Open AccessNeural substrates of levodopa‐responsive gait disorders and freezing in advanced Parkinson's disease: A kinesthetic imagery approach
Author(s) -
Maillet Audrey,
Thobois Stéphane,
Fraix Valérie,
Redouté Jérôme,
Le Bars Didier,
Lavenne Franck,
Derost Philippe,
Durif Franck,
Bloem Bastiaan R.,
Krack Paul,
Pollak Pierre,
Debû Bettina
Publication year - 2015
Publication title -
human brain mapping
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.005
H-Index - 191
eISSN - 1097-0193
pISSN - 1065-9471
DOI - 10.1002/hbm.22679
Subject(s) - levodopa , basal ganglia , psychology , gait , parkinson's disease , putamen , neuroscience , physical medicine and rehabilitation , movement disorders , thalamus , cerebellum , medicine , disease , central nervous system
Gait disturbances, including freezing of gait, are frequent and disabling symptoms of Parkinson's disease. They often respond poorly to dopaminergic treatments. Although recent studies have shed some light on their neural correlates, their modulation by dopaminergic treatment remains quite unknown. Specifically, the influence of levodopa on the networks involved in motor imagery (MI) of parkinsonian gait has not been directly studied, comparing the off and on medication states in the same patients. We therefore conducted an [H 2 15 0] Positron emission tomography study in eight advanced parkinsonian patients (mean disease duration: 12.3 ± 3.8 years) presenting with levodopa‐responsive gait disorders and FoG, and eight age‐matched healthy subjects. All participants performed three tasks (MI of gait, visual imagery and a control task). Patients were tested off , after an overnight withdrawal of all antiparkinsonian treatment, and on medication, during consecutive mornings. The order of conditions was counterbalanced between subjects and sessions. Results showed that imagined gait elicited activations within motor and frontal associative areas, thalamus, basal ganglia and cerebellum in controls. Off medication, patients mainly activated premotor‐parietal and pontomesencephalic regions. Levodopa increased activation in motor regions, putamen, thalamus, and cerebellum, and reduced premotor‐parietal and brainstem involvement. Areas activated when patients are off medication may represent compensatory mechanisms. The recruitment of these accessory circuits has also been reported for upper‐limb movements in Parkinson's disease, suggesting a partly overlapping pathophysiology between imagined levodopa‐responsive gait disorders and appendicular signs. Our results also highlight a possible cerebellar contribution in the pathophysiology of parkinsonian gait disorders through kinesthetic imagery. Hum Brain Mapp 36:959–980, 2015. © 2014 Wiley Periodicals, Inc.