Research center

47 bld de l'Hôpital
75651 Paris
Alexis Brice


Université Pierre et Marie Curie
Université Pierre et Marie Curie


Phone: 01 44 27 25 85
UMRS 1127 UMR 7225
IHU A-ICM, Institut Carnot ICM Hôpital Pitié Salpêtrière

Mots clefs

syndrome Gilles de la Tourette
ganglions de la base


Welter ML, Grabli D, Karachi C, Jodoin N, Fernandez-Vidal S, Brun Y, Navarro S, Rogers A, Cornu P, Pidoux B, Yelnik J, Roze E, Bardinet E, Vidailhet M. Pallidal activity in myoclonus dystonia correlates with motor signs. Mov Disord. 2015 Apr 16. doi: 10.1002/mds.26244. 

Nalls MA, et al. Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson's disease. Nat Genet. 2014 Sep;46(9):989-93. doi: 10.1038/ng.3043. Epub 2014 Jul 27.

García-Lorenzo D, Longo-Dos Santos C, Ewenczyk C, Leu-Semenescu S, Gallea C, Quattrocchi G, Pita Lobo P, Poupon C, Benali H, Arnulf I, Vidailhet M, Lehericy S. (2013) The coeruleus/subcoeruleus complex in rapid eye movement sleep behaviour disorders inParkinson's disease. Brain. 136:2120-9

Nelson M, Bosch C, Venance L, Pouget P. (2013) Microscale inhomogeneity of brain tissue distorts electrical signal propagation. J.Neuroscience 33:2821-7. (IF=7.12)

Corvol JC, Bonnet C, Charbonnier-Beaupel F, Bonnet AM , Roze E, Melyksekian G, Ben Djebara M, Hartmann A, Lacomblez L, Vrignaud C, Zahr N, Agid Y, Costentin J, Hulot JB, Vidailhet M. The non synonymous Val258Met polymorphism in COMT gene impacts entacapone response to L-DOPA in Parkinson’s disease: a randomized cross-over clinical trial. Ann Neurol. 2011;;69:111-8. (IF=10.74)

Lehéricy S, Hartmann A, Lannuzel A, Galanaud D, Delmaire C, Bienaimée MJ, Jodoin N, Roze E, Gaymard B, Vidailhet M. Magnetic resonance imaging lesion pattern in Guadeloupean parkinsonism is distinct from progressive supranuclear palsy Source: Brain. 2010 Mar;133: 2410-2425    (IF=9.5)

 Vidailhet M, Yelnik J, Lagrange C, Fraix V, Grabli D, Thobois S, Burbaud P, Welter ML, Xie-Brustolin J, Braga MC, Ardouin C, Czernecki V, Klinger H, Chabardes S, Seigneuret E, Mertens P, Cuny E, Navarro S, Cornu P, Benabid AL, Lebas JF, Dormont D, Hermier M, Dujardin K, Blond S, Krystkowiak P, Destée A, Bardinet E, Agid Y, Krack P, Broussolle E, Pollak P; for the French SPIDY-2 Study Group Bilateral pallidal deep brain stimulation for the treatment of patients with dystonia-choreoathetosis cerebral palsy: a prospective pilot study Lancet Neurol 8 (8): 709-17, 2009. (IF=18.12)

Fields of research

Neurophysiology / systems neuroscience

Research Theme

Our main research topic is the physiological analysis of both subcortical and cortical brain structures involved in the control of normal and abnormal movements. Dystonia, Gilles de la Tourette syndrome (GTS) and Parkinson’s disease (PD) will be taken as models of basal ganglia dysfunction. The implication of basal ganglia in movement disorders will be analysed by a multimodal approaches in relation with basic science groups and access to platforms (CENIR-imaging; neurophysiology laboratory, functional neurosurgery team and sleep lab). Dystonia is considered as a model of abnormal cortico-striatal integration and GTS as a model of dysfunctional motor and limbic loops. Both pathologies will be explored with similar experimental MRI paradigms in order to detect morphological and biochemical abnormalities (DTI, VBM, spectroscopy). Experimental therapeutic strategies will be developed in two directions with strong clinical implications: a) multiple electrodes neurostimulation in dystonia may increase the improvement of disability. In addition, the targeting of multiples structures (STN, Cm, GPi) within the basal ganglia are potent tools to probe the reactivity of cortico-basal ganglia loops. b) in PD, the aim is to develop pilot pharmacological studies with a combination of potentially neuroprotective compounds, with the hope to target pathways relevant to PD pathogenesis such as oxidative stress, neuroinflammation and mitochondrial function (based on close collaborations with basic science groups involved in research on chronic neurodegenerative diseases). Further, the basal ganglia are also involved in sleep disorders, especially in PD and other parkinsonian syndromes: in previous studies we showed that severe sleepiness in PD is considered a secondary narcolepsy. In line with this result, a selective loss of orexin-positive neurons in PD has been found. We intend to study the mechanisms of sleepiness in PD with 3 main questions: a) the role of sleep apneas in diurnal sleepiness; b) the role of PGP pump polymorphisms on sleepiness induced by dopaminergic agonists; c) the increase of histamine liberation with anti-H3 drugs and the role of these drugs on sleep and motor functioning. REM sleep behaviour disorders (abnormal behaviours while dreaming –acted dreams-) may develop prior to the appearance of PD and are observed in more than 50% of PD patients. We have demonstrated the restoration motor function during RBD (dreams in the absence of normal atonia related to locus sub-coeruleus lesions) in PD and will explore the mechanisms of this normalisation. Finally, at the cortical level, our studies will be centred on the roles of fronto-median areas, supplementary motor area (SMA), pre-SMA, supplementary eye field and cingulate motor areas, and we will use complex eye movement paradigms in order to test processes such as error monitoring, task set inertia or task set reconfiguration. These areas will be selectively and reversibly inactivated with muscimol injections in primates, and by rTMS in humans. The role of their subcortical connections will be analysed in a second phase in parkinsonism and Gilles de la Tourette syndrome.