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.

Friday, May 14, 2021

Effect of post-stroke spasticity on voluntary movement of the upper limb

 Even if this is useful to quantify spasticity, it does absolutely nothing to cure spasticity. That is what survivors want, A CURE. GET THERE!

Effect of post-stroke spasticity on voluntary movement of the upper limb

Abstract

Background

Hemiparesis following stroke is often accompanied by spasticity. Spasticity is one factor among the multiple components of the upper motor neuron syndrome that contributes to movement impairment. However, the specific contribution of spasticity is difficult to isolate and quantify. We propose a new method of quantification and evaluation of the impact of spasticity on the quality of movement following stroke.

Methods

Spasticity was assessed using the Tonic Stretch Reflex Threshold (TSRT). TSRT was analyzed in relation to stochastic models of motion to quantify the deviation of the hemiparetic upper limb motion from the normal motion patterns during a reaching task. Specifically, we assessed the impact of spasticity in the elbow flexors on reaching motion patterns using two distinct measures of the ‘distance’ between pathological and normal movement, (a) the bidirectional Kullback–Liebler divergence (BKLD) and (b) Hellinger’s distance (HD). These measures differ in their sensitivity to different confounding variables. Motor impairment was assessed clinically by the Fugl-Meyer assessment scale for the upper extremity (FMA-UE). Forty-two first-event stroke patients in the subacute phase and 13 healthy controls of similar age participated in the study. Elbow motion was analyzed in the context of repeated reach-to-grasp movements towards four differently located targets. Log-BKLD and HD along with movement time, final elbow extension angle, mean elbow velocity, peak elbow velocity, and the number of velocity peaks of the elbow motion were computed.

Results

Upper limb kinematics in patients with lower FMA-UE scores (greater impairment) showed greater deviation from normality when the distance between impaired and normal elbow motion was analyzed either with the BKLD or HD measures. The severity of spasticity, reflected by the TSRT, was related to the distance between impaired and normal elbow motion analyzed with either distance measure. Mean elbow velocity differed between targets, however HD was not sensitive to target location. This may point at effects of spasticity on motion quality that go beyond effects on velocity.

Conclusions

The two methods for analyzing pathological movement post-stroke provide new options for studying the relationship between spasticity and movement quality under different spatiotemporal constraints.

Introduction

Stroke is one of the leading causes of long-term motor disability [1]. Most individuals with stroke present upper limb sensorimotor deficits that persist into the chronic stage (more than 6 months following the onset of stroke) [1, 2]. Spasticity, a sensorimotor disorder characterized by a velocity-dependent increase in muscle resistance stemming from hyperexcitability of the dysregulated muscle-spindle activity and stretch-reflex arc, is a prevalent sensorimotor deficit following stroke [3,4,5]. As many as 20–50% of patients develop spasticity during the first year after the event [6]. Objective and accurate quantification of spasticity and its effects on voluntary motion is important for guiding rehabilitation of the affected limbs.

While there are several clinical measures of spasticity, controversy remains about the most appropriate ones [7, 8]. Moreover, current measures are not sufficient for determining relationships between spasticity, movement deficits, and functional ability [9, 10]. To establish the effects of spasticity on voluntary motion, prior work has attempted to identify the relationship between the amount of hypertonicity measured at rest and movement disruption of voluntarily activated muscle [10,11,12]. One of the commonly used measures of spasticity is the Modified Ashworth Scale (MAS), which grades the resistance felt during passive stretching of muscles on a 6-point ordinal scale [13, 14]. A major drawback of the MAS is that the passive resistance during stretch characterizes only one aspect of the spasticity phenomenon (i.e., amount of hypertonia at rest). In addition, the scale has low resolution and poor-to-good test–retest reliability [13, 14].

