Basal ganglia dysfunction is implicated in movement disorders including Parkinson Disease, dystonia, and choreiform disorders. Contradicting standard "rate models" of basal ganglia-thalamic interactions, internal pallidotomy improves both hypo- and hyper-kinetic movement disorders. This "paradox of stereotaxic surgery" was recognized shortly after rate models were developed, and is underscored by the outcomes of deep brain stimulation (DBS) for movement disorders. Despite strong evidence that DBS activates local axons, the clinical effects of lesions and DBS are nearly identical. These observations argue against standard models in which GABAergic basal ganglia output gates thalamic activity, and raise the question of how lesions and stimulation can have similar effects. These paradoxes may be resolved by considering thalamocortical loops as primary drivers of motor output. Rather than suppressing or releasing cortex via motor thalamus, the basal ganglia may modulate the timing of thalamic perturbations to cortical activity. Motor cortex exhibits rotational dynamics during movement, allowing the same thalamocortical perturbation to affect motor output differently depending on its timing with respect to the rotational cycle. We review classic and recent studies of basal ganglia, thalamic, and cortical physiology to propose a revised model of basal ganglia-thalamocortical function with implications for basic physiology and neuromodulation.
Keywords: Parkinson disease; deep brain stimulation (DBS); local field potential (LFP); rate model; thalamus.
Copyright © 2021 Magnusson and Leventhal.