Abstract

The sensorimotor cortex is a frequently targeted brain area for the development of Brain-Computer Interfaces (BCIs) for communication in people with severe paralysis and communication problems (locked-in syndrome; LIS). It is widely acknowledged that this area displays an increase in high-frequency band (HFB) power and a decrease in the power of the low frequency band (LFB) during movement of, for example, the hand. Upon termination of hand movement, activity in the LFB band typically shows a short increase (rebound). The ability to modulate the neural signal in the sensorimotor cortex by imagining or attempting to move is crucial for the implementation of sensorimotor BCI in people who are unable to execute movements. This may not always be self-evident, since the most common causes of LIS, amyotrophic lateral sclerosis (ALS) and brain stem stroke, are associated with significant damage to the brain, potentially affecting the generation of baseline neural activity in the sensorimotor cortex and the modulation thereof by imagined or attempted hand movement. In the Utrecht NeuroProsthesis (UNP) study, a participant with LIS caused by ALS and a participant with LIS due to brain stem stroke were implanted with a fully implantable BCI, including subdural electrocorticography (ECoG) electrodes over the sensorimotor area, with the purpose of achieving ECoG-BCI-based communication. We noted differences between these participants in the spectral power changes generated by attempted movement of the hand. To better understand the nature and origin of these differences, we compared the baseline spectral features and task-induced modulation of the neural signal of the LIS participants, with those of a group of able-bodied people with epilepsy who received a subchronic implant with ECoG electrodes for diagnostic purposes. Our data show that baseline LFB oscillatory components and changes generated in the LFB power of the sensorimotor cortex by (attempted) hand movement differ between participants, despite consistent HFB responses in this area. We conclude that the etiology of LIS may have significant effects on the LFB spectral components in the sensorimotor cortex, which is relevant for the development of communication-BCIs for this population.

Highlights

  • The sensorimotor areas of the brain are a promising target area for the control of Brain-Computer Interfaces (BCIs) that aim to provide people with severe paralysis a channel for communication and environmental control

  • For UNP1, these high-frequency band (HFB) responses were all accompanied by a consistent decrease in low frequency band (LFB) power during the active trials and LFB rebound responses immediately thereafter

  • We subsequently studied the consistency of the LFB and HFB response features

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Summary

Introduction

The sensorimotor areas of the brain are a promising target area for the control of Brain-Computer Interfaces (BCIs) that aim to provide people with severe paralysis (locked-in syndrome, LIS) a channel for communication and environmental control. The end of movement is typically associated with a short-lasting increase in beta power (eventrelated synchronization, ERS) (Pfurtscheller et al, 1996) These low-frequency band (LFB) EEG signal changes have been used to accomplish BCI control in able-bodied study participants (e.g., Wolpaw et al, 2000; Scherer et al, 2007; Blankertz et al, 2010; Thomas et al, 2013) as well as in several people with severe paralysis (e.g., Neuper et al, 2003; Kübler et al, 2005; Bai et al, 2010; Daly et al, 2013). HFB activity in the sensorimotor cortex is thought to be highly correlated to lower frequency bands, with the amplitude of HFB activity being coupled to the phase of LFB oscillations during rest (Yanagisawa et al, 2012)

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