Altered muscle resistance at rest may not be the only reason for disruption in voluntary movement [15]. The Tonic Stretch Reflex Threshold (TSRT) identifies where in the biomechanical joint range abnormal muscle resistance begins to contribute to disrupted muscle activation patterns and kinematics [16, 17] providing more specific information about how spasticity and movement deficits are related. TSRT can be determined objectively using the Montreal Spasticity Measure device [18]. The relationship of the TSRT angle with spasticity is based on the threshold control theory of motor control proposed by Feldman [19, 20]. According to the threshold control theory, voluntary movement is generated by regulating the spatial thresholds (of muscle length), at which muscle activation begins. The TSRT, i.e., the spatial threshold at zero velocity, is extrapolated based on the linear regression through measurements representing dynamic spatial thresholds evoked at different stretch velocities.

Upper limb recovery following damage to the brain refers to behavioral restitution (restoring premorbid movement patterns), to which spontaneous restitution is the main contributor. Improvements in upper limb function can also occur through behavioral compensation in which the system accomplishes functional tasks using altered movement patterns [21]. Standard clinical measures of upper limb function do not capture movement quality in a precise manner and therefore are inadequate for differentiating between restitution and compensation [22]. Measurement of movement kinematics and kinetics were suggested as the best way to address this problem. Although some guidelines are available regarding metrics used to characterize motor recovery [23], there is no consensus about how to identify the relationship between spasticity and motor dysfunction. Spasticity is affected by movement velocity and by multiple factors that are difficult to control, such as fatigue, secondary tasks, posture, psychological stress, and time of the day. The variability resulting from these aspects together with the inherent variability of human motion, especially during slow movement, which is typical in people with stroke, complicate the measurement of the effects of spasticity on kinematics. Therefore, a measure that can integrate the spatial and temporal aspects of motion while accounting for motion variability is required.

Stochastic models (based on random variables) offer a comprehensive yet parsimonious representation of motion data. They can capture complex, multi-dimensional, spatiotemporal phenomena while accounting for variability. These features lend stochastic models coupled with a stochastic distance measure (a distance measure between stochastic models) potential advantages over the more commonly used point measures (e.g., mean) for quantifying the effects of spasticity on voluntary motion. However, as the computation of stochastic distance measures is typically more complex, their benefits must be verified. There are several stochastic distance measures that differ according to the characteristics of the differences they capture and the ease of their computation for diverse distributions. Gaussian mixture models (GMMs) are particularly attractive stochastic models for motion representation, since they are easily adapted for spatiotemporal data representation and have standard efficient methods for parameter estimation based on maximum-likelihood estimators via the expectation–maximization algorithm [24] or Bayesian estimation [25]. Two examples of commonly used stochastic measures suitable for measuring distances between GMMs, are the bidirectional Kullback–Leibler divergence (BKLD) and Hellinger’s distance (HD) [26,27,28]. Selecting an appropriate stochastic distance measure is complex since different measures quantify different aspects of dissimilarity between distributions, and thus, are influenced differently by data attributes. HD seems particularly worth exploring in addition to KLD in the context of quantifying the influence of spasticity on voluntary motion. It offers a different perspective regarding the distance between models, and it can rectify some of the shortcomings of the KLD (and BKLD). GMMs, KLD and HD and their shortcomings are described in Appendix 1.

Davidowitz et al. [29] have recently proposed using GMMs and BKLD for quantifying the effects of spasticity (measured by the resistance to passive movement, as reflected in the MAS score) on kinematics of voluntary motion. In a cohort of 16 participants with stroke, spasticity measured by the MAS explained the BKLD of the elbow motion models of reaching movement from nearest neighbor models of healthy individuals. Deviations in individuals with stroke with higher spasticity levels were greater (larger BKLD) than those in individuals with mild spasticity. In the current study, we advanced this effort in two directions. First, we quantified the threshold angle of spasticity using TSRT. In addition, we compared two stochastic distance measures, BKLD and HD, and analyzed the advantages of each for measuring the effects of spasticity on voluntary movement. We hypothesized that both distance measures would be related to TSRT and that differences between the measured distances would highlight different aspects of spasticity, due to the variant sensitivity of BKLD and HD to different confounding variables. Preliminary results have been presented in abstract form [30, 31].

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