Parkinsonism-related β oscillations in the primate basal ganglia networks – Recent advances and clinical implications. (February 2019)

• Record Type: Journal Article
• Authors: Deffains, Marc; Bergman, Hagai
• Is Part Of: Parkinsonism & related disorders. Volume 59(2019)
• Page Start: 2
• Page End: 8
• Publication Date: 2019-02
• Subjects: Basal ganglia -- Parkinson's disease -- Non-human primate -- MPTP -- Oscillations; BG basal ganglia -- DBS deep brain stimulation -- EEG electroencephalogram -- GPe external segment of the globus pallidus -- GPi internal segment of the globus pallidus -- LFP local field potential -- MPTP 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine -- MSN medium spiny neuron -- MUA multi-unit activity -- NHP non-human primate -- PD Parkinson's disease -- SNr substantia nigra pars reticulata -- STN subthalamic nucleus -- TAN tonically active neuron -- 6-OHDA 6-hydroxydopamine; Parkinson's disease -- Periodicals; Movement disorders -- Periodicals; Movement Disorders -- Periodicals; Nerve Degeneration -- Periodicals; Nervous System Diseases -- Periodicals; Parkinson Disease -- Periodicals; Tremor -- Periodicals; Parkinson, Maladie de -- Périodiques; Parkinson's disease; 616.833
• DOI: 10.1016/j.parkreldis.2018.12.015
• Languages: English
• ISSNs: 1353-8020

Abstract

Abstract: Today, the basal ganglia (BG) network can be viewed as a three-layer neural network in which the striatum and the subthalamic nucleus (STN) are the two BG input structures and together innervate BG downstream structures using GABA and glutamate, respectively. The striatum is larger than the STN and is the main site of dopamine depletion in Parkinson's disease (PD). However, STN is the prime target for deep brain stimulation (DBS) of patients with advanced PD. Traditionally, the efficacy of STN-DBS is attributed to the suppression of the pathological synchronous β oscillations along the cortico-thalamo BG network. In conventional DBS, stimulation is delivered continuously and equally influences normal and pathological neural activity. A DBS protocol would be therefore more effective if stimulation was only applied when necessary. We recently showed in the non-human primate model of PD that parkinsonism-related β oscillations resonate across the BG network through the STN, not the striatum. Moreover, we also demonstrated that BG β oscillations are episodic and albeit extended in parkinsonism also exists in the healthy condition. Thus, not all parkinsonian β oscillatory episodes are necessarily pathological. Remarkably, the duration of BG β episodes is more highly impacted than their magnitude in parkinsonism and may be more reliable metric - especially in STN - to discriminate between normal ("good") and pathological ("bad") β episodes. Thus, prolonged STN β episodes is suggested as one of the biomarkers of the pathological neuronal activity in parkinsonism that could be used as a trigger for adaptive DBS. Highlights: The striatum and the subthalamic nucleus (STN) are the basal ganglia (BG) inputs. Parkinsonism-related BG β oscillations resonate through the STN, not the striatum. BG β oscillations are episodic but not necessarily pathological. Episodic BG β oscillatory activity is more prevalent in parkinsonism. Longer STN β episodes are a biomarker of abnormal neuronal activity in parkinsonism.