Background:Forced external rotation of the foot is a mechanism of ankle injuries. Clinical observations include combinations of ligament and osseous injuries, with unclear links between causation and injury patterns. By observing the propagation sequence of ankle injuries during controlled experiments, insight necessary to understand risk factors and potential mitigation measures may be gained.Hypothesis:Ankle flexion will alter the propagation sequence of ankle injuries during forced external rotation of the foot.Study Design:Controlled laboratory study.Methods:Matched-pair lower limbs from 9 male cadaveric specimens (mean age, 47.0 ± 11.3 years; mean height, 178.1 ± 5.9 cm; mean weight, 94.4 ± 30.9 kg) were disarticulated at the knee. Specimens were mounted in a test device with the proximal tibia fixed, the fibula unconstrained, and foot translation permitted. After adjusting the initial ankle position (neutral, n = 9; dorsiflexed, n = 4; plantar flexed, n = 4) and applying a compressive preload to the tibia, external rotation was applied by rotating the tibia internally while either lubricated anteromedial and posterolateral plates or calcaneal fixation constrained foot rotation. The timing of osteoligamentous injuries was determined from acoustic sensors, strain gauges, force/moment readings, and 3-dimensional bony kinematics. Posttest necropsies were performed to document injury patterns.Results:A syndesmotic injury was observed in 5 of 9 (56%) specimens tested in a neutral initial posture, in 100% of the dorsiflexed specimens, and in none of the plantar flexed specimens. Superficial deltoid injuries were observed in all test modes.Conclusion:Plantar flexion decreased and dorsiflexion increased the incidence of syndesmotic injuries compared with neutral matched-pair ankles. Injury propagation was not identical in all ankles that sustained a syndesmotic injury, but a characteristic sequence initiated with injuries to the medial ligaments, particularly the superficial deltoid, followed by the propagation of injuries to either the syndesmotic or lateral ligaments (depending on ankle flexion), and finally to the interosseous membrane or the fibula.Clinical Relevance:Superficial deltoid injuries may occur in any case of hyper–external rotation of the foot. A syndesmotic ankle injury is often concomitant with a superficial deltoid injury; however, based on the research detailed herein, a deep deltoid injury is then concomitant with a syndesmotic injury or offloads the syndesmosis altogether. A syndesmotic ankle injury more often occurs when external rotation is applied to a neutral or dorsiflexed ankle. Plantar flexion may shift the injury to other ankle ligaments, specifically lateral ligaments.
Unpredictable forces which perturb balance are frequently applied to the body through interaction between the upper limb and the environment. Lower limb muscles respond rapidly to these postural disturbances in a highly specific manner. We have shown that the muscle activation patterns of lower limb muscles are organized in a direction specific manner which changes with lower limb stability. Ankle muscles change their activity within 80 ms of the onset of a force perturbation applied to the hand which is earlier than the onset of changes in ground reaction force, ankle angle or head motion. The latency of the response is sensitive to the perturbation direction. However, neither the latency nor the magnitude of the response is affected by stiffening the arm even though this alters the magnitude and timing of motion of the body segments. Based on the short latency, insensitivity of the change in ankle muscle activation to motion of the body segments but sensitivity to perturbation direction we reason that changes in ankle muscle activation are most likely triggered by sensory signals originating from cutaneous receptors in the hand. Furthermore, evidence that the latency of changes in ankle muscle activation depends on the number of perturbation directions suggests that the neural pathway is not confined to the spinal cord.
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