Beta-triggered adaptive deep brain stimulation during reaching movement in Parkinson's disease.

Subthalamic nucleus (STN) beta-triggered adaptive deep brain stimulation (ADBS) has been shown to provide clinical improvement comparable to conventional continuous DBS (CDBS) with less energy delivered to the brain and less stimulation induced side effects. However, several questions remain unanswered. First, there is a normal physiological reduction of STN beta band power just prior to and during voluntary movement. ADBS systems will therefore reduce or cease stimulation during movement in people with Parkinson's disease and could therefore compromise motor performance compared to CDBS. Second, beta power was smoothed and estimated over a time period of 400 ms in most previous ADBS studies, but a shorter smoothing period could have the advantage of being more sensitive to changes in beta power, which could enhance motor performance. In this study, we addressed these two questions by evaluating the effectiveness of STN beta-triggered ADBS using a standard 400 ms and a shorter 200 ms smoothing window during reaching movements. Results from 13 people with Parkinson's disease showed that reducing the smoothing window for quantifying beta did lead to shortened beta burst durations by increasing the number of beta bursts shorter than 200 ms and more frequent switching on/off of the stimulator but had no behavioural effects. Both ADBS and CDBS improved motor performance to an equivalent extent compared to no DBS. Secondary analysis revealed that there were independent effects of a decrease in beta power and an increase in gamma power in predicting faster movement speed, while a decrease in beta event related desynchronization (ERD) predicted quicker movement initiation. CDBS suppressed both beta and gamma more than ADBS, whereas beta ERD was reduced to a similar level during CDBS and ADBS compared with no DBS, which together explained the achieved similar performance improvement in reaching movements during CDBS and ADBS. In addition, ADBS significantly improved tremor compared with no DBS but was not as effective as CDBS. These results suggest that STN beta-triggered ADBS is effective in improving motor performance during reaching movements in people with Parkinson's disease, and that shortening of the smoothing window does not result in any additional behavioural benefit. When developing ADBS systems for Parkinson's disease, it might not be necessary to track very fast beta dynamics; combining beta, gamma, and information from motor decoding might be more beneficial with additional biomarkers needed for optimal treatment of tremor.

Deep brain stimulation of the subthalamic nucleus in Parkinson disease 2013-2023: where are we a further 10 years on?

Deep brain stimulation has been in clinical use for 30 years and during that time it has changed markedly from a small-scale treatment employed by only a few highly specialized centers into a widespread keystone approach to the management of disorders such as Parkinson's disease. In the intervening decades, many of the broad principles of deep brain stimulation have remained unchanged, that of electrode insertion into stereotactically targeted brain nuclei, however the underlying technology and understanding around the approach have progressed markedly. Some of the most significant advances have taken place over the last decade with the advent of artificial intelligence, directional electrodes, stimulation/recording implantable pulse generators and the potential for remote programming among many other innovations. New therapeutic targets are being assessed for their potential benefits and a surge in the number of deep brain stimulation implantations has given birth to a flourishing scientific literature surrounding the pathophysiology of brain disorders such as Parkinson's disease. Here we outline the developments of the last decade and look to the future of deep brain stimulation to attempt to discern some of the most promising lines of inquiry in this fast-paced and rapidly evolving field.