Neurofeedback for Parkinson Disease

---

BETAPARK – Beta-based neurofeedback training procedures to reduce motor symptoms in Parkinson disease

Abstract

Parkinson’s disease (PD) is a complex neurodegenerative disease caused by death of midbrain dopaminergic neurons. It is primarily characterized by motor symptoms (tremor, rigidity, and akinesia) that worsen over time. Treatments include dopamine replacement therapy and deep brain stimulation (DBS) of the subthalamic nucleus (STN) in the basal ganglia (BG). However, each has drawbacks, with pharmacological treatments eventually causing disabling motor complications and losing efficacy in most patients (Obeso et al., 2000), and STN-DBS being an invasive, expensive procedure applicable to only a subset of patients (Benabid et al., 2009; Charles et al., 2002). This calls for better understanding the pathophysiology of PD in order to pave the way to new non-pharmacological and non-invasive treatment options for PD. Abnormal oscillatory brain activity is associated with a range of neurological and psychiatric disorders (Fries 2015; Voytek and Knight 2015). In PD, abnormal activity has been observed in the 13-35 Hz frequency range or so-called beta band, extending into the lower alpha band (8-12 Hz) frequency range (Alonso-Frech et al., 2006; Brown, 2006), thus leading to an enlarged definition of pathological beta as elevated [8-35Hz] activity (Hammond et al. 2007). This activity has been primarily observed in subcortical structures of the BG, including the STN (e.g., Weinberger et al., 2006), but it extends  throughout the BG-cortex network (Eusebio and Brown 2009; Silberstein et al., 2005) and cortical activity appears to lead BG activity in the beta band (Fogelson et al., 2006; Litvak et al. 2011). This suggests that modifying cortical activity in this frequency band may be an entry point for intervening in the BG-cortex network. We propose to use neurofeedback (NF) to test whether PD patients can learn to self-regulate their brain activity to reduce pathological neural activity and thereby motor symptoms.We will leverage NF to target regulation of pathological beta band (8-35 Hz) oscillations, and we will characterize training-induced changes in cortical network activity and their relationship with symptom severity. Our goal is to provide direct evidence of the functional role of beta rhythms in the pathophysiology of PD while assessing NF as a new non-pharmacological and non-invasive tool for ameliorating PD motor symptoms.

First steps: Designing an optimal NF training procedure

The first work-package of this project will be dedicated to the design and evaluation (on healthy controls) of a reliable NF protocol aimed at maximizing learning of beta regulation in PD patients. This protocol will then be used in the clinical study. We will work on all the aspects of the training procedure, i.e., on the training tasks, on the instructions, on the training environment and on the feedback. To do so, I am looking for a post-doc (24 month contract), ideally with experience in the design and implementation of BCI training procedures and knowledge in learning theories.

The team

– Nathalie George (project leader), Ph.D., CNRS Research Director, ICM Paris
– Brian Lau, Ph.D., CNRS Research Scientist, ICM Paris
– Fabrizio de Vico Fallani, Ph.D., Inria Research Director, Inria Paris
– Mario Chavez, Ph.D., CNRS Research Scientist, ICM Paris
– Carine KARACHI, M.D. Ph.D., Neurosurgeon and Pr., ICM Paris
– Marie-Laure WELTER, M.D., Ph.D., Neurologist and Pr., ICM Paris