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Clinical Trial Summary

Dystonia, a disabling disease with uncontrolled movement disorders was considered to be a manifestation of basal ganglia dysfunction, yet there is accumulating evidence from animal and human experiments that the cerebellum plays a prominent role in the pathophysiology of dystonia. Our recent results suggest a deficient cerebellar sensory encoding in dystonia, resulting in a decoupling of the motor component from the afferent information flow resulting from changes in the environment. An overall loss of gabaergic-mediated inhibition is at the forefront in dynamic changes in neural circuitry described in dystonia. In the mature brain gabaergic control the generation of temporal synchronies and oscillations in the glutamatergic neurons. Taken these all together with the results of a pilot experiment, the investigators hypothesize that deficient synchronies in the fast gamma range are one of the key mechanisms leading to abnormal communication inside the cerebello-cortical network in dystonia. The investigators aim first to demonstrate it by means of MEG (Magneto encepholography) recordings allowing to reconstruct the spatio-temporal dynamics of gamma oscillations in the nodes of the cerebello-cortical network. The investigators then aim to re-establish (if lost) or boost (if decreased) the defective synchronies by applying to the cerebellum at high gamma frequency a non invasive transcranial alternative current stimulation.


Clinical Trial Description

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Study Design


Related Conditions & MeSH terms


NCT number NCT02073630
Study type Interventional
Source Institut National de la Santé Et de la Recherche Médicale, France
Contact
Status Completed
Phase N/A
Start date February 2014
Completion date August 2016

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