TY - JOUR
T1 - Sensorimotor ECoG Signal Features for BCI Control
T2 - A Comparison Between People With Locked-In Syndrome and Able-Bodied Controls
AU - Freudenburg, Zachary V
AU - Branco, Mariana P
AU - Leinders, Sacha
AU - van der Vijgh, Benny H
AU - Pels, Elmar G M
AU - Denison, Timothy
AU - van den Berg, Leonard H
AU - Miller, Kai J
AU - Aarnoutse, Erik J
AU - Ramsey, Nick F
AU - Vansteensel, Mariska J
N1 - Funding Information:
We thank the participants for their participation in this research. Also, we thank the clinical staff at the Department of Neurology and Neurosurgery for their contribution to our research, Stavrina Devetzoglou-Toliou for their help with data analysis and Eric Wolters for their help with literature research. Funding. This study was funded by grants from the European Union (ERC-Adv 320708), the Van Wagenen Foundation, the Dutch Technology Foundation STW (grant 14906), and the National Institute On Deafness and Other Communication Disorders of the National Institutes of Health (U01DC016686). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Publisher Copyright:
© Copyright © 2019 Freudenburg, Branco, Leinders, Vijgh, Pels, Denison, Berg, Miller, Aarnoutse, Ramsey and Vansteensel.
PY - 2019/10/16
Y1 - 2019/10/16
N2 - 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.
AB - 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.
KW - amyotrophic lateral sclerosis
KW - brain stem stroke
KW - brain-computer interface
KW - electrocorticography
KW - high-frequency band
KW - implant
KW - low-frequency band
KW - sensorimotor cortex
UR - http://www.scopus.com/inward/record.url?scp=85074278763&partnerID=8YFLogxK
U2 - 10.3389/fnins.2019.01058
DO - 10.3389/fnins.2019.01058
M3 - Article
C2 - 31680806
SN - 1662-4548
VL - 13
JO - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
M1 - 1058
ER -