title: [Parkinson's disease and cortico-Basal Ganglia circuits].
abstract: Cortico-basal ganglia circuit model has been studied extensively after it was first proposed by Alexander and Crutcher in 1990. This model accurately predicted the hyperactivity of indirect pathway and subthalamic nucleus(STN) in the dopamine deficiency state of Parkinson's disease (PD), prompting the experimental approaches of lesioning STN in parkinsonian primates. Application of these successful experiences with STN lesions in the reversal of parkinsonian symptoms to human PD patients facilitates the development of STN deep brain stimulation (DBS), which has become one of the most important therapies for PD in recent years. Although the classical model of the cortico-basal ganglia circuits by Alexander and Crutcher has provided many important insights into the basal ganglia function, the functional role of cortico-subthalamic "hyperdirect" pathway in the circuits has been relatively neglected. The first part of this article summarizes recent development concerning the cortico-basal ganglia circuits, especially emphasizing the importance of the hyperdirect pathway. In the second part of this article, we would describe the analyses of gross corticobasal ganglia circuit electrophysiological findings, especially emphasizing the coherence between two oscillating signals. We would also discuss the correlation between these parameters and the motor dysfunction, and its pathophysiological implications in PD.
authors.affiliation: Department of Physiology, National Taiwan University College of Medicine, and Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Ming-Kai
authors.initials: MK
authors.lastname: Pan
authors.forename: Chun-Hwei
authors.initials: CH
authors.lastname: Tai
authors.forename: Chung-Chin
authors.initials: CC
authors.lastname: Kuo
mesh_terms: D001479:Basal Ganglia / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology*; D046690:Deep Brain Stimulation / Q000379:methods; D006801:Humans; D008954:Models, Biological; D009434:Neural Pathways / Q000473:pathology*; D010300:Parkinson Disease / Q000473:pathology* / Q000628:therapy; D020531:Subthalamic Nucleus / Q000502:physiology