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Behavioural Neurology
Volume 2015 (2015), Article ID 970204, 6 pages
Research Article

Coexistence of Gait Disturbances and Chorea in Experimental Huntington’s Disease

1Department of Neuroscience, Maastricht University Medical Center, 6229 ER Maastricht, Netherlands
2European Graduate School of Neuroscience (EURON), 6229 ER Maastricht, Netherlands
3Department of Neurosurgery, Maastricht University Medical Center, 6229 ER Maastricht, Netherlands

Received 1 March 2015; Revised 6 April 2015; Accepted 17 April 2015

Academic Editor: Barbara Picconi

Copyright © 2015 João Casaca-Carreira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease caused by an expanded CAG repeat. The clinical features are progressive motor dysfunction, cognitive deterioration, and psychiatric disturbances. Unpredictable choreic movements, among the most characteristic hallmarks, may contribute to gait disturbances and loss of balance in HD individuals. In this study, we aimed to investigate and characterize the gait abnormalities and choreic movements in a transgenic rat model of HD (tgHD). TgHD presents typical neuropathological, neurophysiological, and behavioral aspects mimicking some of the key features of human HD and is the only described experimental model for HD that exhibits choreiform movements. We used the Catwalk, with emphasis on static and dynamic gait parameters, to test the hypothesis that at symptomatic age (9 months) the dynamic measures of gait in HD are altered and coexist with choreiform movements. Our results showed that the dynamic parameters seem to be more affected than static parameters at this age in tgHD rats. The number of steps and step cycles and swing speed of the paws were increased in tgHD rat in comparison to wild-type controls. Our study demonstrates that gait abnormalities coexist with chorea rather than being caused by it. These symptoms may originate from distinct networks in the basal ganglia and downstream connections.