[Functional anatomy of the basal ganglia]

The cerebral cortex of mammals is massively interconnected with the basal ganglia. The manner in which the basal ganglia process information has been accepted since it was described in the 1980s. It is not a definitive model and many aspects of it still need clarification.

The corpus striatum (ST) forms the entrance to the basal ganglia circuit (BG) and receives numerous afferent fibres from the cerebral cortex. Similarly, the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNpr) form the main nuclei for exit from the circuit and have an inhibitory effect on the pre-motor neurones of the ventral lamina of the thalamus. Between the entrance nucleus and the exit structures are two parallel systems of projection known as the direct and indirect pathways. The direct pathway projects monosynaptically only on the Gpi/SNpr complex. The indirect pathway projects polysynaptically on to the GR/SNpr complex after passing through the external segment of the globus pallidus (Gpe) and subthalamic nucleus. Imbalance in the activity of these two circuits will lead to alterations in discharge from the Gpi/SNpr complex which will cause bradykinesia or hyperkinesia. The bradykinesia or akinesia would be caused by increased gabaergic inhibition of the thalamic premotor neurones as a result of excessive discharge of the Gpi/SNpr complex.

Current exploration of the electrophysiology of the basal ganglia and careful analysis of the clinical findings in lesions circumscribed to certain parts of the thalamus, subthalamus and internal globus pallidus in patients with Parkinson's disease, have led to the appearance of paradoxical effects, according to the current basal ganglia model.