From the Department of Radiology, Division of Nuclear Medicine (N.I.B., K.A.F., R.A.K., P.J.H.S., M.L.T.M.M.), and Department of Neurology (N.I.B., K.A.F., V.K., R.L.A.), University of Michigan; Neurology Service and GRECC (N.I.B., R.L.A.), VAAAHS, Ann Arbor, MI; and Department of Internal Medicine (S.S.), Division of Geriatrics, University of Pittsburgh, PA.
Neurology. 2013 Oct 29;81(18):1611-6. doi: 10.1212/WNL.0b013e3182a9f558. Epub 2013 Sep 27.
We investigated dopaminergic and cholinergic correlates of gait speed in Parkinson disease (PD) and non-PD control subjects to test the hypothesis that gait dysfunction in PD may result from multisystem degeneration.
This was a cross-sectional study. Subjects with PD but without dementia (n = 125, age 65.6 ± 7.3 years) and elderly subjects without PD (n = 32, age 66.0 ± 10.6 years) underwent [¹¹C]dihydrotetrabenazine dopaminergic and [(11)C]methyl-4-piperidinyl propionate acetylcholinesterase PET imaging, and cognitive and clinical testing, including an 8.5-m walk in the dopaminergic "off" state. The fifth percentile of cortical cholinergic activity in the elderly without PD was used to define normal-range activity in the subjects with PD.
Normal-range cortical cholinergic activity was present in 87 subjects with PD (69.6%). Analysis of covariance using gait speed as the dependent variable demonstrated a significant model (F = 6.70, p < 0.0001) with a significant group effect (F = 3.36, p = 0.037) and significant slower gait speed in the low cholinergic PD subgroup (0.97 ± 0.22 m/s) with no significant difference between the normal-range cholinergic PD subgroup (1.12 ± 0.20 m/s) and control subjects (1.17 ± 0.18 m/s). Covariate effects were significant for cognition (F = 6.58, p = 0.011), but not for striatal dopaminergic innervation, sex, or age.
Comorbid cortical cholinergic denervation is a more robust marker of slowing of gait in PD than nigrostriatal denervation alone. Gait speed is not significantly slower than normal in subjects with PD with relatively isolated nigrostriatal denervation.
我们研究了帕金森病（PD）和非 PD 对照组中多巴胺能和胆碱能与步态速度的相关性，以检验步态功能障碍可能是由于多系统退行性变导致的假说。
这是一项横断面研究。无痴呆的 PD 患者（n = 125，年龄 65.6 ± 7.3 岁）和无 PD 的老年受试者（n = 32，年龄 66.0 ± 10.6 岁）接受了 [¹¹C]二氢四苯并嗪多巴胺能和 [(11)C]甲基-4-哌啶基丙酸乙酰胆碱酯酶 PET 成像，以及认知和临床测试，包括在多巴胺能“关闭”状态下进行 8.5 米步行。无 PD 的老年受试者中皮质胆碱能活性的第 5 百分位数被用于定义 PD 患者的正常范围活性。
87 名 PD 患者（69.6%）存在正常范围的皮质胆碱能活性。使用步态速度作为因变量的协方差分析显示，模型具有显著意义（F = 6.70，p < 0.0001），组间效应显著（F = 3.36，p = 0.037），且低胆碱能 PD 亚组的步态速度显著较慢（0.97 ± 0.22 m/s），而正常范围胆碱能 PD 亚组（1.12 ± 0.20 m/s）和对照组（1.17 ± 0.18 m/s）之间无显著差异。协变量的影响对认知有显著意义（F = 6.58，p = 0.011），但对纹状体多巴胺能神经支配、性别或年龄无显著意义。
皮质胆碱能神经支配的合并缺失是 PD 患者步态减慢的比纹状体多巴胺能神经支配缺失更为有力的标志物。在多巴胺能神经支配相对孤立缺失的 PD 患者中，步态速度并没有明显慢于正常。
