Journal of neurology · 2025
Neural and dopaminergic substrates of festinating gait in Parkinson's disease.
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Lee Eek-Sung, Kim Min Seung, Oh Jungsu S, Seo Seung Yeon, Kim Jae Seung, Han You Mie, Chang Suk Ki, Jo Sang Won, Kang Suk Yun
Аннотация
BACKGROUND: Festinating gait (FSG) is a typical feature of Parkinson's disease (PD). However, the mechanisms are poorly understood. We aimed to determine the neural substrates of FSG in PD and whether the festinating gait is related to striatal dopaminergic activity.
METHODS: A total of 70 PD patients without FSG and 22 PD patients with FSG were recruited for voxel-based morphometry and diffusion tensor imaging analyses. Among the subjects, 55 PD patients without FSG and 13 PD patients with FSG were analyzed for striatal dopaminergic activity. The severity of FSG and freezing were evaluated using a systematic questionnaire.
RESULTS: PD patients with FSG demonstrated significantly lower cognitive scores and higher depression, fatigue, and Unified Parkinson's Disease Rating Scale scores when compared with subjects without FSG. Neuroimaging analysis revealed that PD patients with FSG exhibited decreased white matter integrity in the right frontoparietal and parolfactory cingulum as well as increased gray matter (GM) volume in the right caudate nucleus. FSG severity negatively correlated with GM volume in the left middle frontal gyrus and bilateral hippocampi. Significant differences in striatal dopamine transporter activity were not observed between PD patients with and without FSG, and correlation was not found between FSG severity and dopamine transporter activity, indicating that FSG in PD may be associated with structural brain changes rather than dopaminergic dysfunction.
CONCLUSIONS: The brain areas for cognitive control of complex motor movements, posture regulation, memory function, and emotion may be associated with FSG, and striatal dopaminergic activity may not be involved in FSG.
METHODS: A total of 70 PD patients without FSG and 22 PD patients with FSG were recruited for voxel-based morphometry and diffusion tensor imaging analyses. Among the subjects, 55 PD patients without FSG and 13 PD patients with FSG were analyzed for striatal dopaminergic activity. The severity of FSG and freezing were evaluated using a systematic questionnaire.
RESULTS: PD patients with FSG demonstrated significantly lower cognitive scores and higher depression, fatigue, and Unified Parkinson's Disease Rating Scale scores when compared with subjects without FSG. Neuroimaging analysis revealed that PD patients with FSG exhibited decreased white matter integrity in the right frontoparietal and parolfactory cingulum as well as increased gray matter (GM) volume in the right caudate nucleus. FSG severity negatively correlated with GM volume in the left middle frontal gyrus and bilateral hippocampi. Significant differences in striatal dopamine transporter activity were not observed between PD patients with and without FSG, and correlation was not found between FSG severity and dopamine transporter activity, indicating that FSG in PD may be associated with structural brain changes rather than dopaminergic dysfunction.
CONCLUSIONS: The brain areas for cognitive control of complex motor movements, posture regulation, memory function, and emotion may be associated with FSG, and striatal dopaminergic activity may not be involved in FSG.