Association between cerebral small vessel diseases and mild parkinsonian signs in the elderly with vascular risk factors

Feb. 13, 2016

Highlights

• •Our findings support the contribution of hypertensive microangiopathy to MPS.
• •A high degree of cerebral small vessel disease burden was associated with MPS.
• •MPS may be a reflection of an increased vascular burden or more widespread disease.
• •Reducing the vascular risk factors that cause SVD could be prevented MPS.

Abstract

Introduction

The aim of this study was to examine the association between mild parkinsonian signs (MPS), cerebral small-vessel disease (SVD), and total SVD burden in patients with vascular risk factors.

Methods

We performed a cross-sectional study among 268 patients with vascular risk factors but without parkinsonism or dementia (71.0±7.8 years, 63% male). MPS was evaluated via Unified Parkinson's Disease Rating Scale Part III. Brain MRI was used to determine SVD (cerebral microbleeds [CMBs], lacunar infarctions [LIs], and white matter hyperintensities [WMH]). The presence of each SVD feature was indicated by the total SVD score. Logistic regression analyses were performed adjusting for age, sex, history of stroke, hypertension, diabetes mellitus, and dyslipidemia.

Results

In a multivariate analysis, we found that the presence of CMBs, deep CMBs, mixed (in the basal ganglia and thalamus) LIs, periventricular hyperintensities (PVH), and deep WMH (DWMH), and total SVD score were significantly associated with MPS, whereas strictly lobar CMBs and other LIs (in strictly basal ganglia or strictly thalamus) were not. We also found a significant association between mixed LIs, PVH, DWMH and total SVD score and gait/balance function, between PVH and rigidity, and between mixed LIs and bradykinesia. Among elderly participants (≥73years), the association of total SVD score, deep CMBs, mixed LIs, and PVH, with MPS remained significant.

Conclusion

Our results provide additional evidence that SVD including CMBs, and especially total SVD burden, might be a surrogate marker for MPS and support the contribution of hypertensive microangiopathy as the underlying etiology.

http://dx.doi.org/10.1016/j.parkreldis.2016.02.011

 Hatate

,

 Kaori Miwa

,

 Mari Matsumoto

,

 Tsutomu Sasaki

,

 Yoshiki Yagita

,

 Manabu Sakaguchi

,

Kazuo Kitagawa

,

 Hideki Mochizuki

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