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Objective: The contribution of the contralesional motor cortex to the impaired limbs is still controversial. The aim of this study was to investigate the role of descending projections from the contralesional hemisphere during voluntary elbow flexion on the paretic side. Design: Eleven healthy and 10 stroke subjects performed unilateral isometric elbow flexion tasks at various submaximal levels. Transcranialmagnetic stimulation was delivered to the hotspot of bicepsmuscles ipsilateral to the target side (paretic side in stroke subjects or right side in controls) at rest and during elbow flexion tasks. Motor-evoked potential amplitudes of the contralateral resting biceps muscles, transcranial magnetic stimulation--induced ipsilateral force increment, and reflex torque and weakness of spastic elbow flexors were quantified. Results: The normalized motor-evoked potential amplitude increased with force level in both healthy and stroke subjects. However, stroke subjects exhibited significantly higher force increment compared with healthy subjects only at low level of elbow flexion but similar at moderate to high levels. The greater force increment significantly correlated with reflex torque of the spastic elbow flexors, but not weakness. Conclusions: These results provide novel evidence that ipsilateral projections are not likely to contribute to strength but are correlated to spasticity of spastic-paretic elbow flexors after stroke. [ABSTRACT FROM AUTHOR]

Objectives: Botulinum toxin injection remains the first line management for focal spasticity in stroke patients. Botulinum toxin blocks presynaptic release of acetylcholine at the neuromuscular junction. Current knowledge of the innervation zone (IZ) of motor points is based on histological cadaver studies. The specific aim was to localize IZ non-invasively using high-density EMG recordings in healthy (Exp 1) and stroke (Exp 2) subjects. Design: We enrolled 11 young and healthy subjects in Exp 1 and 10 hemiparetic stroke subjects in Exp 2. The subjects had similar procedures in Exp 1 and 2. A high-density linear electrode array was placed from the proximal to distal tendon junction of biceps brachii muscle. EMG recordings were made on each side in a randomized order during the following two conditions: 1) maximum voluntary contraction (MVC) of elbow flexion and 2) electrical stimulation of the musculocutenous nerve at the intensity that generated maximum responses (M-wave) using an electrical stimulator. Stimulus artifacts were removed from EMG recordings offline. The IZ was localized where the polarity of motor unit action potentials changes, i.e., cross-correlation between adjacent two bipolar signals is the lowest. Results: Innervation zones were easily detected visually and were confirmed by cross-correlation analysis in both MVC and M-wave conditions for both healthy and stroke subjects. There were no differences in IZ locations between two sides in healthy and stroke subjects, and between MVC and M-wave methods. Conclusions: This study demonstrated successful and reliable localization of IZ of biceps muscles in both healthy and stroke subjects. The findings suggest that the M-wave technique could be applied to patients with severe spasticity to detect IZ. These patients usually can not produce voluntary contractions. High-density EMG recordings with M-wave technique could be used for accurate IZ location, which could guide botulinum toxin injection for maximum outcomes. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Spasticity, commonly defined as a phenomenon of velocity-dependent increase in muscle tone, is easily recognized, but difficult to be objectively quantified. The pathophysiological basis of spasticity is not completely understood, but based on the results of our previous studies, we hypothesize that post-stroke spasticity primarily results from hyperexcitability of reticulospinal projections. Clinically, reticulospinal hyperexcitability can be estimated through its antigravity property reflected by the altered resting joint angle of the affected muscles. The objective of this study was to evaluate whether the resting joint angle correlates with severity of spasticity. Specifically, we correlated the resting joint angle with other frequently used clinical and biomechanical methods for assessment of spasticity of the elbow flexors in chronic stroke survivors. METHODS: Seventeen hemiparetic stroke subjects (age: 37-89 years; 11 right and 6 left hemiplegia; averaged 54.8 months after stroke, ranging 12-107 months) participated in the study. Inclusion criteria were: 1) hemiplegia secondary to a single ischemic or hemorrhage stroke; 2) at least 6 months post-stroke; 3) spastic spasticity in elbow flexors of the impaired side, rated as Modified Ashworth Scale (MAS) less than 4; 4) able to understand and follow instructions related to the experiment; and 5) able to give informed written consent. The number of subjects with modified Ashworth scale score (MAS) =0, 1, 1+, 2, 3 was 3, 3, 5, 3, 3, respectively. The study had two sets of experimental measurements, clinical assessment and laboratory biomechanical measurements. The following clinical assessments were performed on each subject: (1) Active range of motion; (2) Passive range of motion; (3) MAS: Resistance to passive elbow flexion was assessed by stretching the muscle at a moderate speed and scoring the resistance using Modified Ashworth Scale; (4) Tardieu scale: Angle measured at a fast speed when the muscle reaction was first felt (if there was no muscle reaction, Tardieu angle was considered as 180°) (5) Resting angle (R): to evaluate gravity effect angle measured while the arm was relaxed. The fully extended position of the elbow was defined as 180°. The first two clinical assessments of spasticity were performed while subjects were comfortably seated. For the MAS, Tardieu and resting angle measurement subjects were explicitly instructed to stand and relax the affected arm. Measurements were taken after they were standing still for at least one minute. Subjects were allowed to take support of a person/chair/walker/ cane with the unaffected arm. Biomechanically, responses to constant velocity stretch of elbow flexors were measured on a customized apparatus. Only the affected side was tested. Three velocities 5°/s, 50°/s, and 100°/s were used. Three trials were performed at each velocity. A total range of 60- stretch was