Quadriceps Inhibition After Naturally Occurring Patellar Tendon Damage and Pain

Abstract

Context After knee-joint injury, pain, effusion, and mechanoreceptor damage alter afferent signaling, which can result in quadriceps inhibition and subsequent weakness. The individual contributions of each factor to inhibition remain unclear due to confounding knee-joint injuries and indirect experimental models. Objective To characterize the influence of naturally occurring knee damage and pain on quadriceps neuromuscular function in individuals with patellar tendinopathy. Design Cross-sectional study. Setting Research laboratory. Patients or Other Participants Twenty participants who self-reported patellar tendinopathy (PT) and 10 healthy control individuals underwent ultrasonic tendon assessment. Injured participants were dichotomized by an orthopaedic surgeon into groups with (1) pain and structural tendon abnormality and (2) regional pain alone. Main Outcome Measure(s) Quadriceps inhibition was assessed with the Hoffman reflex and the central activation ratio via the superimposed-burst technique. Normally distributed measures were analyzed using a 1-way analysis of variance and post hoc independent t tests. Kruskal-Wallis tests with post hoc Mann-Whitney U tests were used to analyze nonnormally distributed data. An a priori α level of P ≤ .05 was set. Results Control participants presented with more spinal-reflex excitability (0.37 ± 0.23) than the PT (0.10 ± 0.06; P = .03) and regional-pain (0.18 ± 0.05; P = .02) groups. Knee-extension strength was greater in the control (3.37 ± 0.59 Nm/kg) than in the PT (2.41 ± 0.67 Nm/kg; P = .01) group but not the regional-pain group (3.05 ± 0.66 Nm/kg; P = .24). Control individuals presented with more quadriceps activation (97.93% ± 3.12) than the PT (84.44% ± 16.98; P < .01) and regional-pain (91.17% ± 10.56; P = .01) groups. No differences were present for any measures between the PT and regional-pain groups (P values > .05). Conclusions Deficits in spinal-reflex excitability, quadriceps activation, and strength were present in both the PT and regional-pain groups. A combination of pain and structural damage appeared to have the greatest negative effect on quadriceps function, as only the PT group presented with neuromuscular outcomes that failed to meet clinical thresholds.

Quadriceps Muscle Action and Association With Knee Joint Biomechanics in Individuals with Anterior Cruciate Ligament Reconstruction

“…46 A shift away from patellar tendon stretch and toward active muscle lengthening as we observed in the ACLR limb may serve to prevent further donor site injury as the patellar tendon defect heals. Indeed, individuals without ACLR but with structural damage to the patellar tendon exhibit quadriceps inhibition 47 ; a similar mechanism of neuromuscular inhibition after ACLR could serve to protect the donor site, shifting lengthening demands from the tendon to the muscle. Certainly, additional studies are warranted to compare muscle-tendon dynamics and quadriceps inhibition between graft types before making conclusions, but their results could have consequences both for graft choice and individualized medicine.…”

Mechanisms of Arthrogenic Muscle Inhibition

“…Namely, spinal-reflexive deficits have routinely been observed in a variety of patient populations, including those with ACL injury and ACLR, patellar tendinopathies, acute ankle sprains, and chronic ankle instability. [30][31][32][33][34][35] To this end, the quadriceps, fibularis longus and brevis, and soleus musculature have all demonstrated reductions in spinal-reflexive excitability following injury, suggesting that changes in reflexive capacities from altered afferent signaling contribute to motor deficits in these populations and muscle groups. Although effusion models were able to show that spinal-reflex inhibition was present acutely without pain or true joint damage, clinical studies have demonstrated that a combination of altered afferent input (ie, concomitant pain, deafferentation, and swelling) appears to be more potent than either one in isolation.…”

“…Although effusion models were able to show that spinal-reflex inhibition was present acutely without pain or true joint damage, clinical studies have demonstrated that a combination of altered afferent input (ie, concomitant pain, deafferentation, and swelling) appears to be more potent than either one in isolation. 35,36 Early AMI paradigms and effusion models suggested that sustained deficits in reflexive excitability contribute to persistent impairments in muscle function. However, contrary to the early paradigm hypotheses, prolonged deficits in reflexive excitability have not been shown in clinical populations.…”

Rehabilitation after a Complete Avulsion of the Proximal Rectus Femoris Muscle: Considerations from a Case Report

“…A potential reason for the observed neuromuscular function could be a muscular inhibition based on the structural damage of the tendon. As the active muscle structure and the innervation path of the muscles are likely intact, inhibition may be triggered by the acute inflammation and/or pain [26]. Thus, the use of surface electromyography during rehabilitation may be helpful to evaluate the ability for the voluntary neuromuscular activation of the injured muscle.…”