If you are seeing this message, you may be experiencing temporary network problems. Please wait a few minutes and refresh the page. If the problem persists, you may wish to report it to your local Network Manager.
It is also possible that your web browser is not configured or not able to display style sheets. In this case, although the visual presentation will be degraded, the site should continue to be functional. We recommend using the latest version of Microsoft or Mozilla web browser to help minimise these problems.
Wiley InterScience | ||
![]() Journal of AnatomySee Also: Volume 196 Issue 4, Pages 519 - 525 Published Online: 13 Dec 2002 Journal compilation © 2009 Anatomical Society of Great Britain and Ireland Published on behalf of the Anatomical Society of Great Britain and Ireland
Abstract | Full Text: PDF (Size: 148K) | Related Articles | Citation Tracking Functional anatomy of movement disorders Copyright KEYWORDS Basal ganglia • Parkinson's disease • akinesia • dyskinesias ABSTRACTModels of basal ganglia function are described which encapsulate the principal pathophysiological mechanisms underlying parkinsonian akinesia on the one hand and abnormal involuntary movement disorders (dyskinesias) on the other. In Parkinson's disease, degeneration of the nigrostriatal dopamine system leads to overactivity of the 'indirect' striatopallidal projection to the lateral (external) segment of the globus pallidus. This causes inhibition of lateral pallidal neurons, which in turn project to the subthalamic nucleus. Disinhibition of the subthalamic nucleus leads to abnormal subthalamic overactivity and, as a consequence, overactivity of medial (internal) pallidal output neurons. Dyskinesias, such as are observed in Huntington's disease, levodopa-induced dyskinesia and ballism, share mechanistic features in common and are associated with decreased neuronal activity in both the subthalamic nucleus and the medial globus pallidus. Accepted: 19 October 1999; |