utilized with the ending position 10 degrees beyond the resting joint angle. Goniometer was used to position arm at the initial angle calculated for each patient. The trial began with the elbow in the initial posture (I), and then a constant velocity extension movement was imposed at the elbow until the elbow reached the predetermined ending posture (E). The elbow was then held in the ending posture for 2 seconds and returned to the initial posture at the same velocity. A rest period of about 20 seconds was allowed between trials to allow adequate recovery and to minimize the influence of stretch history on the response to the subsequent stretch. Subjects were instructed to relax during the trials, neither assisting nor resisting the joint extension to record reflex response. Torque was measured with a torque sensor and angular motion recorded with encoder using custom LabVIEWTM program. Data were analyzed offline using a customized MATLAB® (The MathWorks Inc.) program. Torque data was low-pass filtered to remove outlier noise evident in the raw data. To avoid data variation as a result of anthropometry spread between subjects, torque was normalized by body weight. To characterize the pattern of the response, average torque was calculated across all three trials for each speed. For each subject, peak torque was calculated for all speeds, between the start and end of rotation. The stiffness was computed by finding slope from the linear regression of torque-angle profile. The limits to finding slope were decided to be 25% and 75% of the maximum torque for a given trial. Correlations between clinical assessment (MAS, Tardieu, and resting angle) and biomechanical measures (peak torque and stiffness) were analyzed using spearman's coefficient (r). Furthermore a repeated measures one way analysis of variance (ANOVA) was used to analyze the effect of velocity on peak torque and stiffness. P<0.05 was chosen to indicate statistically significant differences. RESULTS: Peak torque increased with the velocity. A one-way ANOVA showed a significant effect of velocity on both peak torque (F[3,14]=15.63, p<0.0001) and stiffness (F[3,14]=12.68, p=0.0002). There existed strong correlation of the resting angle with peak torque (r ranged from 0.70 to 0.76, p<0.01) and stiffness (r ranged from 0.73 to 0.77, p<0.01). The resting angle also showed a strong positive correlation with Tardieu angle (r = 0.77, pG0.01) and strong negative correlation with MAS (r =- 0.89, p<0.01). All clinical measures, MAS (r ranged from 0.77 to 0.85, p<0.01), the resting angle (r ranged from 0.70 to 0.77, p<0.01) and Tardieu angle (r ranged from 0.57 to 0.65, p<0.05), showed strong correlation with biomechanical measurement (peak torque and stiffness). CONCLUSION: Our results of strong correlation between the resting joint angle and other frequently used clinical and biomechanical measurements indicate that the resting joint angle is valid in estimating severity of poststroke spastic spasticity. Resting angle observation for spasticity estimation can and will be an easy, yet valid method in clinical settings. In particular, resting angle observation will be clinically effective for spasticity estimation for small muscles or muscles which are not easily measurable by common clinical methods. [ABSTRACT FROM AUTHOR]

Objectives: Weakness after stroke is widely seen, and it often has adverse functional sequelae. Peripheral factors such as muscle fiber loss, fat infiltration, altered contractile properties, and an inability to fully activate the muscles on the impaired side are all contributing mechanisms. To further understand peripheral and central contributions, we used M-wave EMG recordings to reflect peripheral neuromuscular capabilities, and EMG recordings during maximal voluntary contraction (MVC) to reveal maximal voluntary activation. The ratio of MVC EMG and M-wave EMG provides an estimate of voluntary activation level. Accordingly, our specific aims were 1) to compare peripheral neuromuscular capabilities (M-wave EMG), maximal voluntary activation (MVC EMG), and voluntary activation level (the ratio) of the biceps brachii muscle between impaired and non-impaired side, 2) to correlate voluntary activation level with weakness. Design: Nine chronic hemiparetic stroke subjects (6 male, 3 female; mean: 62.7 years of age; months after stroke: 45.3, ranging from 28 to 93; MAS 0, 1, and 1+) participated in the experiment. Subjects were seated comfortably on a height- adjustable chair with the arm secured firmly on a customized apparatus. A linear electrode array of 20 bars was placed on the biceps brachii muscle for EMG recordings. Two conditions were tested on each side: 1) maximum voluntary contraction (MVC) of elbow flexion and 2) electrical stimulation of the musculocutaneous nerve at the intensity that generated maximum responses (M-wave). Torque during MVC tasks was recorded. The following variables were calculated: EMGM-wave, EMGMVC, peak torque (TorqueMVC), EMGMVC/M-wave on each side. To normalize individual absolute values, the ratios of EMGM-wave/TorqueMVC and EMGMVC/TorqueMVC were also computed. Weakness in defined as the ratio of TorqueMVC on the impaired side to the non-impaired side. Results: As expected, peak torque was significantly smaller on the impaired than non-impaired side (27.9 Nm vs. 44.5Nm, p=0.04). EMGM-wave was also significantly smaller on the impaired than non-impaired side (1743.7 uV vs. 3269.2 uV, pG0.0002). However, normalized EMGM-wave/TorqueMVC was not significantly different between two sides (85.2 vs. 90.0 uV/Nm, p=0.81). The MVC EMG data showed a different pattern. EMGMVC was smaller on the impaired than non-impaired side (588.0 uV vs. 1410.9 uV, p=0.01). Normalized EMGM-wave/TorqueMVC showed the same (19.6 vs. 32.1 uV/Nm, p=0.04). The voluntary activation level, EMGMVC/M-wave, was also smaller on the impaired than non-impaired side (0.27 vs. 0.40, p=0.08). Using linear regression analysis, the voluntary activation level on the impaired side was highly correlated with weakness (R=0.72), but very low (R=0.32) on non-impaired side. Conclusions: Collectively, our findings suggest that both peripheral and central factors contribute to post-stroke weakness, but activation deficit correlates most closely with weakness. These findings also provide further evidence to highlight the potential benefit from high-intensity exercises to enhance central activation for facilitation of motor recovery. [ABSTRACT FROM AUTHOR]