Related Experiment Video
Updated: Mar 23, 2026

Evaluating Postural Control and Lower-extremity Muscle Activation in Individuals with Chronic Ankle Instability
Published on: September 18, 2020
Effects of an auditory biofeedback device on plantar pressure in patients with chronic ankle instability
Luke Donovan1, Mark A Feger2, Joseph M Hart3
1University of Toledo, Department of Kinesiology, 2801 W. Bancroft St, Toledo, Mail Stop 119, OH, 43606, USA.
Abstract:
Chronic ankle instability (CAI) patients have been shown to have increased lateral column plantar pressure throughout the stance phase of gait. To date, traditional CAI rehabilitation programs have been unable to alter gait. We developed an auditory biofeedback device that can be worn in shoes that elicits an audible cue when an excessive amount of pressure is applied to a sensor. This study determined whether using this device can decrease lateral plantar pressure in participants with CAI and alter surface electromyography (sEMG) amplitudes (anterior tibialis, peroneus longus, medial gastrocnemius, and gluteus medius). Ten CAI patients completed baseline treadmill walking while in-shoe plantar pressures and sEMG were measured (baseline condition). Next, the device was placed into the shoe and set to a threshold that would elicit an audible cue during each step of the participant's normal gait. Then, participants were instructed to walk in a manner that would not trigger the audible cue, while plantar pressure and sEMG measures were recorded (auditory feedback (AUD FB) condition). Compared to baseline, there was a statistically significant reduction in peak pressure in the lateral midfoot-forefoot and central forefoot during the AUD FB condition. In addition, there were increases in peroneus longus and medial gastrocnemius sEMG amplitudes 200 ms post-initial contact during the AUD FB condition. The use of this auditory biofeedback device resulted in decreased plantar pressure in the lateral column of the foot during treadmill walking in CAI patients and may have been caused by the increase in sEMG activation of the peroneus longus.

