Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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.
My back ground story is here:

Thursday, May 24, 2018

Assessing Hand Muscle Structural Modifications in Chronic Stroke

I got nothing useful out of this, but lots of numbers and mathematical signs.
imageYa Zong1,2,3, imageHenry H. Shin3, imageYing-Chih Wang4, imageSheng Li3, imagePing Zhou2,3 and imageXiaoyan Li3*
  • 1Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
  • 2Guangdong Work Injury Rehabilitation Center, Guangzhou, China
  • 3Department of Physical Medicine and Rehabilitation, University of Texas Health Science Center at Houston, TIRR Memorial Hermann Research Center, Houston, TX, United States
  • 4Department of Occupational Science and Technology, University of Wisconsin-Milwaukee, Milwaukee, WI, United States
The purpose of the study is to assess poststroke muscle structural alterations by examining muscular electrical conductivity and inherent electrophysiological properties. In particular, muscle impedance and compound muscle action potentials (CMAP) were measured from the hypothenar muscle bilaterally using the electrical impedance myography and the electrophysiological techniques, respectively. Significant changes of muscle impedance were observed in the paretic muscle compared with the contralateral side (resistance: paretic: 27.54 ± 0.97 Ω, contralateral: 25.46 ± 0.91 Ω, p < 0.05; phase angle: paretic: 8.81 ± 0.61°, contralateral: 10.79 ± 0.69°, p < 0.05). In addition, impedance changes correlated moderately with the CMAP amplitude in the paretic hand (phase angle: r = 0.66, p < 0.05; reactance: r = 0.58, p lt; 0.05). The study discloses significant muscle rearrangements as a result of fiber loss or atrophy, fat infiltration or impaired membrane integrity in chronic stroke.


Muscle weakness is a remarkable symptom in stroke and contributes significantly to impaired motor functions. To understand mechanisms underlying weakness, studies can focus on assessing changes in neural control and muscular properties. In particular, intramuscular electromyography (EMG) and morphological techniques have been applied to examine muscle structural rearrangements poststroke. Increased motor unit fiber density, larger and complex motor unit action potentials (13), small angular fibers, as well as fiber type grouping (4, 5) have been observed in the acute and chronic stages of stroke suggesting the process of muscle denervation and reinnervation. While these studies characterize structural alterations in the paretic muscles, most approaches involve invasive recording and are limited by sampling only small selective areas of the muscle.
Electrical impedance myography (EIM) is an emerging technique for noninvasive evaluation of muscle electrical conductive properties. It applies weak, high-frequency alternating current to the muscles and produces raw bio-impedance data without causing neuronal and muscular depolarization (6, 7). EIM measures three impedance parameters in terms of resistance (R), reactance (X), and phase angle [θ = arctan (X/R)] (7, 8), which represent the inherent resistivity of skeletal muscle relative to extracellular and intracellular fluid, the integrity of cell membranes, tissue interfaces and non-ionic substances, and membrane oscillation properties of the muscle respectively (912).
Electrical impedance myography has been used to examine muscle structural alterations in a number of neuromuscular diseases including amyotrophic lateral sclerosis (ALS), muscular dystrophy, and spinal muscular atrophy (6, 7, 1319). It is sensitive to muscle structural modifications in terms of atrophy, increased fat infiltration or connective tissue growth (2022). In addition, the technique demonstrates strong correlations with standard measures of ALS including ALS functional rating scale-revised, handheld dynamometry, and motor unit number estimation in tracking the progression of the disease (13, 17, 23).
Applications of EIM to assess poststroke muscle conditions are relatively limited in the literature. In a previous study, we examined muscle impedance properties in the biceps brachii and found significant changes of muscle structural properties in the paretic side (24). Since proximal muscles demonstrate different extents of impairment from distal muscles (25), it remains unknown whether findings from biceps brachii are applicable to hand muscles. In this study, we applied EIM technique to examine impedance changes in the hypothenar muscle poststroke. In addition, we measured the compound muscle action potentials (CMAP) of the muscle, to assess inherent electrical properties. CMAP is evoked by electrical activation of all functioning motor units and represents summation of all action potentials in spatial distribution. Application of the two different techniques to the same muscle may disclose different features of the muscle and improve current knowledge on structural changes in the paretic hand muscle.

