In the late 1980's, a model was developed which proposed a framework for the anatomical organization of the basal ganglia, and provided consistent explanations for the clinical syndromes of Parkinson's disease. Some basic knowledge of the anatomical and functional organization of the basal ganglia will help understand the neurological basis of the gait disorders manifested in Parkinson's disease. In addition, because of their close anatomical and functional association with the striatum and pallidum, the substantia nigra and the subthalamic nucleus are now considered an integral part of the basal ganglia. The term extrapyramidal underscores this distinction and calls attention to a set of neurological illnesses caused by lesions that affect the basal ganglia. The striatum receives somatotopic cortical input from the frontal, sensory, motor, and parietotemporal-occipital association areas.
Corticostriatal afferents release the excitatory amino acid glutamate.
The influence of the basal ganglia circuits on the cortical motor areas is completed by means of the excitatory pathway from the thalamus to precentral cortex. Activation of the direct pathway results in net excitation of the thalamocortical circuits and facilitation of cortically initiated movements. Activation of the indirect pathway increases excitatory drive to the STN and the basal ganglia output nuclei, resulting in inhibition of the thalamocortical circuit. The influence of dopamine-containing nigrostriatal afferents is to enhance transmission through the direct pathway and suppress transmission through the indirect pathway. The net effect of dopamine, then, is to enhance positive feedback to the cortical motor areas and facilitate volitional movements.