Deep Brain Stimulation of the Subthalamic Nucleus Enhances Emotional Processing in Parkinson Disease

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Abstract
THE PATHOLOGIC hallmark of Parkinson disease (PD) is the degeneration of dopaminergic cells within the substantia nigra and the subsequent dopamine depletion of the striatum. Studies in monkeys with experimental parkinsonism induced by 1-methyl-4-pheny-1,2,3,6-tetrahydropyridine could demonstrate that the striatal dopamine deficiency leads to abnormally high firing rates and altered neuronal discharge patterns of neurons in the internal globus pallidus and subthalamic nucleus (STN).1 It is assumed that the overactive internal globus pallidus, an output nucleus of the basal ganglia, causes akinesia and rigidity through excessive inhibition of thalamocortical and brainstem motor circuits. The internal globus pallidus is driven in this scheme by excitatory projections from a disinhibited STN.1 Administration of dopamine agonists alleviates motor symptoms of parkinsonism in parallel with a reduction of neuronal firing rates in the internal globus pallidus and STN.2-4 Inactivation of the STN or internal globus pallidus through lesioning or electrical high-frequency stimulation also reverses parkinsonian symptoms1,5-7 by restoring thalamocortical and brainstem motor activity downstream to the site of dopaminergic action.

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