Bernstein Seminar "Pathological oscillatory activity in Parkinson’s and Tremor; what does it mean and how should we treat it?"

February 23, 2021

Freiburg (Visio) (Germany)



The Medical Research Council | Brain Network Dynamics Unit | University of Oxford | UK


For decades we have had cardiac pacemakers that adjust their pacing according to demand and yet therapeutic adaptive stimulation approaches for the central nervous system are still not clinically available. Instead, to treat patients with advanced Parkinson’s disease or Essential Tremor we stimulate the basal ganglia or thalamus with fixed regimes, unvarying in frequency or intensity. Although effective, this comes with side-effects and in terms of sophistication this treatment approach could be compared to having an air-conditioning system on all the time, regardless of temperature. This talk will describe recent steps being taken to define the underlying circuit dysfunction in Parkinson’s and tremor and to improve deep brain stimulation by controlling its delivery according to the state of pathological activity.

Evidence is growing that motor symptoms in Parkinson’s disease and Essential Tremor are due, at least in part, to excessive synchronisation between oscillating neurons. Some degree of transient synchronisation is believed to be beneficial during neural processing by way of improving signal to noise ratios. However, excessive synchronisation, even if transient, reduces the information coding capacity of the system, impairing processing. Recordings in patients with Parkinson’s disease confirm bursts of oscillatory synchronisation in the basal ganglia centred around 20 Hz. The bursts of 20 Hz activity are prolonged in patients withdrawn from their usual medication and the dominance of these long duration bursts negatively correlates with motor impairment. Longer bursts attain higher amplitudes, indicative of more pervasive oscillatory synchronisation within the neural circuit. In contrast, in heathy primates and in treated Parkinson’s disease bursts tend to be short. Accordingly, it might be best to use closed-loop controlled deep brain stimulation to selectively terminate longer, bigger, pathological beta bursts to both save power and to spare the ability of underlying neural circuits to engage in more physiological processing between long bursts. It is now possible to record and characterise bursts on-line during stimulation of the same site and trial adaptive stimulation. Thus far, this has demonstrated improvements in efficiency and side-effects over conventional continuous stimulation,with at least as good symptom control in Parkinsonian patients.

But the presence of abnormal oscillatory synchrony in neural circuits in Parkinson’s and tremor also suggests an alternative strategy for stimulation; phase-locked stimulation to drive oscillations down. This approach has been pioneered in tremor and is now also being explored for the treatment of Parkinson’s disease.

Hosted by Ad Aertsen


Full list of BCF seminars: here



Feb 23, 2021
from05:15 PM to06:00 PM

Zoom Meeting. You can contact Fiona Siegfried for meeting ID and password.

Contact: here