C L Nicholson1, P Coubes2, G Poulen3. 1. Service de neurochirurgie, CHRU Montpellier, 34295 Montpellier, France; Department of Neurosurgery, Newcastle General Hospital, Newcastle, UK. 2. Service de neurochirurgie, CHRU Montpellier, 34295 Montpellier, France; IGF, 34094 Montpellier, France; CNRS UMR5203, 34094 Montpellier, France; Inserm, U661, 34094 Montpellier, France; Université Montpellier I, 34094 Montpellier, France. 3. Service de neurochirurgie, CHRU Montpellier, 34295 Montpellier, France; IGF, 34094 Montpellier, France; CNRS UMR5203, 34094 Montpellier, France; Inserm, U661, 34094 Montpellier, France; Université Montpellier I, 34094 Montpellier, France. Electronic address: g-poulen@chu-montpellier.fr.
Abstract
PURPOSE: To discuss the potential of deep brain stimulation (DBS) of the dentate nucleus as a treatment for dystono-dyskinetic syndromes. METHODS: An extensive literature review covered the anatomy and physiology of the dentate nucleus and the experimental evidence for its involvement in the pathophysiology of dystonia and dyskinesia. RESULTS: Evidence from animal models and from functional imaging in humans is strongly in favor of involvement of the dentate nucleus in dystono-dyskinetic syndromes. Results from previous surgical series of dentate nucleus stimulation were promising but precise description of movement disorders being treated were lacking and outcome measures were generally not well defined. CONCLUSIONS: In the light of new evidence regarding the involvement of the dentate nucleus in dystono-dyskinetic syndromes, we present a review of the current literature and discuss why the question of dentate nucleus stimulation deserves to be revisited.
PURPOSE: To discuss the potential of deep brain stimulation (DBS) of the dentate nucleus as a treatment for dystono-dyskinetic syndromes. METHODS: An extensive literature review covered the anatomy and physiology of the dentate nucleus and the experimental evidence for its involvement in the pathophysiology of dystonia and dyskinesia. RESULTS: Evidence from animal models and from functional imaging in humans is strongly in favor of involvement of the dentate nucleus in dystono-dyskinetic syndromes. Results from previous surgical series of dentate nucleus stimulation were promising but precise description of movement disorders being treated were lacking and outcome measures were generally not well defined. CONCLUSIONS: In the light of new evidence regarding the involvement of the dentate nucleus in dystono-dyskinetic syndromes, we present a review of the current literature and discuss why the question of dentate nucleus stimulation deserves to be revisited.