Gait speed in Parkinson disease correlates with cholinergic degeneration

• DOI: 10.1212/wnl.0b013e3182a9f558
• Publication Date: 2013-09-28T05:19:13Z
• Authors: Nicolaas I. Bohnen; Kirk A. Frey; Stephanie Studenski; Vikas Kotagal; Robert A. Koeppe; Peter J.H. Scott; Roger L. Albin; Martijn L.T.M. Mü...
• Keywords: Aged, 80 and over; Cerebral Cortex; Male; Analysis of Variance; Carbon Isotopes; Tetrabenazine; Dioxolanes; Parkinson Disease; Middle Aged; Neuropsychological Tests; Cross-Sectional Studies; Positron-Emission Tomography; Vesicular Monoamine Transport Proteins; Nerve Degeneration; Acetylcholinesterase; Humans; Female; Cognition Disorders; Gait Disorders, Neurologic; Aged

We investigated dopaminergic and cholinergic correlates of gait speed in Parkinson disease (PD) non-PD control subjects to test the hypothesis that dysfunction PD may result from multisystem degeneration.This was a cross-sectional study. Subjects with but without dementia (n = 125, age 65.6 ± 7.3 years) elderly 32, 66.0 10.6 underwent [¹¹C]dihydrotetrabenazine [(11)C]methyl-4-piperidinyl propionate acetylcholinesterase PET imaging, cognitive clinical testing, including an 8.5-m walk "off" state. The fifth percentile cortical activity used define normal-range PD.Normal-range present 87 (69.6%). Analysis covariance using as dependent variable demonstrated significant model (F 6.70, p < 0.0001) group effect 3.36, 0.037) slower low subgroup (0.97 0.22 m/s) no difference between (1.12 0.20 (1.17 0.18 m/s). Covariate effects were for cognition 6.58, 0.011), not striatal innervation, sex, or age.Comorbid denervation is more robust marker slowing than nigrostriatal alone. Gait significantly normal relatively isolated denervation.