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, October 14, 2022

Quantitative measurement of resistance force and subsequent attenuation during passive isokinetic extension of the wrist in patients with mild to moderate spasticity after stroke

Well, you measured spasticity. WITH NO CURES LISTED, this was all fucking useless. The whole point of stroke research is to cure patients, this did nothing for that.

Quantitative measurement of resistance force and subsequent attenuation during passive isokinetic extension of the wrist in patients with mild to moderate spasticity after stroke

Abstract

Background

Spasticity is evaluated by measuring the increased resistance to passive movement, primarily by manual methods. Few options are available to measure spasticity in the wrist more objectively. Furthermore, no studies have investigated the force attenuation following increased resistance. The aim of this study was to conduct a safe quantitative evaluation of wrist passive extension stiffness in stroke survivors with mild to moderate spastic paresis using a custom motor-controlled device. Furthermore, we wanted to clarify whether the changes in the measured values could quantitatively reflect the spastic state of the flexor muscles involved in the wrist stiffness of the patients.

Materials and methods

Resistance forces were measured in 17 patients during repetitive passive extension of the wrist at velocities of 30, 60, and 90 deg/s. The Modified Ashworth Scale (MAS) in the wrist and finger flexors was also assessed by two skilled therapists and their scores were averaged (i.e., average MAS) for analysis. Of the fluctuation of resistance, we focused on the damping just after the peak forces and used these for our analysis. A repeated measures analysis of variance was conducted to assess velocity-dependence. Correlations between MAS and damping parameters were analyzed using Spearman’s rank correlation.

Results

The damping force and normalized value calculated from damping part showed significant velocity-dependent increases.

There were significant correlations (ρ = 0.53–0.56) between average MAS for wrist and the normalized value of the damping part at 90 deg/s. The correlations became stronger at 60 deg/s and 90 deg/s when the MAS for finger flexors was added to that for wrist flexors (ρ = 0.65–0.68).

Conclusions

This custom-made isokinetic device could quantitatively evaluate spastic changes in the wrist and finger flexors simultaneously by focusing on the damping part, which may reflect the decrease in resistance we perceive when manually assessing wrist spasticity using MAS.

Trial registration UMIN Clinical Trial Registry, as UMIN000030672, on July 4, 2018

Background

Spasticity is a common complication of various neurological diseases and lesions in the central nervous system [1,2,3]. It occurs in 17–46% of stroke patients [4] (17%/1 year [5], 42%/6 months [6], 46%/1 year [7]) within 12 months after onset. Spasticity is primarily observed in the elbow (79% of patients), wrist (66%), and ankle (66%) [8].

Spastic symptoms can induce pain, contractures, abnormal posture, decreased range of joint motion, tendon retraction, and muscle weakness in patients, which may also impair the patient’s quality of life and limit the potential success of rehabilitation [9,10,11]. Accordingly, spasticity management is an essential concept in neurological rehabilitation, and spasticity needs to be measured accurately.

The Modified Ashworth Scale (MAS) measures the level of resistance to passive movement. It is most widely used for evaluating spasticity in a clinical setting and has been investigated in many studies [12], in which the assessor subjectively graded the resistance to manual passive stretch. The MAS grades spasticity as follows: 0 = no increase in muscle tone; 1 = slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part is moved in flexion or extension; 1 +  = slight increase in muscle tone, manifested by a catch followed by minimal resistance throughout the remainder (less than half) of the range of motion (ROM); 2 = more marked increase in muscle tone through most of the ROM, but the affected part is easily moved; 3 = considerable increase in muscle tone, passive movement is difficult; 4 = affected part is rigid in flexion or extension [13]. The MAS is easy to use in clinical practice because it takes little time and no equipment is needed to assess muscle tone [14, 15].

While there have been reports that the MAS shows poor reliability between raters [16,17,18], several other studies have reported good intra- and inter-rater reliability, mostly for the upper extremities [13, 19, 20], and better reliability for evaluations of the wrist flexor compared to those in the proximal elbow flexor or shoulder adductor [21].

Lance [22] defined spasticity as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex” that causes increased muscle tone and, subsequently, increased stiffness to restrict movement. On the other hand, when measuring spasticity in daily clinical practice, especially in patients with mild to moderate spasticity, we often feel not only an increase in muscle tone during passive movement, but also a subsequent sudden decrease in resistance force. This is known as the clasp-knife phenomenon [23]. In addition, in the definition of MAS, "catch and release" and "catch followed by minimum resistance" are mentioned. This sudden decrease in resistance after an increase in resistance during passive extension of the target muscle is a major characteristic of spasticity in patients with mild to moderate spasticity and is a noteworthy change.

To measure and evaluate spasticity more objectively, various quantitative approaches have been tested using different methodologies [24]. Several motor-driven or manually driven devices have been used in patients with stroke, and passive resistance forces have been measured in the ankle [25,26,27,28,29], elbow, [30,31,32,33] wrist [34,35,36,37], and finger [38] joints. Several studies have shown a significant correlation between the MAS and increased resistance to passive movement in the wrist joint [35, 36]. However, no studies have investigated the correlation between the MAS and force attenuation following increased resistance in the wrist joint when measuring spasticity in patients with stroke.

Since most patients with spasticity after stroke in previous studies showed consistent stretch reflexes at less than 100 deg/s in wrist flexor muscles [34] and at 30–60 deg/s in elbow or ankle joints [26, 39, 40], we thought it would be possible to measure spasticity with the instrument at speeds slower than those typically used. Furthermore, we wanted to avoid the appearance of pain after repetitive measurements.

We have developed a device that can measure passive resistance at low angular velocities and reduces excessive resistance to the wrist joint due to extension. We also focused on and analyzed the characteristic damping force observed after the maximum resistance with extension, which could reflect the decrease in resistance we sense while measuring MAS.

We considered that a safe and easy-to-use device that can evaluate such resistance may be useful in introducing the objective measurement of spasticity into daily clinical practice. The purpose of this study was to investigate whether a custom-made motor-controlled device could be used to safely measure extension stiffness in a relatively mild spastic wrist joint in a patient with a post-stroke hemiparetic upper limb. Furthermore, we wanted to clarify whether the subsequent damping changes after the peak resistance could quantitatively reflect the spastic state of the wrist flexors and extrinsic finger flexors involved in wrist stiffness by examining its correlations to the MAS.

More at link.

No comments:

Post a Comment