Brain metabolic abnormalities during gait with freezing in Parkinson's disease. (29th October 2015)

• Record Type: Journal Article
• Authors: Tard, C.; Delval, A.; Devos, D.; Lopes, R.; Lenfant, P.; Dujardin, K.; Hossein-Foucher, C.; Semah, F.; Duhamel, A.; Defebvre, L.; Le Jeune, F.; Moreau, C.
• Is Part Of: Neuroscience. Volume 307(2015)
• Page Start: 281
• Page End: 301
• Publication Date: 2015-10-29
• Subjects: [18F]-FDG-PET [18F]-fluorodeoxyglucose positron emission tomography -- BA Brodmann area -- FEF frontal eye field -- FoG freezing of gait -- MLR mesencephalic locomotor region -- SMA supplementary motor area -- PD Parkinson's disease -- ROI region of interest; PET -- associative somatosensory cortex -- premotor cortex -- temporopolar area -- executive-attention network; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2015.08.063
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: Freezing of gait was related to hypometabolism of premotor area during actual gait. Freezers presented a hypermetabolism of the posterior parietal cortex during gait. Parietofrontal network was involved in freezing phenomenon. Basal ganglia overactivation during gait was observed in freezers patients. The balance between external and internal signals may fail during freezing. Abstract: Introduction: Freezing 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. Methods: Twenty-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. Results: For 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). Conclusion: FoG 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).