Model of basal ganglia dysfunction

This schematic drawing of the basal ganglia and their connections illustrates the main striato-fugal pathways. In Parkinson disease (PD), the indirect inhibitory pathway mediated via D2 striatal receptors is postulated to be overactive, whereas the direct inhibitory pathway mediated via D1 striatal receptors is underactive. As a result, the main pallidal-thalamic outflow pathway provides excessive inhibitory input to the thalamus, which causes suppression of thalamo-cortical-spinal pathway, manifested clinically by paucity and slowness of movement (bradykinesia). In contrast, altered function in the basal ganglia that occurs with hyperkinetic movement disorders presumably leads to disinhibition of the thalamo-cortical-striatal pathway, manifested clinically by abnormal involuntary movements such as chorea, hemiballism, tics (as seen in Tourette syndrome), and dystonia.