Objective:

To compare cerebral metabolic patterns and dopaminergic function in patients with freezing of gait (FOG) associated with cerebral small vessel disease (CSVD) and Parkinson's disease (PD) using 18F-FDG and 11C-CFT PET imaging.

Background:

FOG is a disabling motor symptom commonly seen in PD, but also present in patients with CSVD. While PD is characterized by dopaminergic neuronal degeneration, the mechanism underlying FOG in CSVD remains poorly understood. This study aims to investigate the differences in the metabolic and dopaminergic profiles between CSVD and PD patients with FOG to better understand their underlying pathophysiology.

Design/Methods:

This cross-sectional study included 7 CSVD patients with FOG, 7 PD patients with FOG, and 20 healthy controls. All subjects underwent clinical assessment and PET imaging using 18F-FDG and 11C-CFT tracers. Visual and quantitative analyses were conducted to compare cerebral metabolism and dopamine transporter binding in key brain regions across the three groups. Clinical correlations were assessed using Pearson's tests and adjusted general linear models.

Results:

CSVD patients exhibited reduced 18F-FDG metabolism in the frontal lobe, striatum, and posterior cingulate cortex, with increased metabolism in the temporal lobe, occipital lobe, and cerebellum. In contrast, PD patients showed increased metabolism in the striatum and reduced metabolism in the parietal and temporal lobes. 11C-CFT PET imaging revealed significant reductions in DAT binding in the bilateral striatum of PD patients, while CSVD patients showed no such deficits. In CSVD patients, higher putamen metabolism was correlated with faster gait speed and lower FOG scores.

Conclusions:

FOG may arise through different mechanisms in CSVD and PD. While PD patients exhibit dopaminergic deficits, CSVD patients show metabolic alterations without significant DAT binding reductions, suggesting that FOG in CSVD may not be primarily driven by dopaminergic dysfunction. These findings emphasize the importance of understanding distinct pathophysiological pathways in FOG, which could aid in tailored therapeutic strategies.