Category: Parkinson's disease: Neuroimaging
Objective: To assess clinical and cerebellar volume differences in Parkinson’s disease (PD) patients with and without freezing of gait (PD-FoG and PD-NOFoG).
Background: Cerebellum plays an increasingly recognized role in gait modulation and FoG in PD patients [1, 2].
Method: Thirty-four PD-FoG, 35 PD-NOFoG, and 23 healthy controls underwent clinical assessment and structural MRI. Clinical evaluation included walking, balance, and a comprehensive neuropsychological battery. Grey matter cerebellar volumes were assessed using SUIT atlas. Analyses were Bonferroni-corrected for number of groups.
This study was funded by Italian Ministry of Health grant number GR-2021-12374005.
Results: Compared to healthy controls, both PD-FoG and PD-NOFoG groups showed reduced walking speed, lower balance confidence (ABC scale), impaired balance (MiniBESTest), and an increased number of steps to walk 10 meters both at comfortable and maximal speed. Additionally, they exhibited a worse performance in memory, attention, and executive functions. Only PD-FoG patients showed increased Timed-Up-and-Go test (TUG) completion time both with and without a cognitive dual-task, and a worse visuospatial performance, delayed recall of Rey’s word list, Trail-Making-Test B-A, and phonemic fluency. Both PD groups exhibited reduced cerebellar lobule X volumes, but only PD-FoG patients had a reduced vermis VIIb volume compared to controls. When directly compared, PD-FoG patients demonstrated a greater number of steps in the 10-meter walking test at maximal speed, lower balance confidence, and worse phonemic fluency relative to PD-NOFoG patients. Additionally, PD-FoG patients exhibited increased volumes in cerebellar lobules VIIIb and IX, as well as vermis crus II.
Conclusion: These findings suggest that structural alterations in specific cerebellar regions, involved in motor and cognitive control of movement, may be linked to the pathophysiology of FoG in patients with PD. Further research is needed to determine if these changes reflect compensatory mechanisms or contribute directly to the development of FoG.
References: 1] Fasano A, Laganiere SE, Lam S, Fox MD. Lesions causing freezing of gait localize to a cerebellar functional network. Ann Neurol. 2017 Jan;81(1):129-141. doi: 10.1002/ana.24845. PMID: 28009063; PMCID: PMC5266642.
2] Dijkstra BW, Gilat M, D’Cruz N, Zoetewei D, Nieuwboer A. Neural underpinnings of freezing-related dynamic balance control in people with Parkinson’s disease. Parkinsonism Relat Disord. 2023 Jul;112:105444. doi: 10.1016/j.parkreldis.2023.105444. Epub 2023 May 12. PMID: 37257264.
To cite this abstract in AMA style:
E. Sarasso, A. Gardoni, A. Grassi, L. Zenere, S. Basaia, G. Bonardi, S. Carta, I. Di Vico, E. Mantovani, E. Canu, M. Bressan, V. Castelnovo, E. Sibilla, C. Tripodi, F. Freri, R. Balestrino, M. Trentinaglia, F. Maffei, V. Chiodega, S. Tamburin, MA. Volontè, S. Mariotto, M. Tinazzi, M. Filippi, F. Agosta. Clinical And Cerebellar Structural Alterations In Parkinson’s Disease Patients With Freezing Of Gait [abstract]. Mov Disord. 2025; 40 (suppl 1). https://www.mdsabstracts.org/abstract/clinical-and-cerebellar-structural-alterations-in-parkinsons-disease-patients-with-freezing-of-gait/. Accessed October 5, 2025.« Back to 2025 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/clinical-and-cerebellar-structural-alterations-in-parkinsons-disease-patients-with-freezing-of-gait/