These results suggest vulnerability of the smooth pursuit and saccadic systems in mTBI. Eye tracking shows promise as an objective, sensitive assessment of damage after mTBI. (ClinicalTrials.gov number, NCT01611194, NCT01925963.).

The spinal stretch reflex is a fundamental building block of motor function, modulating sensitivity across tasks to augment volitional control. Stretch reflex sensitivity can vary continuously during movement and changes between movement and posture. While there have been many demonstrations of reflex modulation and investigations into the underlying mechanisms, there have been few attempts to provide simple, quantitative descriptions of the relationship between the volitional control and stretch reflex sensitivity throughout tasks that require the coordinated activity of several muscles. Here we develop such a description and use it to test the hypothesis that the modulation of stretch reflex sensitivity during movement can be explained by the balance of activity within the relevant agonist and antagonist muscles better than by the activity only in the muscle homonymous with the elicited reflex. We applied continuous pseudo-random perturbations of elbow angle as subjects completed approximately 500 movements in elbow flexion and extension. Measurements were averaged across the repeated movements to obtain continuous estimates of stretch reflex amplitude and background muscle activity. We also ran a control experiment on a subset of subjects performing postural tasks at muscle activity levels matched to those measured in the movement task. For both experiments, we assessed the relationship between background activity in the agonist and antagonist muscles controlling elbow movement and the stretch reflexes elicited in them. We found that modulation in the stretch reflexes during movement can be described by modulation of the background activity in the agonist and antagonist muscles, and that models incorporating agonists and antagonists are significantly better than those considering only the homonymous muscle. Increases in agonist muscle activity enhanced stretch reflex sensitivity whereas increases in antagonist activity suppressed reflex activity. Surprisingly, the magnitude of these effects was similar, suggesting a balance of control between agonists and antagonist that is very different than the dominance of sensitivity to agonist activity during postural tasks. This greater relative sensitivity to antagonist background activity during movement is due to a large decrease in sensitivity to homonymous muscle activity during movement rather than substantial changes in the influence of antagonist muscle activity.

The spinal stretch reflex is a fundamental building block of motor function, with a sensitivity that varies continuously during movement and when changing between movement and posture. Many have investigated task-dependent reflex sensitivity, but few have provided simple, quantitative analyses of the relationship between the volitional control and stretch reflex sensitivity throughout tasks that require coordinated activity of several muscles. Here we develop such an analysis and use it to test the hypothesis that modulation of reflex sensitivity during movement can be explained by the balance of activity within agonist and antagonist muscles better than by activity only in the muscle homonymous with the reflex. Subjects completed hundreds of flexion and extension movements as small, pseudo-random perturbations of elbow angle were applied to obtain estimates of stretch reflex amplitude throughout the movement. A subset of subjects performed a postural control task at muscle activities matched to those during movement. We found that reflex modulation during movement can be described by background activity in antagonist muscles about the elbow much better than by activity only in the muscle homonymous to the reflex (p<0.001). Agonist muscle activity enhanced reflex sensitivity whereas antagonist activity suppressed it. Surprisingly, the magnitude of these effects was similar, suggesting a balance of control between agonists and antagonists very different from the dominance of sensitivity to homonymous activity during posture. This balance is due to a large decrease in sensitivity to homonymous muscle activity during movement rather than substantial changes in the influence of antagonistic muscle activity.

Ankle sprains are the most common musculoskeletal injury, typically resulting from excessive inversion of the ankle. One way to prevent excessive inversion and maintain ankle stability is to generate a stiffness that is sufficient to resist externally imposed rotations. Frontal-plane ankle stiffness increases as participants place more weight on their ankle, but whether this effect is due to muscle activation or axial loading of the ankle is unknown. Identifying whether and to what extent axial loading affects ankle stiffness is important to understanding what role the passive mechanics of the ankle joint play in maintaining its stability. The objective of this study was to determine the effect of passive axial load on frontal-plane ankle stiffness. We had subjects seated in a chair as an axial load was applied to the ankle ranging from 10% to 50% body weight. Small rotational perturbations were applied to the ankle in the frontal plane to estimate stiffness. We found a significant, linear, 3-fold increase in ankle stiffness with axial load from the range of 0% bodyweight to 50% bodyweight. This increase could not be due to muscle activity as we observed no significant axial-load-dependent change in any of the recorded muscle activations. These results demonstrate that axial loading is a significant contributor to maintaining frontal-plane ankle stability, and that disruptions to the mechanism mediating this sensitivity of stiffness to axial loading may result in pathological cases of ankle instability.