Cholinergic brain network deficits associated with vestibular sensory conflict deficits in Parkinson's disease: correlation with postural and gait deficits.
Cholinergic brain network deficits associated with vestibular sensory conflict deficits in Parkinson's disease: correlation with postural and gait deficits.
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DOI：
10.1007/s00702-022-02523-3
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发表时间：
2022-08
影响因子：
3.3
通讯作者：
Muller, Martijn L. T. M.
中科院分区：
文献类型：
--
作者：
Bohnen, Nicolaas, I;Kanel, Prabesh;Roytman, Stiven;Scott, Peter J. H.;Koeppe, Robert A.;Albin, Roger L.;Kerber, Kevin A.;Muller, Martijn L. T. M.
关键词：
探讨局部脑泡乙酰胆碱转运体（VAChT）配体[18F]氟乙氧基苯并维酰胺（[18F]-FEOBV） PET在伴有和不伴有前庭感觉冲突缺陷（VSCD）帕金森病（PD）患者中的结合情况。研究与vscd相关的胆碱能脑缺陷与姿势不稳定和步态困难（PIGD）之间的关系。PD患者（M70/F22，平均年龄67.6±7.4岁）完成了失衡、跌倒、步态冻结（FoG）、改良Romberg感觉冲突测试的临床评估，并进行了VAChT PET检查。基于兴趣量（VOI）的分析包括详细的丘脑和小脑包裹。vscd相关VAChT VOI选择采用逐步logistic回归分析。囊泡单胺转运蛋白2型（VMAT2） [11C]二氢四苯那嗪（DTBZ） PET显像54例。在考虑混杂因素的情况下，进行协方差分析，比较有和没有PIGD运动特征的患者与vscd相关的胆碱能缺陷。73例患者PET取样通过验收标准。这项数据驱动的分析确定了与VSCD存在相关的5个脑voi的胆碱能缺陷：内侧膝状核（MGN） （P<0.0001）、海马旁回（P=0.0043）、枕状核下核（P=0.047）、梭状回（P=0.035）和杏仁核（P=0.019）。与年龄、病程、性别和黑质纹状体多巴胺能丧失无关，失衡（- 8.3%，F=6.5， P=0.015；总模型：F=5.1， P=0.0008）、跌倒（- 6.9%，F=4.9， P=0.03；总模型F=4.7， P=0.0015）和FoG （- 14.2%， F=9.0， P=0.0043；总模型F=5.8， P=0.0003）患者这5个区域的FEOBV结合缺陷均显著降低[18F]。使用MGN VAChT结合作为单一胆碱能VOI的事后分析显示，与失衡、跌倒和FoG有类似的显著关联。vscd相关的胆碱能网络变化定位于不同的结构，涉及多感觉，特别是前庭，以及多模态认知和运动整合脑区域。VSCD相关胆碱能网络缺陷的相对临床效果在FoG中最大，其次是姿势不平衡和跌倒。mgnn是最显著的区域。
To examine regional cerebral vesicular acetylcholine transporter (VAChT) ligand [18F]fluoroethoxybenzovesamicol ([18F]-FEOBV) PET binding in Parkinson’s disease (PD) patients with and without vestibular sensory conflict deficits (VSCD). To examine associations between VSCD-associated cholinergic brain deficits and postural instability and gait difficulties (PIGD). PD persons (M70/F22; mean age 67.6±7.4 years) completed clinical assessments for imbalance, falls, freezing of gait (FoG), modified Romberg sensory conflict testing, and underwent VAChT PET. Volumes-of-interest (VOI)-based analyses included detailed thalamic and cerebellar parcellations. VSCD-associated VAChT VOI selection used stepwise logistic regression analysis. Vesicular monoamine transporter type 2 (VMAT2) [11C]dihydrotetrabenazine (DTBZ) PET imaging was available in 54 patients. Analyses of covariance were performed to compare VSCD-associated cholinergic deficits between patients with and without PIGD motor features while accounting for confounders. PET sampling passed acceptance criteria in 73 patients. This data-driven analysis identified cholinergic deficits in five brain VOIs associating with the presence of VSCD: Medial geniculate nucleus (MGN) (P<0.0001), parahippocampal gyrus (P=0.0043), inferior nucleus of the pulvinar (P=0.047), fusiform gyrus (P=0.035) and the amygdala (P=0.019). Composite VSCD-associated [18F]FEOBV binding deficits in these 5 regions was significantly lower in patients with imbalance (−8.3%, F=6.5, P=0.015; total model: F=5.1, P=0.0008), falls (−6.9%, F=4.9, P=0.03; total model F=4.7, P=0.0015), and FoG (−14.2%, F=9.0, P=0.0043; total model F=5.8, P=0.0003), independent of age, duration of disease, gender and nigrostriatal dopaminergic losses. Post-hoc analysis using MGN VAChT binding as the single cholinergic VOI demonstrated similar significant associations with imbalance, falls and FoG. VSCD-associated cholinergic network changes localize to distinct structures involved in multi-sensory, in particular vestibular, and multimodal cognitive and motor integration brain regions. Relative clinical effects of VSCD associated cholinergic network deficits were largest for FoG followed by postural imbalance and falls. The MGN was the most significant region identified.
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影响因子：
4.3
作者：
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通讯作者：
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