Parkinsonism-related β oscillations in the primate basal ganglia networks – Recent advances and clinical implications

Deffains M(1), Bergman H(2).

Author information:
(1)Institute of Neurodegenerative Diseases – CNRS UMR 5293, University of
Bordeaux, Bordeaux, 33076, France.
(2)Department of Medical Neurobiology, Institute of Medical Research Israel –
Canada (IMRIC), The Hebrew University – Hadassah Medical School, Jerusalem,
91120, Israel; The Edmond and Lily Safra Center for Brain Sciences, The Hebrew
University, Jerusalem, 91904, Israel; Department of Neurosurgery, Hadassah
University Hospital, Jerusalem, 91120, Israel. Electronic address:
.

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.

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