# Cortical basal ganglia network dynamics during human gait control

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2023 · $406,601

## Abstract

PROJECT SUMMARY/ ABSTRACT
 The long-term goal of this project is to understand the cortical-basal ganglia network activities that are
involved with human gait control, and reveal the abnormalities in this circuit that underlie gait disorders in patients
with Parkinson’s disease (PD). Human gait is a complex motor task that requires the flexible coordination of both
cortical and subcortical structures within the brain. However, the neural encoding for gait initiation, continuous
rhythmic walking, and gait adaptation is largely unknown due largely to methodological constraints. Decoding
the neural control of gait is not only important for understanding a fundamental human behavior, but is also
important for developing novel neuromodulation paradigms to treat gait problems in PD.
 We propose to study the neurophysiology of human gait control by capturing simultaneous local field
potentials from bilateral motor cortex and globus pallidus interna (GPi) of ten PD patients implanted with
bidirectional sensing and stimulating devices. We plan to decode the cortical and pallidal neural activities that
underlie effective and abnormal gait initiation, continuous walking, and gait modification under different
medication states and stimulation cycles in the naturalistic environment in addition to the laboratory setting. Our
working model is that continuous gait is generated by rhythmic low frequency fluctuations—theta (4-8Hz), alpha
(8-12Hz), and beta oscillations (13-30Hz) in the GPi and does not require much cortical input except periodic
beta desynchronization required to disinhibit the motor cortex. Motor cortical involvement is greater during gait
initiation and gait adaptation, where top-down cortical command is necessary to modify basal ganglia activities
to maintain postural balance. We theorize that in PD, where increased beta synchrony throughout the motor
system is associated with an akinetic state, gait impairments are caused by this excessive cortical-pallidal
synchronization and disrupt the dynamic and transient synchronization required for normal gait.
 To test this hypothesis, we will study gait initiation (Aim 1) in the laboratory setting under different
medication and stimulation conditions, continuous locomotion (Aim 2) both in the laboratory setting and in the
home setting to capture dynamic changes of gait in the naturalistic setting, and a visually guided gait adaptation
task (Aim 3) under different medication and stimulation conditions in the laboratory. The impact of this study will
be 1) perform the first chronic network analysis of human gait using cortical and pallidal recordings, 2) investigate
the human brain activities underlying walking in the natural environment, and 3) provide a conceptual framework
for understanding the mechanism of supraspinal network control of gait and pathophysiology of gait impairments
in PD.

## Key facts

- **NIH application ID:** 10567272
- **Project number:** 1R01NS130183-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Doris Du Wang
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $406,601
- **Award type:** 1
- **Project period:** 2023-01-15 → 2027-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10567272

## Citation

> US National Institutes of Health, RePORTER application 10567272, Cortical basal ganglia network dynamics during human gait control (1R01NS130183-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10567272. Licensed CC0.

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