Effect of small vessel disease burden and lacunes on gait/posture impairment in Parkinson’s disease
Huimin Chena b c, Meimei Zhanga b c, Gengliang Liua b c, Xuemei Wanga b c, Zhan Wanga b c, Huizi Maa b c, Yuesong Pana b c, David Wangd, Yilong Wanga b c, Tao Fengb e f g✉
- aAdvanced Innovation Center for Human Brain Projection, Capital Medical University, Beijing, China
- bChina National Clinical Research Center for Neurological Diseases (NCRC-ND), Beijing, China
- cDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
- dIllinois Neurological Institute Stroke Network, Sisters of the Third Order of St Francis Healthcare System, University of Illinois College of Medicine, Peoria, USA
- eAdvanced Innovation Center for Human Brain Projection, Capital Medical University, Beijing, China. bxbkyjs@sina.com
- fChina National Clinical Research Center for Neurological Diseases (NCRC-ND), Beijing, China. bxbkyjs@sina.com
- gDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. bxbkyjs@sina.com
- ✉Corresponding author
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Abstract
Introduction: The comorbidity of cerebral small vessel disease (CSVD) may worsen gait impairment of Parkinson's disease (PD). However, the evidence remains scarce and controversial, and the mechanism of their potential interaction remains largely unknown. The present study aimed to investigate the overall impact of quantity and location of CSVD on gait/posture function in PD. Methods: This cross-sectional study included 315 consecutive eligible patients with PD from Beijing Tiantan Hospital from May 2016 to August 2018. Associations of gait/posture subscores with the burden score of CSVD and four CSVD imaging markers were assessed using multivariate linear regression models. Results: Burden of CSVD was significantly associated with more severe gait/posture impairment in PD in the unadjusted model (β = 0.521, P = 0.011, 95% CI 0.118-0.923) and in the model adjusted for age, hypertension, ischemic stroke, low-density lipoprotein level, cholesterol level, and cognitive statues (β = 0.448, P = 0.047, 95% CI 0.006-0.891). The presence of lacunes, but not other CSVD markers, was significantly associated with higher gait/posture subscores after the adjustment (β = 0.492, P = 0.041, 95% CI 0.021-0.964), and the number of lacunes in the basal ganglia significantly correlated with the gait/posture subscores in patients with PD (P = 0.012, Spearman r = 0.161). Conclusions: CSVD and lacunes in the basal ganglia may independently contribute to gait/posture dysfunction in PD. Promoting neurovascular health may preserve some gait/posture function of PD.