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Background: Anklebot therapy has proven to be effective in improving hemiparetic gait. However, neither ankle torque steadiness nor the relationship between changes in force control and functional tasks after therapy with Anklebot were described. Objective: To assess whether a single session of robotic therapy promotes short-term ankle adaptations that influence ankle torque steadiness and walking speed in individuals with chronic hemiparesis. Methods: A sample of participants who had residual hemiparesis deficits (hemiparesis group; n = 13) and age- and sex-matched healthy control participants (control group; n = 13). For sample characterization, balance, mobility, sensorimotor impairment, and daily living activities performance were measured. Results: Differences in functional tests were identified only when the control and hemiparesis groups (F = 29.1; p = .001) were compared during the 10-metre Walking Test. Regarding the pre- and post-robotic assistance session, no significant difference was observed for any comparison (p > .05), except for the steadiness test, as demonstrated by the standard deviation (F = 7.10; p = .01) and coefficient of variation (F = 6.20; p = .02). The hemiparesis group showed better torque steadiness during dorsiflexion post-robotic assistance therapy (p ≥ 0.02) when compared with pre-robotic assessment. Correlations were identified between steadiness and walking speed variables. Conclusion :  People with chronic hemiparesis presented short-term performance gains in torque steadiness, especially during dorsiflexion, after a single robotic therapy session. The robotic therapy did not influence the walking speed, although low to moderate correlations between torque steadiness variables and walking speed were observed.

Background: Research over the last two decades has highlighted the critical role of Brain-derived neurotrophic factor (BDNF) in brain neuroplasticity. Studies suggest that physical exercise may have a positive impact on the release of BDNF and therefore, brain plasticity. These results in animal and human studies have potential implications for the recovery from damage to the brain and for interventions that aim to facilitate neuroplasticity and, therefore, the rehabilitation process. Purpose: The aim of this study was to carry out a systematic review of the literature investigating how aerobic exercises and functional task training influence BDNF concentrations post-stroke in humans and animal models. Data Sources: Searches were conducted in PubMed (via National Library of Medicine), SCOPUS (Elsevier), CINAHL with Full Text (EBSCO), MEDLINE 1946-present with daily updates (Ovid) and Cochrane. Study Selection: All of the database searches were limited to the period from January, 2004 to May, 2017. Data Extraction: Two reviewers extracted study details and data. The methodological quality of the studies that used animal models was assessed using the ARRIVE Guidelines, and the study that evaluated human BDNF was assessed using the PEDro Scale. Data Synthesis: Twenty-one articles were included in this review. BDNF measurements were performed systemically (serum/plasma) or locally (central nervous system). Only one study evaluated human BDNF concentrations following physical exercise, while 20 studies were experimental studies using a stroke model in animals. A wide variation was observed in the training protocol between studies, although treadmill walking was the most common type of intervention among the studies. Studies were of variable quality: the studies that used animal models scored from 8/20 to 15/20 according to the ARRIVE Guidelines. The only study that evaluated human subjects scored 5/10 according to the PEDro scale and, which indicates a quality classified as "fair". Conclusions: The results of the current systematic review suggest that aerobic exercise promotes changes in central BDNF concentrations post-stroke. On the other hand, BDNF responses following functional exercises, such as reaching training and Constraint Induced Movement Therapy (CIMT), seem to be still controversial. Given the lack of studies evaluating post-stroke BDNF concentration following physical exercise in humans, these conclusions are based on animal work.

Background and Purpose: Muscle and bone form a functional unit. Residual physical poststroke impairments such as muscle weakness, spasticity, and decrease in function can promote metabolic bone changes. Moreover, muscle strength can influence this process. Thus, the purpose of the present study was to investigate bone volume and mobility performance in subjects with chronic hemiparesis post stroke., Methods: A cross-sectional study was performed on 14 subjects post stroke who were paired with healthy controls. Bone volume, isometric muscle performance, and mobility levels were measured. Midfemoral bone volumes were determined using magnetic resonance imaging, and muscular performance was measured by dynamometry. Mobility was measured using the Timed Up and Go Test and the 10-Meter Walk Test., Results: Regarding bone volume total, there was no difference in the medullary and cortical groups (P ≥ .05). During torque peak isometric flexion, the paretic group was significantly different compared with the other groups (P = .001). However, the control presented no difference compared with the nonparetic limb (P = .40). With regard to the extension isometric torque peak, the paretic limb was significantly different compared with the nonparetic (P = .033) and the control (P = .001) limbs, and the control was different from the nonparetic limb (P = .045). Bone volume variables correlated with the isometric torque peak., Conclusions: Chronic hemiparetic subjects maintain bone geometry compared with healthy volunteers matched by age, body mass index, and gender. The correlation between bone volume midfemoral structures and knee isometric torque was possible., (Copyright © 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Background: Brain-derived neurotrophic factor (BDNF) plays a critical role in sensorimotor recovery after a stroke. However, few studies have assessed the circulating BDNF levels in post-stroke humans to understand its changes. This study was conducted to measure BDNF serum concentrations in subjects with chronic hemiparesis, as well as to correlate serum concentrations with age, post-stroke time, total score of Stroke Specific Quality of Life Scale (SS-QOL), mobility subscale score, and motor function of SS-QOL., Methods: Seventeen chronic post-stroke subjects matched by age and gender with healthy controls took part in the study. Personal data (age, hemiparesis side, and post-stroke time) were collected, and a physical examination (weight, height, body mass index) and SS-QOL assessment were carried out. On the same day, after the initial evaluation, venous blood samples were collected from the chronic post-stroke subjects and the healthy subjects. The BDNF serum concentrations were measured blindly by enzyme-linked immunosorbent assay., Results: Subjects with chronic hemiparesis presented a decrease in BDNF serum compared with healthy subjects (P < .01). There was no correlation between BDNF serum levels with post-stroke time, age or quality of life, mobility, and the upper extremity motor function (P > .05). BDNF concentrations are related to structural and functional recovery after stroke; thus, this reduction is important to understand the rehabilitation process more clearly. However, more studies are needed considering the genetic variations and other tools to assess motor impairment and functional independence., Conclusion: Chronic post-stroke subjects presented a decrease in BDNF serum concentrations, without a correlation with post-stroke time, age, and quality of life., (Copyright © 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Introduction: Stretching (St) has been used for treating denervated muscles. However, its effectiveness and safety claims require further study., Methods: Rats were divided into: (1) those with denervated (D) muscles, evaluated 7 or 15 days after sciatic nerve crush injury; (2) those with D muscles submitted to St during 7 or 15 days; and (3) those with normal muscles. Muscle fiber cross-sectional area, serial sarcomere number, sarcomere length, and connective tissue density were measured. MMP-2, MMP-9, TIMP-1, TGF-β1, and myostatin mRNAs were determined by real-time polymerase chain reaction. MMP-2 and MMP-9 activity was evaluated by zymography. Collagen I was localized using immunofluorescence., Results: St did not prevent muscle atrophy due to denervation, but it increased fibrosis and collagen I deposition at day 15. St also upregulated MMP-9 and TGF-β1 gene expressions at day 7, and myostatin at day 15., Conclusions: Stretching denervated muscle does not prevent atrophy, but it increases fibrosis via temporal modulation of TGF-β1/myostatin and MMP-9 cascades., (© 2015 Wiley Periodicals, Inc.)