The Strength-Dexterity (SD) test measures the ability of the pulps of the thumb and index finger to compress a compliant and slender spring prone to buckling at low forces (<3N). We know that factors such as aging and neurodegenerative conditions bring deteriorating physiological changes (e.g., at the level of motor cortex, cerebellum, and basal ganglia), which lead to an overall loss of dexterous ability. However, little is known about how these changes reflect upon the dynamics of the underlying biological system. The spring-hand system exhibits nonlinear dynamical behavior and here we characterize the dynamical behavior of the phase portraits using attractor reconstruction. Thirty participants performed the SD test: 10 young adults, 10 older adults, and 10 older adults with Parkinson's disease (PD). We used delayed embedding of the applied force to reconstruct its attractor. We characterized the distribution of points of the phase portraits by their density (number of distant points and interquartile range) and geometric features (trajectory length and size). We find phase portraits from older adults exhibit more distant points (p = 0.028) than young adults and participants with PD have larger interquartile ranges (p = 0.001), trajectory lengths (p = 0.005), and size (p = 0.003) than their healthy counterparts. The increased size of the phase portraits with healthy aging suggests a change in the dynamical properties of the system, which may represent a weakening of the neural control strategy. In contrast, the distortion of the attractor in PD suggests a fundamental change in the underlying biological system, and disruption of the neural control strategy. This ability to detect differences in the biological mechanisms of dexterity in healthy and pathological aging provides a simple means to assess their disruption in neurodegenerative conditions and justifies further studies to understand the link with the physiological changes.

Characterization of the disruption of neural control strategies for dynamic fingertip forces from attractor reconstruction

PEPPOLONI, LORENZO;RUFFALDI, EMANUELE;
2017-01-01

Abstract

The Strength-Dexterity (SD) test measures the ability of the pulps of the thumb and index finger to compress a compliant and slender spring prone to buckling at low forces (<3N). We know that factors such as aging and neurodegenerative conditions bring deteriorating physiological changes (e.g., at the level of motor cortex, cerebellum, and basal ganglia), which lead to an overall loss of dexterous ability. However, little is known about how these changes reflect upon the dynamics of the underlying biological system. The spring-hand system exhibits nonlinear dynamical behavior and here we characterize the dynamical behavior of the phase portraits using attractor reconstruction. Thirty participants performed the SD test: 10 young adults, 10 older adults, and 10 older adults with Parkinson's disease (PD). We used delayed embedding of the applied force to reconstruct its attractor. We characterized the distribution of points of the phase portraits by their density (number of distant points and interquartile range) and geometric features (trajectory length and size). We find phase portraits from older adults exhibit more distant points (p = 0.028) than young adults and participants with PD have larger interquartile ranges (p = 0.001), trajectory lengths (p = 0.005), and size (p = 0.003) than their healthy counterparts. The increased size of the phase portraits with healthy aging suggests a change in the dynamical properties of the system, which may represent a weakening of the neural control strategy. In contrast, the distortion of the attractor in PD suggests a fundamental change in the underlying biological system, and disruption of the neural control strategy. This ability to detect differences in the biological mechanisms of dexterity in healthy and pathological aging provides a simple means to assess their disruption in neurodegenerative conditions and justifies further studies to understand the link with the physiological changes.
2017
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11382/514803
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