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Context: Quadriceps activation failure has been observed following various pathological conditions in a knee joint such as knee surgery, pain, effusion in knee, and osteoarthritis also could be aging matter. Those patients are unable to attain maximal quadriceps strength for a long period of time although their quadriceps itself is not damaged. This impairment is termed arthrogenic muscle inhibition (AMI). AMI has been of concern to clinicians because this weakness hinders the rehabilitation process considerably and delays recovery because strengthening protocols for the AMI could be largely ineffective. Clinically, it is important to understand neurophysiological mechanisms of the AMI to treat patients with the impairment. Objectives: This is a narrative review of the literature. The purpose of this review is to understand the following: (1) Why investigations of only peripheral spinal reflexive pathways are not enough for elucidation of the mechanisms of the AMI? (2) What we know about the role of the gamma spindle system in AMI so far? (3) Could a dysfunctional gamma spindle system contribute to AMI lead neural changes in upper central nervous system? and (4) Concerns that a clinician should take into consideration when deciding whether to apply therapeutic interventions for AMI. Data Sources: The databases PubMed, MEDLINE, SPORTDiscus, and CINAHL were searched with the terms arthrogenic muscle inhibition (AMI), reflex inhibition, joint mechanoreceptor, gamma loop, corticospinal pathway, spinal reflex, effusion, and joint injury. The remaining citations were collected from references of similar papers. Conclusions: AMI is a limiting factor in the rehabilitation of joint injury. Motor unit recruitment could be hindered in patients with AMI as a result of a dysfunctional gamma spindle system. Clinicians should understand the mechanism of AMI well in order to establish effective rehabilitation programs for AMI. Indeed, AMI is not caused by a single factor, but rather, multiple neural factors can change over time following the appearance of AMI. Therefore, multiple interventions targeting different neural pathways should be combined to achieve the ideal therapeutic goal for the treatment of AMI.

The purpose of this case study was to determine the effect of patellar taping, patellar bracing, and control condition on (a) patellofemoral congruence angle (PFC), (b) lateral patellar angle (LPA), (c) lateral patellar displacement (LPD), and (d) pain, as determined by the visual analog scale (VAS) during an 8-in. step-down. The subject was a 15-year-old female with a 3-year history of recurrent patellar subluxations and anterior knee pain syndrome. Results revealed the following: control condition—PFC 41.4-1.1°, LPA 19.9-6.9°, LPD 18.6-8.3 mm, VAS 8.8 cm; tape—PFC 46.2-2.3°, LPA 25.1-2.9°, LPD 24.2-7.5 mm, VAS 0.8 cm; brace—PFC 3.4-16.5°, LPA 7.9-0.8°, LPD 9.4-4.7 mm, VAS 0.3 cm. Patellar bracing was effective in centralizing the patella as revealed by the PFC, LPA, and LPD measures; however, patellar taping did not improve patellar position, and in some positions taping actually worsened patellar position. A large reduction in pain as measured by the VAS occurred during an 8-in. step-down for both taping and bracing. More research is necessary to explain the pain reduction without a change in patellar position using tape.

Context: Central activation ratio (CAR) is a common outcome measure used to quantify gross neuromuscular function of the quadriceps using the superimposed burst technique, yet this outcome measure has not been validated in the gluteal musculature. Objective: To quantify gluteus medius (GMed) and gluteus maximus (GMax) CAR in a healthy population and evaluate its validity and reliability over a 1-week period. Design: Descriptive. Setting: Laboratory. Patients or Other Participants: A total of 20 healthy participants (9 males and 11 females; age 22.2 [1.4] y, height 173.4 [11.1] cm, mass 84.8 [25.8] kg) were enrolled in this study. Interventions: Participants were assessed at 2 sessions, separated by 1 week. Progressive electrical stimuli (25%, 50%, 75%, and 100%) were delivered to the GMed and GMax at rest, and 100% stimuli were delivered during progressive hip abduction and extension contractions (25%, 50%, 75%, and 100% maximal voluntary isometric contraction). Main Outcome Measures: GMed and GMax CAR, and hip abduction and hip extension maximal voluntary isometric contraction torque. Line of best fit and coefficient of determination (r ²) were used to assess the relationship between torque output and CAR at varying levels of stimuli. Intraclass correlation coefficients, ICCs(3,k), were used to assess the between-session reliability. Results: GMed CAR was 96.1% (3.4%) and 96.6% (3.2%), on visits 1 and 2, respectively, whereas GMax CAR was 86.5% (7.5%) and 87.2% (10.7%) over the 2 sessions. A third-order polynomial demonstrated the best line of fit between varying superimposed burst intensities at rest for both GMed (r ² = .156) and GMax (r ² = .602). Linear relationships were observed in the CAR during progressive contractions with a maximal superimposed burst, GMed (r ² = .409) and GMax (r ² = .639). Between-session reliability was excellent for GMed CAR, ICC(3,k) = .911, and moderate for GMax CAR, ICC(3,k) = .704. Conclusion: CAR appears to be an acceptable measure of GMed and GMax neuromuscular function in healthy individuals. Gluteal CAR measurements are reliable measures over a 1-week test period.