Abnormal center of mass control during balance: a new biomarker of falls in people with Parkinson’s disease

Abstract

Although Parkinson disease (PD) causes profound balance impairments, we know very little about how PD impacts the sensorimotor networks we rely on for automatically maintaining balance control. In young healthy people and animals, muscles are activated in a precise temporal and spatial organization when the center of body mass (CoM) is unexpectedly moved.This organization is largely automatic and determined by feedback of CoM motion. Here, we show that PD alters the sensitivity of the sensorimotor feedback transformation. Importantly, sensorimotor feedback transformations for balance in PD remain temporally precise, but become spatially diffuse by recruiting additional muscle activity in antagonist muscles during balance responses. The abnormal antagonist muscle activity remains precisely time-locked to sensorimotor feedback signals encoding undesirable motion of the body in space. Further, among people with PD, the sensitivity of abnormal antagonist muscle activity to CoM motion varies directly with the number of recent falls. Our work shows that in people with PD, sensorimotor feedback transformations for balance are intact but disinhibited in antagonist muscles, likely contributing to balance deficits and falls.

Cortical Beta Oscillatory Activity Evoked during Reactive Balance Recovery Scales with Perturbation Difficulty and Individual Balance Ability

“…Sensorimotor beta oscillatory activity is sustained throughout balance recovery with a time course resembling balance-correcting muscle activation. Our lab previously demonstrated that during reactive balance recovery the central nervous system directly scales the initial automatic motor response with body motion at a delay of 100 ms [ 4 , 5 , 60 , 65 ]. The similarity of the time course of the initial beta activity to that of the motor responses suggests the possibility that a common source of integrated sensory inputs [ 66 , 67 ] may drive both the initial automatic motor response (at ~100 ms delay) and the early phase of evoked cortical beta activity (at ~50 ms delay) during balance reactions.…”

Cortical beta oscillatory activity evoked during reactive balance recovery scales with perturbation difficulty and individual balance ability

“…Sensorimotor beta oscillatory activity is sustained throughout balance recovery with a time course resembling balance-correcting muscle activation. Our lab previously demonstrated that during reactive balance recovery the central nervous system directly scales the initial automatic motor response with body motion at a delay of 100 ms (McKay et al, 2020;Welch & Ting, 2008. The similarity of the time course of the initial beta activity to that of the motor responses suggests the possibility that a common source of integrated sensory inputs (He et al, 1991;Lockhart & Ting, 2007) may drive both the initial automatic motor response (at ~100 ms delay) and the early phase of evoked cortical beta activity (at ~50 ms delay) during balance reactions.…”

Delayed Center of Mass Feedback in Elderly Humans Leads to Greater Muscle Co-Contraction and Altered Balance Strategy under Perturbed Balance: a Predictive Musculoskeletal Simulation Study

“…Three fixed COM feedback delay conditions were used to investigate the effect of delayed feedback: 𝑡 𝐷 = 100, 150, and 200 ms. These delay conditions were modeled to reflect the sensory feedback delay observed in the elderly population [46]. The magnitude of the sinusoidal perturbation applied to the platform was increased from 0 to 80 mm, where the 0 to 10 mm range was incremented by 2 mm and the 10 mm to 80 mm was incremented by 20 mm.…”

“…where 𝑝 indicates the position and 𝑝 indicates the velocity of the foot or wholebody COM; and 𝐾 𝐶𝑃 and 𝐾 𝐶𝑉 are the feedback control gains for position and velocity respectively, and 𝑡 𝐷 is the COM feedback delay. The range of delays used were adapted from the study by McKay et al [46], which looked at sensory feedback and balance in individuals with Parkinson's disease compared to elderly individuals without Parkinson's disease; in this study they provided a sensorimotor feedback model that successfully reproduced muscle activations as seen in experimental trials with healthy, aging, and Parkinson's disease subject groups. Equation (3) differs from the equation used in McKay et al's study by using a comparison of whole body COM position to foot COM position.…”

“…where 𝑝 indicates the position and 𝑝 indicates the velocity of the foot or wholebody COM; and 𝐾 𝐶𝑃 and 𝐾 𝐶𝑉 are the feedback control gains for position and velocity respectively, and 𝑡 𝐷 is the COM feedback delay. The range of delays used were adapted from the study by McKay et al [46], which looked at sensory…”