Aims: We evaluated a Selective Bladder Denervation (SBD) device, which uses radiofrequency ablation, for the treatment of overactive bladder syndrome in terms of its nerve denervation, ablation characteristics, and post-treatment healing. Methods: Using the SBD device, eight fresh extirpated ovine bladder trigones were treated (90°C set point for 60 s) and nitroblue tetrazolium viability stained to characterize the ablation. In addition, 12 trigones were treated in vivo with three adjacent ablations and divided into survival cohorts: Day 7, Day 30, and Day 90 to assess the ablations and their associated healing. Results: The ex vivo single trigone ablations had a 7.9 ± 0.9 mm width and 5.7 ± 1.0 mm thickness that involved the submucosa, detrusor muscle, adventitia, and vagina. Microscopic viability staining confirmed complete nerve necrosis within the targeted tissue. The in vivo Day 7 trigones supported the ex vivo ablation characteristics and showed up to minimal inflammation, granulation tissue, and collagen fibrosis. Day 30 trigones had essentially absent inflammation and granulation tissue with evolving collagen fibrosis at the ablation's periphery. Day 90 trigones had essentially absent acute inflammation, minimal chronic inflammation, essentially absent granulation tissue, and up to mild collagen fibrosis. No ureteral/urethral alterations, vesico-vaginal fistulas, or other complications were identified. Conclusions: The SBD device provided a targeted trigone ablation with resultant denervation. The tissue healing timeline followed that expected for a hyperthermic ablation and was characterized by a fibroproliferative healing response with limited inflammation and granulation tissue. The ablations did not impact the overlying bladder mucosal surface.

Context: Performance on single-leg hopping (SLH) assessments is commonly included within return-to-sport criteria for rehabilitating athletes. Triaxial accelerometers have been used to quantify impact loading in a variety of movements, including hopping; however, they have never been attached to the tibia during SLH, and their method of fixation has not been investigated. Objective: The purpose of this study was to quantify triaxial accelerations and evaluate the influence of the fixation method of a lightweight inertial measurement unit (Blue Trident) mounted to the tibia during SLH performance. Design: Single cohort, repeated-measures experimental design. Participants: Sixteen healthy participants (10 females and 6 males; 20 [0.9] y; 1.67 [0.08] m; 66.0 [8.5] kg) met the inclusion criteria, volunteered, and completed this study. Interventions: Participants performed 2 sets of 3 SLH trials with an inertial measurement unit (1500 Hz) fixated to the tibia, each set with 1 of 2 attachment methods (double-sided tape [DST] with athletic tape and silicon strap [SS] with Velcro adhesion). Main Outcome Measures: Hop distance, peak tibial acceleration (PTA), time to PTA, and the acceleration slope were assessed during each hop landing. Results: Repeated-measures analysis of variance determined no significant effect of the attachment method on hop metrics (P = .252). Across 3 trials, both fixation methods (DST and SS) had excellent reliability values (intraclass correlation coefficient: .868–.941) for PTA and acceleration slope but not for time to PTA (intraclass correlation coefficient: .397–.768). The PTA for DST (27.22 [7.94] g) and SS (26.21 [10.48] g) was comparable and had a moderate, positive relationship (DST: r = .72, P < .01; SS: r = .77, P < .01) to SLH distance. Conclusions: Tibial inertial measurement units with triaxial accelerometers can reliably assess PTA during performance of the SLH, and SS is a viable alternative tibial attachment to DST.

Objective measures of disease progression are critically needed in research on Parkinson’s disease (PD) and atypical Parkinsonism but may be hindered by both practicality and cost. The Purdue Pegboard Test (PPT) is objective, has high test-retest reliability, and has a low cost. The goals of this study were to determine: (1) longitudinal changes in PPT in a multisite cohort of patients with PD, atypical Parkinsonism, and healthy controls; (2) whether PPT performance reflects brain pathology revealed by neuroimaging; (3) quantify kinematic deficits shown by PD patients during PPT. Parkinsonian patients showed a decline in PPT performance that correlated with motor symptom progression, which was not seen in controls. Neuroimaging measures from basal ganglia were significant predictors of PPT performance in PD, whereas cortical, basal ganglia, and cerebellar regions were predictors for atypical Parkinsonism. Accelerometry in a subset of PD patients showed a diminished range of acceleration and irregular patterns of acceleration, which correlated with PPT scores.