Short-latency stretch reflexes depend on the balance of activity in agonist and antagonist muscles during ballistic elbow movements.

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, pseudorandom 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 with 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.NEW & NOTEWORTHY This study examined the sensitivity of the stretch reflexes elicited in elbow muscles to the background activity in these same muscles during movement and postural tasks. We found a heightened reciprocal control of reflex sensitivity during movement that was not present during maintenance of posture. These results help explain previous discrepancies in reflex sensitivity measured during movement and posture and provide a simple model for assessing their contributions to muscle activity in both tasks.

Frontal plane ankle stiffness increases with axial load independent of 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 in 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% body weight to 50% body weight. 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.

Eye Tracking Results in Postconcussive Syndrome Versus Normative Participants.

Purpose: Standard physical, neurologic, and neuropsychologic examinations may not detect abnormalities after mild traumatic brain injury (mTBI). An analysis of eye movements may be more sensitive to neurologic dysfunction. Methods: We performed eye tracking assessments in 71 active duty and veteran military personnel with persistent postconcussive symptoms (3 months to 5 years after mTBI) and 75 volunteers with no history of brain injury. Both eyes were sampled at 500 Hz and analyzed for various eye measurement parameters during visual tasks involving the saccadic and smooth systems. Results: No difference between mTBI and normal participants in main sequence profiles was observed. On the circular task, intersaccadic interval duration was shorter in mTBI compared with normal subjects (horizontal: Cohen's D = -0.65; vertical: Cohen's D = -0.75). For reading, absolute saccadic amplitudes (Cohen's D = -0.76) and average forward saccadic amplitudes were lower (Cohen's D = -0.61). Absolute fixation velocity was higher (Cohen's D = 1.02), and overall fixation durations (Cohen's D = 0.58), regression durations (Cohen's D = 0.49), and forward saccadic durations (Cohen's D=0.54) were longer. mTBI participants had more fixations (Cohen's D = 0.54) and regressions per line (Cohen's D = 0.70) and read fewer lines (Cohen's D = -0.38) than normal subjects. On the horizontal ramp task, mTBI participants had lower weighted smooth pursuit gains (Cohen's D = -0.55). On the horizontal step task, mTBI participants had shorter mean fixation times (Cohen's D = -0.55). Conclusions: 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.).