Abstract
Current intracortical probe technology is limited in clinical implementation due to the short functional lifetime of implanted devices. Devices often fail several months to years post-implantation, likely due to the chronic immune response characterized by glial scarring and neuronal dieback. It has been demonstrated that this neuroinflammatory response is influenced by the mechanical mismatch between stiff devices and the soft brain tissue, spurring interest in the use of softer polymer materials for probe encapsulation. Here, we demonstrate stable recordings and electrochemical properties obtained from fully encapsulated shape memory polymer (SMP) intracortical electrodes implanted in the rat motor cortex for 13 weeks. SMPs are a class of material that exhibit modulus changes when exposed to specific conditions. The formulation used in these devices softens by an order of magnitude after implantation compared to its dry, room-temperature modulus of ~2 GPa.
Highlights
Successful clinical application of brain-machine interfaces (BMIs) requires stable, chronic, selective recordings from task-associated neural networks
While several styles of intracortical microelectrode arrays (MEAs) are commercially available, they are limited in clinical implementation due to a relatively short functional lifetime, only recording distinguishable units in non-human primates for an average of 1-6 years post-implantation [7,8,9,10]
While there are various factors that contribute to MEA failure, findings suggest that the tissue response may be one component that contributes to the premature loss of stable neural recordings [11,12,13,14]
Summary
Successful clinical application of brain-machine interfaces (BMIs) requires stable, chronic, selective recordings from task-associated neural networks. Multichannel intracortical microelectrode arrays (MEAs) are able to record single units and local field potentials from adjacent neural tissue within the brain. The chronic foreign body response stems from the recruitment of activated support cells to the injury site, initiating signaling cascades that result in upregulated local production of inflammatory and neurotoxic cytokines [14,15]. This leads to the accumulation of glial cells around the implant (i.e., encapsulation) concurrent with local neuronal death [11,15,16,17,18], both of which are obstacles for reliable signal acquisition
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
