Models 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.