TY - JOUR
T1 - The characteristics of pallidal low-frequency and beta bursts could help implementing adaptive brain stimulation in the parkinsonian and dystonic internal globus pallidus
AU - Piña-Fuentes, Dan
AU - van Zijl, Jonathan C.
AU - van Dijk, J. Marc C.
AU - Little, Simon
AU - Tinkhauser, Gerd
AU - Oterdoom, D. L. Marinus
AU - Tijssen, Marina A. J.
AU - Beudel, Martijn
PY - 2019
Y1 - 2019
N2 - Introduction: Adaptive deep brain stimulation (aDBS) has been applied in Parkinson's disease (PD), based on the presence of brief high-amplitude beta (13–35 Hz) oscillation bursts in the subthalamic nucleus (STN), which correlate with symptom severity. Analogously, average low-frequency (LF) oscillatory power (4–12 Hz) in the internal globus pallidus (GPi) correlates with dystonic symptoms and might be a suitable physiomarker for aDBS in dystonia. Characterization of pallidal bursts could facilitate the implementation of aDBS in the GPi of PD and dystonia patients. Objective and methods: We aimed to describe the bursting behaviour of LF and beta oscillations in a cohort of five GPi-DBS PD patients and compare their amplitude and length with those of a cohort of seven GPi-DBS dystonia, and six STN-DBS PD patients (n electrodes = 34). Furthermore, we used the information obtained to set up aDBS and test it in the GPi of both a dystonia and a PD patient (n = 2), using either LF (dystonia) or beta oscillations (PD) as feedback signals. Results: LF and beta oscillations in the dystonic and parkinsonian GPi occur as phasic, short-lived bursts, similarly to the parkinsonian STN. The amplitude profile of such bursts, however, differed significantly. Dystonia showed higher LF burst amplitudes, while PD presented higher beta burst amplitudes. Burst characteristics in the parkinsonian GPi and STN were similar. Furthermore, aDBS applied in the GPi was feasible and well tolerated in both diseases. Conclusion: Pallidal LF and beta burst amplitudes have different characteristics in PD and dystonia. The presence of increased burst amplitudes could be employed as feedback for GPi-aDBS.
AB - Introduction: Adaptive deep brain stimulation (aDBS) has been applied in Parkinson's disease (PD), based on the presence of brief high-amplitude beta (13–35 Hz) oscillation bursts in the subthalamic nucleus (STN), which correlate with symptom severity. Analogously, average low-frequency (LF) oscillatory power (4–12 Hz) in the internal globus pallidus (GPi) correlates with dystonic symptoms and might be a suitable physiomarker for aDBS in dystonia. Characterization of pallidal bursts could facilitate the implementation of aDBS in the GPi of PD and dystonia patients. Objective and methods: We aimed to describe the bursting behaviour of LF and beta oscillations in a cohort of five GPi-DBS PD patients and compare their amplitude and length with those of a cohort of seven GPi-DBS dystonia, and six STN-DBS PD patients (n electrodes = 34). Furthermore, we used the information obtained to set up aDBS and test it in the GPi of both a dystonia and a PD patient (n = 2), using either LF (dystonia) or beta oscillations (PD) as feedback signals. Results: LF and beta oscillations in the dystonic and parkinsonian GPi occur as phasic, short-lived bursts, similarly to the parkinsonian STN. The amplitude profile of such bursts, however, differed significantly. Dystonia showed higher LF burst amplitudes, while PD presented higher beta burst amplitudes. Burst characteristics in the parkinsonian GPi and STN were similar. Furthermore, aDBS applied in the GPi was feasible and well tolerated in both diseases. Conclusion: Pallidal LF and beta burst amplitudes have different characteristics in PD and dystonia. The presence of increased burst amplitudes could be employed as feedback for GPi-aDBS.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85053831652&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/30227227
U2 - https://doi.org/10.1016/j.nbd.2018.09.014
DO - https://doi.org/10.1016/j.nbd.2018.09.014
M3 - Article
C2 - 30227227
SN - 0969-9961
VL - 121
SP - 47
EP - 57
JO - Neurobiology of Disease
JF - Neurobiology of Disease
ER -