| Description |
Intracortical microelectrode arrays have incredible potential to help treat patients with CNS damage. Unfortunately, widespread clinical use of this technology is hindered due to the lack of reliability and longevity in chronicrecordings, for which a major mechanism is the host's foreign body response (FBR). It negatively affects the health and viability of adjacent tissue and eventually diminishes device performance. The FBR has been classically described by the expression of neuroinflammatory biomarkers including activated macrophages/microglia, astrogliosis, blood brain barrier disruption, and loss of neuronal cells and their processes. Improvements of recording microelectrode arrays have proceeded at a slow pace due to various factors. One primary reason is that the FBR is not well understood from a device design perspective. Another critical element is that most attempts to decrease the FBR have only been applied to single-shank devices intended for research applications. It is unknown whether the same approach(es) would benefit more clinically relevant, high-density, penetrating devices that have been cleared by the FDA. To address these shortfalls, this dissertation will build upon published studies and focus on: 1) Clarifying the role and developmental lineage of macrophages/microglia involved in the FBR to chronically implanted penetrating arrays; 2) Determining whether reducing the penetrating profile of a high density microelectrode array can reduce the FBR to devices chronically implanted in rat cortex; 3) Evaluating whether incorporating a soft, permeable base on a high density microelectrode array reduces the brain's FBR following a chronic indwelling period. Accomplishing these aims may provide further details about the FBR to CNS implants and develop biologically informed design strategies for advancement towards clinical translation. |
