Phase resetting and intermittent control at critical edge of stability as major mechanisms of fractality in human gait cycle variability

TL;DR

This paper presents a computational model explaining gait fractality as arising from phase resetting and intermittent control mechanisms at the edge of stability, linking these to healthy gait variability and potential pathologies.

Contribution

It introduces a novel model connecting gait fractality with control mechanisms like phase resetting and intermittent control, highlighting their role in stability and pathology.

Findings

Gait fractality emerges from control mechanisms at the stability edge.

Pathological gait may result from dysfunction in these control mechanisms.

Model links gait variability to sensorimotor control dynamics.

Abstract

The fractality of human gait, namely, the long-range correlation that characterizes scale-free fluctuations of gait descriptors, such as the stride intervals during steady-state walking, depends on the well-tuned organization of the sensorimotor controller. Gait fractality is apparent in healthy young adults but tends to disappear in elderly individuals and neurological patients. Therefore, its partial loss may be indicative of pathological conditions. Despite its potential to be used as a dynamical biomarker for fall risk assessment, the mechanistic origin of gait fractality has been investigated by only a few studies, and even less attention has been devoted to the link between gait fractality and gait stability. Here, we propose a novel computational model of gait by addressing the flexibility-stability trade-off first, and then by showing that gait fractality is a natural consequence of the developed control mechanisms, including phase resetting and intermittent control, which supplement instability in a linear feedback controller operated at stability's edge. The results suggest that pathological gait, characterized by joint-rigidity and/or loss of fractality, may be caused by dysfunction in some of these mechanisms.