexion may disrupt impact force regulation during weight acceptance and lead to instability that ultimately delays and prolongs weight transfer timing during locomotion. Alternatively, excessive ankle and knee joint flexion during loading may precipitate limb collapse and destabilize balance during weight transfer. Thus, both insufficient and excessive joint movement could affect weight transfer processes. In addition to the amplitude of paretic ankle and knee joint angular displacements, abnormalities in the relative timing of these joint motions (i.e., inter-joint coordination) may also contribute to impaired weight transfer following stroke.

Another key factor affecting functional weight transfer is the ability to regulate the center of pressure (COP) beneath the feet in relation to the body center of mass (COM). During locomotion, effective neuromotor control of the lower extremities contributes to regulating COM position and movement relative to the base of support to maintain stability and prevent falling. Compared with able-bodied adults, persons with chronic stroke have a reduced capacity to rapidly shift their COP to the stance limb during gait initiation [28], reflecting abnormalities in balance control during weight transfer. Because hip and ankle musculature regulates COM and COP movements [29], difficulties in controlling hip kinematics and hip-ankle joint coordination may contribute to delayed and reduced weight transfer after a stroke.

To further address the foregoing issues, this study examined the potential biomechanical factors that could affect lower paretic limb weight bearing and weight transfer performance following stroke. After stroke individuals often limit their use of the paretic limb by favoring the use of the less affected leg during stance and gait [30]. An approach that forces individuals to fully load the paretic limb is warranted to reveal the performance capacity and assess the control of weight bearing and weight transfer. Accordingly, we designed a novel system that vertically displaces the support surface underneath one leg and therefore imposes weight transfer. By unilaterally introducing a perturbation that drops the standing support surface, this approach forces a rapid alteration in inter-limb weight bearing distribution and challenges medial–lateral balance control.

The primary purpose of this study was to characterize the kinematics and kinetics of the paretic lower extremity during an externally induced weight transfer towards the paretic limb in chronic stroke compared to age-matched controls. We hypothesized that, compared with able-bodied individuals, those with chronic stroke would show reduced and uncoordinated paretic limb joint angular displacements, and prolonged stabilization time of the COP velocity following an externally induced weight transfer. In addition, relationships between measurements during imposed weight transfer, motor recovery assessment (i.e. Chedoke McMaster Stroke Assessment leg and foot subscale), and clinical limb loading and balance performance (i.e. Four-Square Step Test (FSST) and Step Test (ST)) were explored. We expected that COP velocity stabilization time and CMSA scores would be associated with FSST and ST scores.

 

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