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Dorsolateral prefrontal cortex-based control with an implanted brain-computer interface.

ABSTRACT: The objective of this study was to test the feasibility of using the dorsolateral prefrontal cortex as a signal source for brain-computer interface control in people with severe motor impairment. We implanted two individuals with locked-in syndrome with a chronic brain-computer interface designed to restore independent communication. The implanted system (Utrecht NeuroProsthesis) included electrode strips placed subdurally over the dorsolateral prefrontal cortex. In both participants, counting backwards activated the dorsolateral prefrontal cortex consistently over the course of 47 and 22 months, respectively. Moreover, both participants were able to use this signal to control a cursor in one dimension, with average accuracy scores of 78?±?9% (standard deviation) and 71?±?11% (chance level: 50%), respectively. Brain-computer interface control based on dorsolateral prefrontal cortex activity is feasible in people with locked-in syndrome and may become of relevance for those unable to use sensorimotor signals for control.

SUBMITTER: Leinders S

PROVIDER: S-EPMC7508852 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Dorsolateral prefrontal cortex-based control with an implanted brain-computer interface.

Leinders Sacha S Vansteensel Mariska J MJ Branco Mariana P MP Freudenburg Zac V ZV Pels Elmar G M EGM Van der Vijgh Benny B Van Zandvoort Martine J E MJE Ramsey Nicolas F NF Aarnoutse Erik J EJ

Scientific reports 20200922 1

The objective of this study was to test the feasibility of using the dorsolateral prefrontal cortex as a signal source for brain-computer interface control in people with severe motor impairment. We implanted two individuals with locked-in syndrome with a chronic brain-computer interface designed to restore independent communication. The implanted system (Utrecht NeuroProsthesis) included electrode strips placed subdurally over the dorsolateral prefrontal cortex. In both participants, counting b ...[more]

PMID: 32963279

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Project description:BackgroundMethamphetamine (MA), is an extremely addictive stimulant that adversely affects the central nervous system. Accumulating evidence indicates that molecular mechanisms such as oxidative stress, apoptosis, and autophagy are involved in the toxicity of MA. Considering experimental animal studies exhibiting MA-induced neurotoxicity, the relevance of these findings needs to be evidently elucidated in human MA users. It is generally assumed that multiple chemical substances released in the brain following MA-induced metabolic activation are primary factors underlying damage of neural cells. Hence, this study aimed to investigate the role of autophagy and apoptosis as well as oxidative stress in the brain of postmortem MA-induced toxicity.Materials and methodsIn this study, we determine the gene expression of autophagy and apoptosis, including BECN1, MAP1ALC3, CASP8, TP53, and BAX genes in ten healthy controls and ten chronic users of MA postmortem dorsolateral prefrontal cortex (DLPFC) by real-time polymerase chain reaction. Also, we applied immunohistochemistry in formalin-fixed and paraffin-embedded human brain samples to analyze brain-derived neurotrophic factor (BDNF). Also, spectrophotometry was performed to measure glutathione (GSH) content.ResultsThe expression level of apoptotic and autophagic genes (BECN1, MAP1ALC3, CASP8, TP53, and BAX) were significantly elevated, while GSH content and BDNF showed substantial reductions in DLPFC of chronic MA users. Discussion: Our data showed that MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. Also, MA induces multiple functional and structural perturbations in the brain, determining its toxicity and possibly contributing to neurotoxicity.DiscussionOur study showed BDNF-positive cells as well as GSH amount, displayed significant declines in DLPFC of MA user. MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. However, further investigations are needed to throw light on the cellular and molecular mechanisms that act in the various regions of the addicted brain, especially in DLPFC.

Project description:Brain-computer interfaces are being developed to restore movement for people living with paralysis due to injury or disease. Although the therapeutic potential is great, long-term stability of the interface is critical for widespread clinical implementation. While many factors can affect recording and stimulation performance including electrode material stability and host tissue reaction, these factors have not been investigated in human implants. In this clinical study, we sought to characterize the material integrity and biological tissue encapsulation via explant analysis in an effort to identify factors that influence electrophysiological performance. We examined a total of six Utah arrays explanted from two human participants involved in intracortical BCI studies. Two platinum (Pt) arrays were implanted for 980 days in one participant (P1) and two Pt and two iridium oxide (IrOx) arrays were implanted for 182 days in the second participant (P2). We observed that the recording quality followed a similar trend in all six arrays with an initial increase in peak-to-peak voltage during the first 30-40 days and gradual decline thereafter in P1. Using optical and two-photon microscopy we observed a higher degree of tissue encapsulation on both arrays implanted for longer durations in participant P1. We then used scanning electron microscopy and energy dispersive X-ray spectroscopy to assess material degradation. All measures of material degradation for the Pt arrays were found to be more prominent in the participant with a longer implantation time. Two IrOx arrays were subjected to brief survey stimulations, and one of these arrays showed loss of iridium from most of the stimulated sites. Recording performance appeared to be unaffected by this loss of iridium, suggesting that the adhesion of IrOx coating may have been compromised by the stimulation, but the metal layer did not detach until or after array removal. In summary, both tissue encapsulation and material degradation were more pronounced in the arrays that were implanted for a longer duration. Additionally, these arrays also had lower signal amplitude and impedance. New biomaterial strategies that minimize fibrotic encapsulation and enhance material stability should be developed to achieve high quality recording and stimulation for longer implantation periods.

Dataset Information

Dorsolateral prefrontal cortex-based control with an implanted brain-computer interface.

Publications

Dorsolateral prefrontal cortex-based control with an implanted brain-computer interface.

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