Forrest, A. M. | bioRxiv Science

bioRxiv2025

Finite element model predicts micromotion-induced strain profiles that correlate with the functional performance of Utah arrays in humans and non-human primates

ObjectiveUtah arrays are widely used in both humans and non-human primates (NHPs) for intracortical brain-computer interfaces (BCIs), primarily for detecting electrical signals from cortical tissue to decode motor commands. Recently, these arrays have also been applied to deliver electrical stimulation aimed at restoring sensory functions. A key challenge limiting their longevity is the micromotion between the array and cortical tissue, which may induce mechanical strain in surrounding tissue and contribute to performance decline. This strain, due to mechanical mismatch, can exacerbate glial scarring around the implant, reducing the efficacy of Utah arrays in recording neuronal activity and delivering electrical stimulation. ApproachTo investigate this, we employed a finite element model (FEM) to predict tissue strains resulting from micromotion. Main ResultsOur findings indicated that strain profiles around edge and corner electrodes were greater than those around interior shanks, affecting both maximum and average strains within 50 {micro}m of the electrode tip. We then correlated these predicted tissue strains with in-vivo electrode performance metrics. We found negative correlations between 1 kHz impedance and tissue strains in human motor arrays and NHP area V4 arrays at 1-mo, 1-yr, and 2-yrs post-implantation. In human motor arrays, the peak-to-peak waveform voltage (PTPV) and signal-to-noise ratio (SNR) of spontaneous activity were also negatively correlated with strain. Conversely, we observed a positive correlation between the evoked SNR of multi-unit activity and strain in NHP area V4 arrays. SignificanceThis study establishes a spatial dependence of electrode performance in Utah arrays that correlates with tissue strain.

neuroscience↗

bioRxiv2024

Dynamic changes in structure and function of brain mural cells around chronically implanted microelectrodes

1.0Integration of neural interfaces with minimal tissue disruption in the brain is ideal to develop robust tools that can address essential neuroscience questions and combat neurological disorders. However, implantation of intracortical devices provokes severe tissue inflammation within the brain, which requires a high metabolic demand to support a complex series of cellular events mediating tissue degeneration and wound healing. Pericytes, peri-vascular cells involved in blood-brain barrier maintenance, vascular permeability, waste clearance, and angiogenesis, have recently been implicated as potential perpetuators of neurodegeneration in brain injury and disease. While the intimate relationship between pericytes and the cortical microvasculature have been explored in other disease states, their behavior following microelectrode implantation, which is responsible for direct blood vessel disruption and dysfunction, is currently unknown. Using two-photon microscopy we observed dynamic changes in the structure and function of pericytes during implantation of a microelectrode array over a 4-week implantation period. Pericytes respond to electrode insertion through transient increases in intracellular calcium and underlying constriction of capillary vessels. Within days following the initial insertion, we observed an influx of new, proliferating pericytes which contribute to new blood vessel formation. Additionally, we discovered a potentially novel population of reactive immune cells in close proximity to the electrode-tissue interface actively engaging in encapsulation of the microelectrode array. Finally, we determined that intracellular pericyte calcium can be modulated by intracortical microstimulation in an amplitude- and frequency-dependent manner. This study provides a new perspective on the complex biological sequelae occurring the electrode-tissue interface and will foster new avenues of potential research consideration and lead to development of more advanced therapeutic interventions towards improving the biocompatibility of neural electrode technology.

bioengineering↗