Materials and Methods



Fourteen chronic stroke survivors participated in the study (8 female, 6 male, age: 63 ± 10 years, mean ± SD). They had a single incidence of stroke with the time course of stroke varying from 8 month to 15 years (80 ± 55 months, mean ± SD). All subjects were free of any other known neurological disorders or symptoms including neuropathy, radiculopathy, cervical spondylosis, or hyperglycemia. All subjects gave written informed consent in accordance with the Declaration of Helsinki. The protocol was approved by the Protection of Human Subjects (CPHS) at University of Texas Health Science Center at Houston.
Clinical assessment: hand recovery was evaluated using grip force and the Chedoke–McMaster assessment.


Experimental protocol included EIM and electrophysiological tests in the hypothenar muscle.
EIM Measurement
Subjects were seated upright with the examined arm in a natural, resting position on a height-adjustable table. Muscle impedance was measured using the mView EIM system (Myolex Inc., Boston, MA, USA). A handheld electrode array (P/N number: 20-00036) was placed on the muscle bulk with slight pressure applied by the experimenter. To further improve contact between the electrode and skin, saline wipe was used to moisten the skin before each trial. During the trial, alternating current at high frequencies from 1 kHz to 10 MHz was delivered to the muscle in discrete steps. Stimulation intensity was less than 1 mA which did not involve any neuronal or muscular depolarization. Impedance measurement was applied to each muscle multiple times until three consistent trials were saved. In this study, impedance was obtained from the pair of current electrodes with the largest inter-electrode distance of 32 mm in parallel to muscle fiber direction.
Muscle Response Measurement
Subsequent to the EIM test, CMAP was collected from the hypothenar muscle using an UltraPro S100 EMG system (Natus Neurology Incorporated, Middleton, WI, USA). Two disposable electrodes (Ag–AgCl electrode, 10-mm diameter) were placed on the motor point of the muscle and the distal phalanx of the little finger, respectively, as the active and reference electrodes. The ground electrode was positioned on the dorsal side of the hand. A standard bar electrode was placed on the ulnar nerve, 2 cm proximal to the wrist crease with the cathode oriented distally. After the electrodes were securely attached, the examined hand was restrained in pronation by Nylatex® wraps (4″ width).
Electrical stimulation was applied in single impulses of 200 µs width. It was initiated from relatively low intensity and increased at 2 mA per step until the maximum muscle response was reached. To guarantee all motor units were activated, supramaximal stimulation was applied to record the CMAP. Muscle responses were sampled at a frequency of 48 kHz and band-pass filtered between 1 Hz and 10 kHz.

Data Analysis

Electrical impedance myography and muscle response data were processed using the Matlab software (MathWorks, Natick, MA, USA).

EIM Analysis

Impedance variables including resistance (R), reactance (X), and phase angle (θ) were averaged across three trials at the frequency of 100 kHz for comparison.

Muscle Responses

Compound muscle action potential amplitude was measured as the difference between negative peak and baseline of the waveform.
All data were screened for outliers and normality of distribution. Paired t-test was applied to compare the differences of impedance variables (R, X, and θ) and muscle responses (CMAP amplitude) between paretic and contralateral muscles. Pearson correlation analysis was used to assess linear relationships between EIM variables and the CMAP amplitude. Clinical relevance was examined by calculating Spearman ρ coefficients between impedance variables or muscle responses and the Chedoke scores. Pearson coefficients were calculated between two clinical measures of grip force and duration of the stroke, and the EIM or CMAP amplitude. Statistical significance was set as p < 0.05. Results are reported in a mean ± SE format unless specified.


Impedance variables and CMAP amplitude were averaged across 14 subjects and compared between the paretic and contralateral muscles as illustrated in Figure 1. Among them, eight subjects had paresis in the dominant hand and six subjects had paresis in the non-dominant side. Statistical analysis indicated a significant increase of resistance (R) and a significant decrease of phase angle (θ) in the paretic hypothenar muscle compared with the contralateral side (R: paretic: 27.54 ± 0.97 Ω, contralateral: 25.46 ± 0.91 Ω, p lt; 0.05; θ: paretic: 8.81 ± 0.61°, 10.79 ± 0.69°, p < 0.05). On the other hand, no significant differences in the reactance (X) and the CMAP amplitude were observed between two sides (X: paretic: 4.32 ± 0.37 Ω, contralateral: 4.91 ± 0.43 Ω, p = 0.19; CMAP: paretic: 9.34 ± 0.79 mV, contralateral: 10.28 ± 0.7 mV, p = 0.19).

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