# EFFECTS OF DISEASE AND PALLIDAL DEEP BRAIN STIMULATION ON ANKLE MUSCLE CONTROL IN PARKINSON'S DISEASE > **NIH NIH F31** · UNIVERSITY OF MINNESOTA · 2024 · $35,290 ## Abstract Project Abstract Postural instability and gait deficits are common causes of falls, decreased mobility, and increased morbidity in people with Parkinson's disease (PD). These axial motor signs are often resistant to current treatments, including dopamine replacement therapy (levodopa) and deep brain stimulation (DBS). Currently, the mechanisms contributing to the impaired control of the lower limbs are poorly understood. Extensor muscles of the lower limbs are critical for maintaining vertical support against gravity and generating power during gait. In people with PD, impairment in extensor muscle strength is greater than the flexors. Levodopa and subthalamic DBS (STN DBS) improve strength in both the flexors and extensors but have less of an effect in the extensors. Similarly, levodopa and STN DBS do not significantly improve plantar flexor torque generation during gait. Currently, the mechanisms contributing to greater defici ts in extensor compared to flexor muscle function in PD are unknown, but likely reflect differences in corticospinal, basal ganglia and brainstem contributions to the control of these muscles. This project aims to understand how flexors (tibialis anterior) and extensors (gastrocnemius, soleus) of the ankle contribute to leg rigidity and bradykinesia and gait in people with PD. Aim 1a will use transcranial magnetic stimulation of the leg region of the motor cortex to examine the excitability of corticomotoneuronal and intracortical pathways controlling the ankle flexors and extensors in PD, and controls. Aim 1b will examine the relationships between intracortical and corticomotoneuronal responses and quantitative measures of ankle bradykinesia and rigidity, and gait. Aim 2 will evaluate the response dynamics (60 minute wash-out, 60 minute wash-in) of globus pallidus DBS (GP DBS) on ankle rigidity, bradykinesia, and gait in PD to test the hypothesis that the acute and steady-state effects of GP DBS are different between the ankle flexors and extensors. Response dynamics across these behavioral measures will be examined in relation to the activation of neural pathways in and around the globus pallidus (estimated via patient-specific computational modeling of DBS) to determine which pathways are associated with which motor outcomes. The results of this project will provide an increased understanding of how PD and targeted TMS and GP DBS interventions impact the function of the ankle dorsi and plantar flexors. This knowledge will be important for the development and testing of novel interventions to treat postural and gait disorders and improve quality of life in people with PD. ## Key facts - **NIH application ID:** 10929394 - **Project number:** 5F31HD112086-02 - **Recipient organization:** UNIVERSITY OF MINNESOTA - **Principal Investigator:** emily Elizabeth lecy - **Activity code:** F31 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 2024 - **Award amount:** $35,290 - **Award type:** 5 - **Project period:** 2023-09-01 → 2025-03-10 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/10929394 ## Citation > US National Institutes of Health, RePORTER application 10929394, EFFECTS OF DISEASE AND PALLIDAL DEEP BRAIN STIMULATION ON ANKLE MUSCLE CONTROL IN PARKINSON'S DISEASE (5F31HD112086-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10929394. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*