Volumetric Imaging Biomarkers of Freezing of Gait (FoG) in Patients with Parkinson’s Disease
Nestor Beltre1, Sarah Marmol1, Ihtsham Haq2, Corneliu Luca2
1Department of Neurology, 2Department of Neurology, Movement Division, University of Miami
Objective:

To determine whether imaging biomarkers exist to correlate with existing freezing of gait (FoG) in patients with Parkinson’s disease (PD).

Background:

FoG is a disabling motor symptom of PD, affecting ~25% of patients with early PD and more than half with advanced PD. FoG is a paroxysmal, brief, involuntary, and unexpected disruption of gait that can last for a few seconds. FoG has been linked to postural instability and executive dysfunction. FoG remains challenging to predict, as it is sporadic and has multiple motor, limbic, and cognitive triggers.

Design/Methods:

We analyzed the T1-weighted MRI scans of 50 people with PD with and without FoG using FreeSurfer software, which automatically measured cortical and subcortical volumes.  Patients were included in the FoG+ group if they were observed to have FoG during a clinic visit, self-reported FoG, or had a gait freezing score ≥1 on UPDRS.

Results:

30 patients with and 20 without FOG comprised our cohort. Overall male predominance (68%), more pronounced in the FoG+ group but not statistically significant. Mean age was 60.58, mean disease duration was 8.76 years, with no statistically significant difference between groups. When normalized to total intracranial volume (ICV), there were significant volumetric differences for mean cerebellar cortex (p = 0.03), right and left ventral diencephalon (VDC) (p = 0.005 and 0.009), and brainstem volumes (p = 0.02), with volumes being lower for FoG+.

Conclusions:

Although total ICV and total cerebral cortex volumes were greater for the FoG+ group, normalized volumes for cerebellar cortex, brainstem, and VDC were lower. These preliminary findings suggest the possibility of using volume loss as a predictor of FoG. Notably, inhibition of brainstem  and cerebellar structures have been theorized to contribute to FoG. Limitations include small sample sizes. Next steps include comparing these values to matched healthy controls and correlation between structural atrophy and FoG severity.

10.1212/WNL.0000000000205308