Effect GPi Stimulation on Human Thalamic Neuronal Activity: A DecadeLater

Copyright: © 2017 Pralong E. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. It is now more than 14 years that we first published observations of the effect of motor internal pallidum (mGPi) stimulation on the neuronal activity in the thalamic nucleus ventralis oralis anterior (VOA) [1]. One of the main conclusions of this study was that DBS of mGPi decreased firing activity of a subpopulation of VOA neurones. This fact was against the admitted theory of dystonia as a hyperkinetic movement disorder resulting from disinhibition of the motor thalamus [2]. Three years later, Montgomery [3] published similar observations of decreased neuronal activity in 48% of recorded thalamic neurones in the nucleus ventralis oralis posterior during mGPi stimulation this again invalidated motor thalamus disinhibition as the main pathophysiological mechanism for dystonia. Since, GPi DBS or even pallidotomy have imposed themselves as validated techniques for functional treatment for isolated, generalized or focal dystonias and related disorders [4] such as Lesch-Nyhan syndrome [5].