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      Adaptive Deep Brain Stimulation for Movement Disorders: The Long Road to Clinical Therapy

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          Abstract

          Continuous high-frequency DBS is an established treatment for essential tremor and Parkinson’s disease. Current developments focus on trying to widen the therapeutic window of DBS. Adaptive DBS (aDBS), where stimulation is dynamically controlled by feedback from biomarkers of pathological brain circuit activity, is one such development. Relevant biomarkers may be central, such as local field potential activity, or peripheral, such as inertial tremor data. Moreover, stimulation may be directed by the amplitude or the phase (timing) of the biomarker signal. In this review, we evaluate existing aDBS studies as proof-of-principle, discuss their limitations, most of which stem from their acute nature, and propose what is needed to take aDBS into a chronic setting.

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          High-frequency stimulation of the subthalamic nucleus suppresses oscillatory beta activity in patients with Parkinson's disease in parallel with improvement in motor performance.

          Andrea Kühn, Florian C D Kempf, Christof Brücke … (2008)
          High-frequency stimulation (HFS) of the subthalamic nucleus (STN) is a well-established therapy for patients with severe Parkinson's disease (PD), but its mechanism of action is unclear. Exaggerated oscillatory synchronization in the beta (13-30 Hz) frequency band has been associated with bradykinesia in patients with PD. Accordingly, we tested the hypothesis that the clinical benefit exerted by STN HFS is accompanied by suppression of local beta activity. To this end, we explored the after effects of STN HFS on the oscillatory local field potential (LFP) activity recorded from the STN immediately after the cessation of HFS in 11 PD patients. Only patients that demonstrated a temporary persistence of clinical benefit after cessation of HFS were analyzed. STN HFS led to a significant reduction in STN LFP beta activity for 12 s after the end of stimulation and a decrease in motor cortical-STN coherence in the beta band over the same time period. The reduction in LFP beta activity correlated with the movement amplitude during a simple motor task, so that a smaller amount of beta activity was associated with better task performance. These features were absent when power in the 5-12 Hz frequency band was considered. Our findings suggest that HFS may act by modulating pathological patterns of synchronized oscillations, specifically by reduction of pathological beta activity in PD.
          Article 0 comments Cited 144 times – based on 0 reviews     Review now
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            Pathological synchronisation in the subthalamic nucleus of patients with Parkinson's disease relates to both bradykinesia and rigidity.

            Andrea A Kühn, Alexander Tsui, Tipu Aziz … (2009)
            Parkinson's disease (PD) is associated with exaggerated oscillatory synchrony in the basal ganglia at frequencies over 8-35 Hz. Studies have demonstrated a suppression of local field potential (LFP) activity in the subthalamic nucleus (STN) upon treatment with the dopamine prodrug, levodopa, with the degree of suppression of power in the 8-35 Hz band correlating with the improvement in combined measures of bradykinesia and rigidity. However, these studies do not explicitly address the question of what is more important in predicting clinical change - synchronisation of neuronal activity or the specific frequency within the 8-35 Hz band over which the latter occurs. In addition, they have not demonstrated a relationship between treatment-induced changes in synchronisation and changes in bradykinesia or rigidity on their own. To this end, we collected and analysed LFP and clinical data in 30 patients with PD. We found significant correlations between levodopa-induced power suppression and rigidity and bradykinesia, when these clinical features were considered separately, but only when power suppression profiles were re-aligned to the frequency of peak synchronisation. Under these circumstances correlations with rigidity persisted despite partialising out the effect of bradykinesia and vice versa. These data suggest that levodopa-induced improvements in both rigidity and bradykinesia scale with the degree of suppression of oscillatory power in the STN LFP, and that this is true irrespective of the frequency at which synchronisation occurs across a broad band from 8-35 Hz.
            Article 0 comments Cited 111 times – based on 0 reviews     Review now
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              Exaggerated phase-amplitude coupling in the primary motor cortex in Parkinson disease.

              C. de Hemptinne, E. S. Ryapolova-Webb, E Air … (2013)
              An important mechanism for large-scale interactions between cortical areas involves coupling between the phase and the amplitude of different brain rhythms. Could basal ganglia disease disrupt this mechanism? We answered this question by analysis of local field potentials recorded from the primary motor cortex (M1) arm area in patients undergoing neurosurgery. In Parkinson disease, coupling between β-phase (13-30 Hz) and γ-amplitude (50-200 Hz) in M1 is exaggerated compared with patients with craniocervical dystonia and humans without a movement disorder. Excessive coupling may be reduced by therapeutic subthalamic nucleus stimulation. Peaks in M1 γ-amplitude are coupled to, and precede, the subthalamic nucleus β-trough. The results prompt a model of the basal ganglia-cortical circuit in Parkinson disease incorporating phase-amplitude interactions and abnormal corticosubthalamic feedback and suggest that M1 local field potentials could be used as a control signal for automated programming of basal ganglia stimulators.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 8610688
                Journal ID (pubmed-jr-id): 5937
                Journal ID (nlm-ta): Mov Disord
                Journal ID (iso-abbrev): Mov. Disord.
                Title: Movement disorders : official journal of the Movement Disorder Society
                ISSN (Print): 0885-3185
                ISSN (Electronic): 1531-8257
                Publication date Nihms-submitted: 21 June 2017
                Publication date (Print): June 2017
                Publication date PMC-release: 23 June 2017
                Volume: 32
                Issue: 6
                Pages: 810-819
                Affiliations
                [1 ]Medical Research Council Brain Network Dynamics Unit at the University of Oxford, Oxford, UK
                [2 ]Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK
                [3 ]Department of Neurology, Bern University Hospital and University of Bern, Bern, Switzerland
                [4 ]Institute of Neurology, University College London, London, UK
                Author notes
                [* ] Corresponding author: Dr. Anders Christian Meidahl, Nuffield Department of Clinical Neurosciences, University of Oxford, Level 6, West Wing, John Radcliffe Hospital, OX3 9DU, UK; Anders.meidahl@ 123456ndcn.ox.ac.uk
                Article
                Manuscript ID: EMS73196
                DOI: 10.1002/mds.27022
                PMC ID: 5482397
                PubMed ID: 28597557
                SO-VID: 83c39758-c2f3-46e0-be10-ac4041da66bd
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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                Subject: Article

                ScienceOpen disciplines: Medicine
                Keywords: deep brain stimulation,parkinson’s disease,brain–computer interface,essential tremor,closed-loop
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                ScienceOpen disciplines: Medicine
                Keywords: deep brain stimulation, parkinson’s disease, brain–computer interface, essential tremor, closed-loop

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