Abstract
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been used since the mid-1990s as a treatment for patients with Parkinson's disease, and more recently also in other conditions, such as dystonia or obsessive compulsive disorder. Non-invasive studies of cortical evoked potentials (EPs) that follow individual STN–DBS stimuli has provided us with insights about the conduction of the DBS pulses to the cortex. Such EPs have multiple components of different latencies, making it possible to distinguish short-latency and long-latency responses (3–8 ms and 18–25 ms latency, respectively). The available evidence indicates that these short- and long-latency EPs correspond to conduction from the STN stimulation site to the cortical recording location via anti- and orthodromic pathways, respectively. In this review we survey the literature from recording studies in human patients treated with STN–DBS for Parkinson's disease and other conditions, as well as recent animal studies (including our own) that have begun to elucidate details of the pathways, frequency dependencies, and other features of EPs. In addition, we comment on the possible clinical utility of this knowledge.
Highlights
High-frequency stimulation of subcortical brain targets, of the subthalamic nucleus (STN) is an effective clinical treatment for patients with advanced Parkinson’s disease
We review the literature on cortical evoked potentials (EPs) induced by STN–Deep brain stimulation (DBS), and supplement this material with some of our own primate recording studies
We found that only stimulation in the STN produced short-latency cortical EPs, while stimulation at either site produced long-latency EPs, suggesting that only STN stimulation, but not globus pallidus (GPi) stimulation, antidromically activated fibers related to the motor cortical recording site
Summary
Non-invasive studies of cortical evoked potentials (EPs) that follow individual STN–DBS stimuli has provided us with insights about the conduction of the DBS pulses to the cortex. Such EPs have multiple components of different latencies, making it possible to distinguish short-latency and long-latency responses (3–8 ms and 18–25 ms latency, respectively). In this review we survey the literature from recording studies in human patients treated with STN–DBS for Parkinson’s disease and other conditions, as well as recent animal studies (including our own) that have begun to elucidate details of the pathways, frequency dependencies, and other features of EPs. In addition, we comment on the possible clinical utility of this knowledge
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