Pathological synchronization in Parkinson's disease: networks, models and treatments

被引:1202
作者
Hammond, Constance
Bergman, Hagai
Brown, Peter
机构
[1] Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1N 3BG, England
[2] Univ Bordeaux 2, CNRS, UMR 5543, F-33076 Bordeaux, France
[3] Univ Aix Marseille 2, INSERM, U29, Inst Neurobiol Mediterranee, F-13284 Marseille 07, France
[4] Hebrew Univ Jerusalem, Dept Physiol, Eric Roland Ctr Neurodegenerat Dis, Hadassah Med Sch, IL-91120 Jerusalem, Israel
[5] Hebrew Univ Jerusalem, Ctr Neural Computat, Hadassah Med Sch, IL-91120 Jerusalem, Israel
基金
英国医学研究理事会;
关键词
D O I
10.1016/j.tins.2007.05.004
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Parkinson's disease is a common and disabling disorder of movement owing to dopaminergic denervation of the striatum. However, it is still unclear how this denervation perverts normal functioning to cause slowing of voluntary movements. Recent work using tissue slice preparations, animal models and in humans with Parkinson's disease has demonstrated abnormally synchronized oscillatory activity at multiple levels of the basal ganglia-cortical loop. This excessive synchronization correlates with motor deficit, and its suppression by dopaminergic therapies, ablative surgery or deep-brain stimulation might provide the basic mechanism whereby diverse therapeutic strategies ameliorate motor impairment in patients with Parkinson's disease. This review is part of the INMED/TINS special issue, Physiogenic and pathogenic oscillations: the beauty and the beast, based on presentations at the annual INMED/ TINS symposium (http://inmednet.com/).
引用
收藏
页码:357 / 364
页数:8
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