Showing papers by "Gordon L. Warren published in 2014"
TL;DR: The research literature supports constraint-induced movement therapy as an effective intervention to improve arm function in children with cerebral palsy.
Abstract: Objective: To systematically examine the research literature on the effectiveness of constraint-induced movement therapy on improving arm function in children with cerebral palsy, and to assess the association between the study effect size and the characteristics of the patients and intervention protocol. Data sources: A systematic literature search was conducted in PubMed, PsycINFO, Cochrane, CINAHL, Web of Science, and TRIP Database up to May 2014. Review methods: Studies employing randomized controlled trial design, children with cerebral palsy, comparing constraint-induced movement therapy with another intervention with a focus on arm function, and upper-extremity measures were included in this review. Methodological quality was evaluated using the Physiotherapy Evidence-based Database (PEDro) scale. Results: The literature search resulted in 27 randomized controlled trial studies with good methodological quality that compared constraint-induced movement therapy with other intervention therapy. Overall, constraint-induced movement therapy provided a medium beneficial effect (d = 0.546; p < 0.001) when compared with conventional therapy. For the subgroup analyses, presence of a dose-equivalent comparison group, intervention location, and time of follow-up were significant factors. Studies examining constraint-induced movement therapy effect without a dose-equivalent comparison group showed a large effect in children with cerebral palsy, but studies with a dose-equivalent group only showed a small effect. Children who received home-based constraint-induced movement therapy had a better improvement in arm function than those who received constraint-induced movement therapy elsewhere. Conclusion: The research literature supports constraint-induced movement therapy as an effective intervention to improve arm function in children with cerebral palsy.
67 citations
TL;DR: This new model with quantitative functional outcome measures offers a platform on which to evaluate treatment strategies designed to regenerate muscle tissue volume and restore limb function, consistent with clinical findings of reduced muscle function in large VML injuries.
65 citations
TL;DR: The preservation of muscle function and morphology in mdx mice indicates vibration is not deleterious to muscle lacking dystrophin, and vibration training at 45 Hz and 0.6 g did not significantly impact the tibial bone and the surrounding musculature, but may influence fat distribution in mice.
Abstract: The objective of the study was to determine if low intensity, high frequency vibration training impacted the musculoskeletal system in a mouse model of Duchenne muscular dystrophy, relative to healthy mice. Three-week old wildtype (n = 26) and mdx mice (n = 22) were randomized to non-vibrated or vibrated (45 Hz and 0.6 g, 15 min/d, 5 d/wk) groups. In vivo and ex vivo contractile function of the anterior crural and extensor digitorum longus muscles, respectively, were assessed following 8 wks of vibration. Mdx mice were injected 5 and 1 days prior to sacrifice with Calcein and Xylenol, respectively. Muscles were prepared for histological and triglyceride analyses and subcutaneous and visceral fat pads were excised and weighed. Tibial bones were dissected and analyzed by micro-computed tomography for trabecular morphometry at the metaphysis, and cortical geometry and density at the mid-diaphysis. Three-point bending tests were used to assess cortical bone mechanical properties and a subset of tibiae was processed for dynamic histomorphometry. Vibration training for 8 wks did not alter trabecular morphometry, dynamic histomorphometry, cortical geometry, or mechanical properties (P ≥ 0.34). Vibration did not alter any measure of muscle contractile function (P ≥ 0.12); however the preservation of muscle function and morphology in mdx mice indicates vibration is not deleterious to muscle lacking dystrophin. Vibrated mice had smaller subcutaneous fat pads (P = 0.03) and higher intramuscular triglyceride concentrations (P = 0.03). These data suggest that vibration training at 45 Hz and 0.6 g did not significantly impact the tibial bone and the surrounding musculature, but may influence fat distribution in mice.
16 citations
TL;DR: There is minimal evidence that CCR2 elimination provides protection against bone loss during disuse and estrogen loss, and the majority of the tibia’s structural and functional responses to OVX and DEN were similar regardless of the lack or presence of CCR1, indicating that C CR2 is not protective against bone Loss per se.
Abstract: Bone loss due to age and disuse contributes to osteoporosis and increases fracture risk. It has been hypothesized that such bone loss can be attenuated by modulation of the C-C chemokine receptor 2 (CCR2) and/or its ligands. The objectives of this study were to examine the effects of genetic elimination of CCR2 on cortical and trabecular bones in the mouse tibia and how bone loss was impacted following disuse and estrogen loss. Female CCR2 knockout (CCR2(-/-)) and wildtype mice underwent ovariectomy (OVX) or denervation of musculature adjacent to the tibia (DEN) to induce bone loss. Cortical and trabecular structural properties as well as mechanical properties (i.e., strength) of tibial bones were measured. Compared to wildtype mice, CCR2(-/-) mice had tibiae that were up to 9% larger and stronger; these differences could be explained mainly by the 17% greater body mass (P < 0.001) of CCR2(-/-) mice. The majority of the tibia's structural and functional responses to OVX and DEN were similar regardless of the lack or presence of CCR2, indicating that CCR2 is not protective against bone loss per se. These findings indicate that while CCR2(-/-) mice do have larger and stronger bones than do wildtype mice, there is minimal evidence that CCR2 elimination provides protection against bone loss during disuse and estrogen loss.
11 citations