PURPOSE: In order to develop retinal implants with a large number of electrodes, it is necessary to ensure that they do not cause damage to the neural tissue by the heat that the electrical circuits generate. Knowledge about the threshold of the amount of power that induces damage will assist in developing power budgets for retinal implants. METHODS: Heat-induced retinal damage was evaluated by measuring changes in the morphology of the resident immune cells, the microglia, which are the first cells to respond to retinal trauma. Microglial soma and arbor areas were assessed in rat retinal tissues in vitro to determine the effects of increasing temperatures, implant contact, and heating and implant contact combined. RESULTS: In response to increasing incubation temperatures (no implant), microglial somas enlarged and arbor areas retracted, indicative of retinal stress. Thermal damage thresholds, defined as a significant change in microglial morphology from that observed at the upper limit of normal body temperature, occurred at a temperature of 38.7 °C. Implant contact, induced when a passive implant was placed on the retina, also caused similar morphological alterations in microglia, indicating retinal damage. Heated-implant contact exacerbated the effects of temperature alone but still resulted in a thermal damage threshold of 38.7 °C, the same as with heating alone. CONCLUSIONS: Our conservative recommendations are that implanted retinal electronics keep power dissipations to less than 19 mW/mm(2) to stay below the microglial thermal damage threshold (2.1 °C) and to comply with international standards for implantable devices (2 °C).
PURPOSE: In order to develop retinal implants with a large number of electrodes, it is necessary to ensure that they do not cause damage to the neural tissue by the heat that the electrical circuits generate. Knowledge about the threshold of the amount of power that induces damage will assist in developing power budgets for retinal implants. METHODS: Heat-induced retinal damage was evaluated by measuring changes in the morphology of the resident immune cells, the microglia, which are the first cells to respond to retinal trauma. Microglial soma and arbor areas were assessed in rat retinal tissues in vitro to determine the effects of increasing temperatures, implant contact, and heating and implant contact combined. RESULTS: In response to increasing incubation temperatures (no implant), microglial somas enlarged and arbor areas retracted, indicative of retinal stress. Thermal damage thresholds, defined as a significant change in microglial morphology from that observed at the upper limit of normal body temperature, occurred at a temperature of 38.7 °C. Implant contact, induced when a passive implant was placed on the retina, also caused similar morphological alterations in microglia, indicating retinal damage. Heated-implant contact exacerbated the effects of temperature alone but still resulted in a thermal damage threshold of 38.7 °C, the same as with heating alone. CONCLUSIONS: Our conservative recommendations are that implanted retinal electronics keep power dissipations to less than 19 mW/mm(2) to stay below the microglial thermal damage threshold (2.1 °C) and to comply with international standards for implantable devices (2 °C).
Authors: Shawn K Kelly; William F Ellersick; Ashwati Krishnan; Patrick Doyle; Douglas B Shire; John L Wyatt; Joseph F Rizzo Journal: IEEE Biomed Circuits Syst Conf Date: 2014-10
Authors: Ursula Greferath; Kirstan A Vessey; Andrew I Jobling; Samuel A Mills; Bang V Bui; Zheng He; Nupur Nag; Hiroshi Ohtsu; Erica L Fletcher Journal: PLoS One Date: 2014-12-29 Impact factor: 3.240
Authors: Fahimeh Dehkhoda; Ahmed Soltan; Nikhil Ponon; Andrew Jackson; Anthony O'Neill; Patrick Degenaar Journal: J Neural Eng Date: 2018-04 Impact factor: 5.379