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Current retinal prostheses (RPs) have not achieved useful vision restoration, as their resolution is limited by power dissipation and complexity of interconnect. This article presents an inductively powered wireless system on a chip (SoC) for an electrically controlled, optically addressed retinal prosthetic system. The SoC interfaces to a co-fabricated nanoengineered photosensitive electrode array using only two wires. To reduce the thermal dissipation near sensitive retinal tissue, the proposed design pushes voltage regulation and charge-balanced stimulation control off the implant via a duty-cycled wireless charge metering technique. A calibration technique compensating for power fluctuation caused by eye movement is also presented. Implemented in 180-nm CMOS and delivering up to $3~\mu \text{C}$ of charge at 20-nC resolution, the SoC achieves 73% RF-to-stimulation power efficiency.

Recent approaches toward a functional retinal prosthesis to restore vision in neurodegenerative patients have been limited by the number of pixels that can be individually stimulated. The conventional approach, shown in Fig. 18.1.1 (left), uses an external camera to capture video, whose information is then wirelessly delivered to a hermetic housing (typically a titanium can) for conversion to N distinct stimulation pulses fed transocularly to an $N -$ channel microelectrode array (MEA) placed epi- or subretinally. While this approach has proven long-term biocompatibility, translation to 1000s of channels with hermetic and durable transocular connections is not achievable with current technology, limiting existing designs to at most 256 channels, barely sufficient for 20/400 vision restoration [1] –[3]. Instead, recent work has suggested a full-CMOS solution, where an image sensor, stimulation circuits, and an MEA are integrated directly onto a single CMOS chip, thereby eliminating the interconnect challenge and providing a pathway to scalability [4], [5] (Fig. 18.1.1, middle). However, co-location of photoreceptors, amplifiers, and stimulation circuits imposes difficult fill-factor issues, while also significantly increasing heat dissipation near sensitive ocular and neural tissue due to the need to perform voltage regulation, amplification, and charge-balanced stimulation waveform generation (typical end-to-end efficiency of $\sim20$%) right next to the retina. Most importantly, since the CMOS chip must also include electrodes and yet be sufficiently thin to fit epi- or sub-retinally, current encapsulation methods rely on thin-film deposition to enable patterned electrode windows, which has unproven long-term hemiticity or biocompatibility when encapsulating CMOS which has known biological toxins (e.g., copper), limiting practical implementation.

Routine general anesthesia is considered to be safe in healthy individuals. However, pre-clinical studies in mice, rats, and monkeys have repeatedly demonstrated that exposure to anesthetic agents during early post-natal periods can lead to acute neurotoxicity. More concerning, later-life defects in cognition, assessed by behavioral assays for learning and memory, have been reported. Although the potential for anesthetics to damage the neonatal brain is well-documented, the clinical significance of the pre-clinical models in which damage is induced remains quite unclear. Here, we systematically evaluate critical physiological parameters in post-natal day 7 neonatal mice exposed to 1.5% isoflurane for 2-4 hours, the most common anesthesia induced neurotoxicity paradigm in this animal model. We find that 2 or more hours of anesthesia exposure results in dramatic respiratory and metabolic changes that may limit interpretation of this paradigm to the clinical situation. Our data indicate that neonatal mouse models of AIN are not necessarily appropriate representations of human exposures.

Background Almost one million prematurely born infants die annually from respiratory insufficiency, predominantly in countries with limited access to respiratory support for neonates. The primary hypothesis tested in the present study was that a modified device for bubble nasal continuous positive airway pressure (Bn-CPAP) would provide lower work of spontaneous breathing, estimated by esophageal pressure-rate products. Methods Infants born