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.

Thursday, June 17, 2021

Markedly impaired bilateral coordination of gait in post-stroke patients: Is this deficit distinct from asymmetry? A cohort study

You didn't answer the obvious question. What protocols cure these problems? Or don't you understand you are to solve stroke problems? Not just describe them. 

Markedly impaired bilateral coordination of gait in post-stroke patients: Is this deficit distinct from asymmetry? A cohort study

2011, Journal of NeuroEngineering and Rehabilitation
 Ronald Meijer 1,2,3*, 
Meir Plotnik4,5, 
Esther Groot Zwaaftink 1, 
Rob C van Lummel 6, 
Erik Ainsworth 6, 
Juan D Martina 1
and Jeffrey M Hausdorff  4,7

Abstract

Background:
 Multiple aspects of gait are typically impaired post-stroke. Asymmetric gait is common as a consequence of unilateral brain lesions. The relationship between the resulting asymmetric gait and impairments in the ability to properly coordinate the reciprocal stepping activation of the legs is not clear. The objective of this exploratory study is to quantify the effects of hemiparesis on two putatively independent aspects of the bilateral coordination of gait to gain insight into mechanisms and their relationship and to assess their potential as clinical markers.
Methods:
 Twelve ambulatory stroke patients and age-matched healthy adults wore a triaxial piezo-resistive accelerometer and walked back and forth along a straight path in a hall at a comfortable walking speed during 2minutes. Gait speed, gait asymmetry (GA), and aspects of the bilateral coordination of gait (BCG) were determined.Bilateral coordination measures included the left-right stepping phase for each stride Øi, consistency in the phase generationØ_CV, accuracy in the phase generationØ_ABS, and Phase Coordination Index (PCI), a combination of accuracy and consistency of the phase generation.
Results:
 Group differences (p < 0.001) were observed for gait speed (1.1 ± 0.1 versus 1.7 ± 0.1 m/sec for patients and controls, respectively), GA (26.3 ± 5.6 versus 5.5 ± 1.2, correspondingly) and PCI (19.5 ± 2.3 versus 6.2 ± 1.0,correspondingly). A significant correlation between GA and PCI was seen in the stroke patients (r = 0.94; p <0.001), but not in the controls.
Conclusions:
 In ambulatory post-stroke patients, two gait coordination properties, GA and PCI, are markedly impaired. Although these features are not related to each other in healthy controls, they are strongly related in stroke patients, which is a novel finding. A measurement approach based on body-fixed sensors apparently may provide sensitive markers that can be used for clinical assessment and for enhancing rehabilitation targeting in post stroke patients.

Background

Among patients who experience a stroke, an altered gait pattern and impaired functional mobility are common,even at the conclusion of the typical rehabilitation process. Changes in gait post-stroke include reduced speed and increased energy expenditure. Gait asymmetry (GA)is also quite prevalent and is recognized as a key to understanding of the post-stroke deficits in gait and to improving the rehabilitation process in order to maximize mobility after a stroke [1,2]. However, a complete understanding of all of the factors that contribute to GA in post-stroke patients is lacking [2]. GA is only one aspect of bilateral activation of gait.When evaluating symmetry of walking, we address the question as to what extent the limbs perform similar walking movements. For example, one can compare the swing times performed by each leg. Usually, these measures are compared over series of steps and not per
 individual gait cycles [3]. Another feature is the timingof the left-right coordination of gait, namely the bilateralcoordination of gait (BCG). This feature is distinctivefrom GA since it evaluates the level of coordination between the ongoing stepping movements of both legs.In other words: the individual performance of each leg is not evaluated but rather the interaction between their activation. Evaluating the left-right stepping phasing pat-tern (ideally 180°) is a convenient way to assess this interaction and is also done based on a series of steps.These two aspects of bilateral activation of gait are not necessarily strongly correlated with one another nor are they simply synonymous terms [4,5]. In amputees, for example, the relative timing pattern of the gait cycle, the BCG, can remain constant while one leg will have much shorter swing times than the other, implying high asymmetry  [6]. Consistent with the idea that these two properties are independent, only a weak correlation between GA and BCG was observed in patients with Parkinson’s disease (PD)[4]; in these patients, unlike in amputees, a central nervous system asymmetric degenerative process likely leads both to increased GA and impaired BCG.The present exploratory study was designed to investigate the nature of the relationship between BCG and GA in patients with hemiparesis due to stroke and to examine the potential clinical utility of measures based on BCG. For this purpose, we utilized recently introduced metrics of BCG that were found to be sensitive in other cohorts of subjects (e.g., elderly and young), but have not yet been applied to post stroke patients [4]. In addition, we based our methods on body-fixed sensors(an accelerometer), an approach that could, theoretically,allow for easy implementation in clinical settings. We hypothesized that BCG and GA would both be impaired, compared to age-matched control subjects.Moreover, in contrast to what was observed in other populations, we speculated that impairment of BCG and increased GA are the result of the same underlying pathology in post stroke patients, and, therefore, that these measures would be closely related to each other. 
More at link.

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