Radboud University Medical Centre, Donders Institute for Brain, Cognition and Behaviour, Centre for Cognitive Neuroscience, Department of Neurology, Nijmegen, the Netherlands.
Radboud University Medical Centre, Diagnostic Image Analysis Group, Department of Radiology and Nuclear Medicine, Nijmegen, the Netherlands; Radboud University, Institute for Computing and Information Sciences, Nijmegen, the Netherlands.
Parkinsonism Relat Disord. 2019 Apr;61:94-100. doi: 10.1016/j.parkreldis.2018.11.010. Epub 2018 Nov 8.
Incident parkinsonism in patients with comparable cerebral small vessel disease (SVD) burden is not fully explained by presence of SVD alone. We therefore investigated if severity of SVD, SVD location, incidence of SVD and/or brain atrophy plays a role in this distinct development of parkinsonism.
Participants were from the RUN DMC study, a prospective cohort of 503 individuals with SVD. Parkinsonism was diagnosed according to the UKPDS brain bank criteria. Fine and Gray method was used to assess the association between SVD and incident parkinsonism. Differences in white matter hyperintensities (WMH) progression and brain atrophy were calculated with a linear mixed effect analysis.
After a median follow-up of 8.6 years, 32 of 501 participants developed parkinsonism (6.4%). The highest WMH load was found in the frontal lobe for both groups. Presence of more than one lacune at baseline was higher in the group who developed parkinsonism, especially in the frontal lobe (22% versus 3%, p < 0.001) and basal ganglia (12.5% versus 1%, p-value <0.001). The annual rate of total brain atrophy was significantly higher for those who developed parkinsonism compared to those who did not (8.7 ml [95%CI 7.1-10.3] and 4.9 ml [95%CI 4.5-5.3], respectively). While WMH progression was not different, incidence of lacunes and microbleeds was higher in the group with parkinsonism.
The risk of parkinsonism in patients with SVD is especially increased when WMH and lacunes are present in the frontal lobe. A higher brain atrophy rate might further increase this risk.
在具有相似脑小血管疾病(SVD)负担的患者中,单纯 SVD 并不能完全解释偶发性帕金森病。因此,我们研究了 SVD 严重程度、SVD 位置、SVD 发生率和/或脑萎缩是否在帕金森病的这种特殊发展中起作用。
参与者来自 RUN DMC 研究,这是一项对 503 名 SVD 患者的前瞻性队列研究。帕金森病的诊断符合英国帕金森病脑库标准。精细和灰色方法用于评估 SVD 与偶发性帕金森病之间的关联。线性混合效应分析计算了脑白质高信号(WMH)进展和脑萎缩的差异。
中位随访 8.6 年后,501 名参与者中有 32 名(6.4%)发展为帕金森病。两组的额叶 WMH 负荷最高。基线时存在多个腔隙的患者在发展为帕金森病的组中更高,尤其是在额叶(22%比 3%,p 值<0.001)和基底节(12.5%比 1%,p 值<0.001)。与未发生帕金森病的患者相比,发生帕金森病的患者总脑萎缩的年增长率明显更高(8.7 ml [95%CI 7.1-10.3]和 4.9 ml [95%CI 4.5-5.3])。虽然 WMH 进展无差异,但帕金森病组的腔隙和微出血发生率更高。
当额叶存在 WMH 和腔隙时,SVD 患者发生帕金森病的风险尤其增加。较高的脑萎缩率可能进一步增加这种风险。