Do horizontal propulsive forces influence the nonlinear structure of locomotion?

<p>Abstract</p> <p>Background</p> <p>Several investigations have suggested that changes in the nonlinear gait dynamics are related to the neural control of locomotion. However, no investigations have provided insight on how neural control of the locomotive pattern may be directly reflected in changes in the nonlinear gait dynamics. Our simulations with a passive dynamic walking model predicted that toe-off impulses that assist the forward motion of the center of mass influence the nonlinear gait dynamics. Here we tested this prediction in humans as they walked on the treadmill while the forward progression of the center of mass was assisted by a custom built mechanical horizontal actuator.</p> <p>Methods</p> <p>Nineteen participants walked for two minutes on a motorized treadmill as a horizontal actuator assisted the forward translation of the center of mass during the stance phase. All subjects walked at a self-select speed that had a medium-high velocity. The actuator provided assistive forces equal to 0, 3, 6 and 9 percent of the participant's body weight. The largest Lyapunov exponent, which measures the nonlinear structure, was calculated for the hip, knee and ankle joint time series. A repeated measures one-way analysis of variance with a t-test post hoc was used to determine significant differences in the nonlinear gait dynamics.</p> <p>Results</p> <p>The magnitude of the largest Lyapunov exponent systematically increased as the percent assistance provided by the mechanical actuator was increased.</p> <p>Conclusion</p> <p>These results support our model's prediction that control of the forward progression of the center of mass influences the nonlinear gait dynamics. The inability to control the forward progression of the center of mass during the stance phase may be the reason the nonlinear gait dynamics are altered in pathological populations. However, these conclusions need to be further explored at a range of walking speeds.</p

Estimating Dynamic Gait Stability Using Data from Non-aligned Inertial Sensors

Recently, two methods for quantifying the stability of a dynamical system have been applied to human locomotion: local stability (quantified by finite time maximum Lyapunov exponents, λs and λL) and orbital stability (quantified by maximum Floquet multipliers, MaxFm). In most studies published to date, data from optoelectronic measurement systems were used to calculate these measures. However, using wireless inertial sensors may be more practical as they are easier to use, also in ambulatory applications. While inertial sensors have been employed in some studies, it is unknown whether they lead to similar stability estimates as obtained with optoelectronic measurement systems. In the present study, we compared stability measures of human walking estimated from an optoelectronic measurement system with those calculated from an inertial sensor measurement system. Subjects walked on a treadmill at three different speeds while kinematics were recorded using both measurement systems. From the angular velocities and linear accelerations, λs, λL, and MaxFm were calculated. Both measurement systems showed the same effects of walking speed for all variables. Estimates from both measurement systems correlated high for λs and λL, (R > 0.85) but less strongly for MaxFm (R = 0.66). These results indicate that inertial sensors constitute a valid alternative for an optoelectronic measurement system when assessing dynamic stability in human locomotion, and may thus be used instead, which paves the way to studying gait stability during natural, everyday walking

Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury

Delayed vasospasm that develops 3–7 days after aneurysmal subarachnoid hemorrhage (SAH) has traditionally been considered the most important determinant of delayed ischemic injury and poor outcome. Consequently, most therapies against delayed ischemic injury are directed towards reducing the incidence of vasospasm. The clinical trials based on this strategy, however, have so far claimed limited success; the incidence of vasospasm is reduced without reduction in delayed ischemic injury or improvement in the long-term outcome. This fact has shifted research interest to the early brain injury (first 72 h) evoked by SAH. In recent years, several pathological mechanisms that activate within minutes after the initial bleed and lead to early brain injury are identified. In addition, it is found that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome. Therefore, a therapy or therapies focused on these early mechanisms may not only prevent the early brain injury but may also help reduce the intensity of later developing neurological complications. This manuscript reviews the pathological mechanisms of early brain injury after SAH and summarizes the status of current therapies