[Deep brain stimulation and gait disorders in Parkinson disease].

Abstract : INTRODUCTION: Gait disorders and freezing of gait (FOG) are seen in most patients with advanced Parkinson disease. Response to levodopa and deep brain stimulation is variable across patients. STATE OF ART: Thalamic stimulation is ineffective on gait and can even worsen balance when bilaterally applied. Pallidal stimulation moderately improves gait disorders and FOG although this effect tends to wane after three to five years. Stimulation of the subthalamic nucleus (STN) improves levodopa-responsive gait disorders and FOG. However, some patients worsen after STN stimulation and others are better improved under levodopa than under STN stimulation. Synergistic effects of the two treatments have been reported. As for pallidal stimulation, there is a failure of long-term STN stimulation to improve gait, probably due to the involvement of non-dopaminergic pathways as the disease progresses. Levodopa-resistant gait disorders and FOG do not usually benefit from STN stimulation. In the rare cases of levodopa-induced FOG, STN stimulation may be indirectly effective, as it enables reduction or arrest of the levodopa treatment. PERSPECTIVES: Pedunculopontine nucleus stimulation has recently been performed in small groups of patients with disabling gait disorders and FOG. Although encouraging, the first results need to be confirmed by controlled studies involving larger series of patients. CONCLUSIONS: Overall, gait disorders remain a motor PD symptom that is little improved, or only temporarily, by current pharmacological and surgical treatments. Patient management is complex.
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Article dans une revue
Revue Neurologique, Elsevier Masson, 2010, 166 (2), pp.178-87. 〈10.1016/j.neurol.2009.07.018〉
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Contributeur : Marc Savasta <>
Soumis le : vendredi 30 septembre 2011 - 10:08:55
Dernière modification le : jeudi 1 février 2018 - 01:11:39

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Murielle Ferraye, Bettina Debû, Pierre Pollak. [Deep brain stimulation and gait disorders in Parkinson disease].. Revue Neurologique, Elsevier Masson, 2010, 166 (2), pp.178-87. 〈10.1016/j.neurol.2009.07.018〉. 〈inserm-00627987〉

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