Projections from basal ganglia to tegmentum: a subcortical route for explaining the pathophysiology of Parkinson's disease signs?

Functional changes in the organisation of neuronal circuitries are generall y used to explain parkinsonian motor symptoms and levodopa-induced dyskines ias. Based on information from histology and neurophysiological microrecord ings of specific basal ganglia nuclei, the most widely accepted scheme is b ased on a central loop which starts: in the cerebral cortex, makes multiple relays in the basal ganglia, and returns to the cerebral cortex. Transcran ial magnetic stimulation studies, however, reveal no significant difference s in the excitability of the motor cortex between normal subjects and patie nts with Parkinson's disease. Furthermore, electrophysiological and audiosp inal facilitation studies indicate that the activity of reticular nuclei is altered in Parkinson's disease. It therefore appears that a circuit with t he cortex as the only recipient of basal ganglia output is an oversimplific ation. This paper explores the relationships between various basal ganglia nuclei and proposes a subcortical pathway via which modifications in the ba sal ganglia may influence motor function.