Four weeks of balance training significantly improved self-reported function, static postural control as detected by TTB measures, and dynamic postural control as assessed with the SEBT. TTB measures were more sensitive at detecting improvements in static postural control compared with summary COP-based measures.

Context: Arthrogenic muscle inhibition is an important underlying factor in persistent quadriceps muscle weakness after knee injury or surgery.Objective: To determine the magnitude and prevalence of volitional quadriceps activation deficits after knee injury.Data Sources: Web of Science database. Study Selection: Eligible studies involved human participants and measured quadriceps activation using either twitch interpolation or burst superimposition on patients with knee injuries or surgeries such as anterior cruciate ligament deficiency (ACLd), anterior cruciate ligament reconstruction (ACLr), and anterior knee pain (AKP).Data Extraction: Means, measures of variability, and prevalence of quadriceps activation (QA) failure (,95%) were recorded for experiments involving ACLd (10), ACLr (5), and AKP (3).Data Synthesis: A total of 21 data sets from 18 studies were initially identified. Data from 3 studies (1 paper reporting data for both ACLd and ACLr, 1 on AKP, and the postarthroscopy paper) were excluded from the primary analyses because only graphical data were reported. Of the remaining 17 data sets (from 15 studies), weighted mean QA in 352 ACLd patients was 87.3% on the involved side, 89.1% on the uninvolved side, and 91% in control participants. The QA failure prevalence ranged from 0% to 100%. Weighted mean QA in 99 total ACLr patients was 89.2% on the involved side, 84% on the uninvolved side, and 98.5% for the control group, with prevalence ranging from 0% to 71%. Thirty-eight patients with AKP averaged 78.6% on the involved side and 77.7% on the contralateral side. Bilateral QA failure was commonly reported in patients.Conclusions: Quadriceps activation failure is common in patients with ACLd, ACLr, and AKP and is often observed bilaterally.

Objectives:To define the concept of arthrogenic muscle inhibition (AMI), to discuss its implications in the rehabilitation of joint injury, to discuss the neurophysiologic events that lead to AMI, to evaluate the methods available to measure AM1 and the models that might be implemented to examine AMI, and to review therapeutic interventions that might reduce AMI.Data Sources:The databases MEDLINE, SPORTDiscus, and CIHNAL were searched with the termsreflex inhibition, joint mechanoreceptor, Ib interneuron, Hoffmann reflex, effusion, andjoint injury. The remaining citations were collected from references of similar papers.Conclusions:AMI is a limiting factor in the rehabilitation of joint injury. It results in atrophy and deficiencies in strength and increases the susceptibility to further injury. A therapeutic intervention that results in decreased inhibition, allowing for active exercise, would lead to faster and more complete recovery.