Smaller Cortical Responses to Balance Perturbations in Parkinson's Disease with Freezing of Gait
- 1University of Vermont
Abstract
Freezing of gait (FoG) is among the most disabling symptoms of Parkinson's disease (PD) and is associated with balance impairment and increased falls risk, yet remains challenging to understand due to its episodic and context-dependent nature. Altered supplementary motor area (SMA) function at rest and before self-initiated movements has been implicated in FoG; however, whether this extends to functionally relevant balance behavior is unknown. A loss of balance in response to support surface translations during standing elicits a perturbation-evoked N1 potential, an error assessment signal linked to SMA activity. We therefore predicted that people with FoG would have smaller and later N1 responses than people with PD without FoG and older adults. We recorded electroencephalography (EEG) during backward support-surface translations in 29 people with PD (71 {+/-} 7 years), including 13 people with a history of FoG (FoG+) and 16 people without FoG (FoG-), and 26 older adults (OA; 67 {+/-} 6 years). N1 amplitude and latency were quantified at a central midline electrode and defined as the largest negative peak 100-300 ms post-perturbation. N1 responses were similar between OA and FoG- ({Delta} = 4.0 {micro}V and 2.8 ms, respectively). In contrast, FoG+ had smaller N1 amplitudes than FoG- ({Delta} = 18.1 {micro}V, p = 0.001) and OA ({Delta} = 14.1 {micro}V, p = 0.003), and both differences persisted after adjusting for age. FoG+ also had later N1 latencies than OA ({Delta} = 26.5 ms, p = 0.029), with a similar but non-significant difference versus FoG- ({Delta} = 23.6 ms, p = 0.091); after adjusting for age, these latency differences were not retained. These findings suggest that perturbation-evoked cortical activity is altered in FoG, potentially reflecting altered SMA function, and may provide a functionally relevant marker of FoG susceptibility.
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BibTeX
@misc{monaghan2026smaller,
title = {{Smaller Cortical Responses to Balance Perturbations in Parkinson's Disease with Freezing of Gait}},
author = {A. S. Monaghan and I. J. Lachica and J. Protzak and S. A. Factor and J. L. McKay and M. R. Borich and L. H. Ting and J. L. Mirdamadi},
howpublished = {medRxiv},
year = {2026},
month = nov,
doi = {10.64898/2026.11.03.26367107},
url = {https://www.medrxiv.org/content/10.64898/2026.11.03.26367107v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Smaller Cortical Responses to Balance Perturbations in Parkinson's Disease with Freezing of Gait
AU - A. S. Monaghan
AU - I. J. Lachica
AU - J. Protzak
AU - S. A. Factor
AU - J. L. McKay
AU - M. R. Borich
AU - L. H. Ting
AU - J. L. Mirdamadi
PY - 2026
DA - 2026/11/03
PB - medRxiv
DO - 10.64898/2026.11.03.26367107
UR - https://www.medrxiv.org/content/10.64898/2026.11.03.26367107v1
AB - Freezing of gait (FoG) is among the most disabling symptoms of Parkinson's disease (PD) and is associated with balance impairment and increased falls risk, yet remains challenging to understand due to its episodic and context-dependent nature. Altered supplementary motor area (SMA) function at rest and before self-initiated movements has been implicated in FoG; however, whether this extends to functionally relevant balance behavior is unknown. A loss of balance in response to support surface translations during standing elicits a perturbation-evoked N1 potential, an error assessment signal linked to SMA activity. We therefore predicted that people with FoG would have smaller and later N1 responses than people with PD without FoG and older adults. We recorded electroencephalography (EEG) during backward support-surface translations in 29 people with PD (71 {+/-} 7 years), including 13 people with a history of FoG (FoG+) and 16 people without FoG (FoG-), and 26 older adults (OA; 67 {+/-} 6 years). N1 amplitude and latency were quantified at a central midline electrode and defined as the largest negative peak 100-300 ms post-perturbation. N1 responses were similar between OA and FoG- ({Delta} = 4.0 {micro}V and 2.8 ms, respectively). In contrast, FoG+ had smaller N1 amplitudes than FoG- ({Delta} = 18.1 {micro}V, p = 0.001) and OA ({Delta} = 14.1 {micro}V, p = 0.003), and both differences persisted after adjusting for age. FoG+ also had later N1 latencies than OA ({Delta} = 26.5 ms, p = 0.029), with a similar but non-significant difference versus FoG- ({Delta} = 23.6 ms, p = 0.091); after adjusting for age, these latency differences were not retained. These findings suggest that perturbation-evoked cortical activity is altered in FoG, potentially reflecting altered SMA function, and may provide a functionally relevant marker of FoG susceptibility.
ER -