• C Tard, A Delval, D Devos, R Lopes, P Lenfant, K Dujardin, C Hossein-Foucher, F Semah, A Duhamel, L Defebvre, F Le Jeune, and C Moreau.
• Service de Neurologie et Pathologie du mouvement, Hôpital Roger Salengro, CHRU de Lille, Lille, France; U1171, Université Lille, Lille, France. Electronic address: celinetard@gmail.com.
• Neuroscience. 2015 Oct 29; 307: 281-301.

IntroductionFreezing of gait (FoG) is a debilitating gait disorder in Parkinson's disease (PD). In advanced PD patients with FoG, the supraspinal locomotor network may be dysregulated (relative to similar patients without FoG) during gait. Here, we sought to characterize the metabolism of locomotor networks involved in FoG.MethodsTwenty-two PD patients (11 with off-drug FoG and 11 without) each underwent two [(18)F]-fluorodeoxyglucose PET brain scans in the off-drug state: one at rest and another during radiotracer uptake while performing a standardized gait trajectory that incorporated the usual triggers for FoG.ResultsFor the 11 freezers, FoG was present for 39% (± 23%) of the time during the gait trajectory. The FoG-associated abnormalities were characterized by (i) hypometabolism in frontal regions (the associative premotor, temporopolar and orbitofrontal areas, i.e. Brodmann areas 6 and 8), (ii) hypermetabolism in the paracentral lobule (Brodmann area 5), and (iii) deregulation of the basal ganglia output (the globus pallidus and the mesencephalic locomotor region).ConclusionFoG during a real gait task was associated with impaired frontoparietal cortical activation, as characterized by abnormally low metabolic activity of the premotor area (involved in the indirect locomotor pathway) and abnormally high metabolic activity of the parietal area (reflecting the harmful effect of external cueing).Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

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