Background: Neurogenic detrusor overactivity (NDO) often results in decreased bladder capacity, urinary incontinence, and vesico-ureteral reflux. NDO can trigger autonomic dysreflexia and can impair quality of life. Electrical stimulation of the genital nerves (GNS) acutely inhibits reflex bladder contractions and can increase bladder capacity. Quantifying the effect of GNS on bladder capacity and determining what study factors and subject factors influence bladder capacity improvements will inform the design of clinical GNS interventions. Methods: We measured bladder capacity in 33 individuals with NDO, with and without GNS. These data were combined with data from seven previous GNS studies (n=64 subjects). A meta-analysis of the increase in bladder capacity and potential experimental factors was conducted (n=97 subjects total). Results: Bladder capacity increased 131±101 ml with GNS across subjects in all studies. The number of individuals whose bladder capacity was greater than 300 ml increased from 24% to 62% with GNS. Stimulus amplitude was a significant factor predicting bladder capacity gain. The variance of the bladder capacity gain significantly increased with increasing infusion rate. Other factors did not contribute to bladder capacity gain. Conclusion: GNS acutely increases bladder capacity in individuals with NDO. The consistent increase in magnitude of bladder capacities across the eight studies, and the lack of dependence on individual-specific factors, provide confidence that GNS could be an effective tool for many individuals with NDO. Studies of the chronic effect of GNS on bladder control, with clinical measures such as urinary continence, are needed.

Objective . Recent advances in neural engineering have restored mobility to people with paralysis, relieved symptoms of movement disorders, reduced chronic pain, restored the sense of hearing, and provided sensory perception to individuals with sensory deficits. Approach . This progress was enabled by the team-based, interdisciplinary approaches used by neural engineers. Neural engineers have advanced clinical frontiers by leveraging tools and discoveries in quantitative and biological sciences and through collaborations between engineering, science, and medicine. The movement toward bioelectronic medicines, where neuromodulation aims to supplement or replace pharmaceuticals to treat chronic medical conditions such as high blood pressure, diabetes and psychiatric disorders is a prime example of a new frontier made possible by neural engineering. Although one of the major goals in neural engineering is to develop technology for clinical applications, this technology may also offer unique opportunities to gain insight into how biological systems operate. Main results . Despite significant technological progress, a number of ethical and strategic questions remain unexplored. Addressing these questions will accelerate technology development to address unmet needs. The future of these devices extends far beyond treatment of neurological impairments, including potential human augmentation applications. Our task, as neural engineers, is to push technology forward at the intersection of disciplines, while responsibly considering the readiness to transition this technology outside of the laboratory to consumer products. Significance . This article aims to highlight the current state of the neural engineering field, its links with other engineering and science disciplines, and the challenges and opportunities ahead. The goal of this article is to foster new ideas for innovative applications in neurotechnology.

Continuous monitoring of bladder activity during normal daily activities would improve clinical diagnostics and understanding of the mechanisms underlying bladder function, or help validate how differing neuromodulation strategies affect the bladder. This work describes a urological monitor of conscious activity (UroMOCA). The UroMOCA included a pressure sensor, urine impedance-sensing electrodes, and wireless battery recharge and data transmission circuitry. Components were assembled on a circuit board and encapsulated with an epoxy/silicone molded package that allowed Pt-Ir electrode feedthrough for urine contact. Packaged UroMOCAs measured $12\times 18\times6$ mm. UroMOCAs continuously transmitted data from all onboard sensors at 10 Hz at a 30 cm range, and ran for up to 44 h between wireless recharges. After in vitro calibration, implantations were performed in 11 animals. Animals carried the device for 28 days, enabling many observations of bladder behavior during natural, conscious behavior. In vivo testing confirmed the UroMOCA did not impact bladder function after a two-week healing period. Pressure data in vivo were highly correlated with a reference catheter used during an anesthetized follow-up. Static volume sensor data were less accurate, but demonstrated reliable detection of bladder volume decreases, and distinguished between voiding and non-voiding bladder events.

Individuals with spinal cord injury (SCI) usually develop neurogenic detrusor overactivity (NDO), resulting in bladder urgency and incontinence, and reduced quality of life. Electrical stimulation of the genital nerves (GNS) can inhibit uncontrolled bladder contractions in individuals with SCI. An automated closed-loop bladder neuromodulation system currently does not exist but could improve this approach. We have developed a custom algorithm to identify bladder contractions and trigger stimulation from bladder pressure data without need for abdominal pressure measurement. The goal of this pilot study was to test the feasibility of automated closed-loop GNS using our custom algorithm to identify and inhibit reflex bladder contractions in real time. Experiments were conducted in a single session in a urodynamics laboratory in four individuals with SCI and NDO. Each participant completed standard cystometrograms without and with GNS. Our custom algorithm monitored bladder vesical pressure and controlled when GNS was turned on and off. The custom algorithm detected bladder contractions in real time, successfully inhibiting a total of 56 contractions across all four subjects. There were eight false positives, six of those occurring in one subject. It took approximately 4.0 ± 2.6 s for the algorithm to detect the onset of a bladder contraction and trigger stimulation. The algorithm maintained stimulation for approximately 3.5 ± 1.7 s, which was enough to inhibit activity and relieve feelings of urgency. Automated closed-loop stimulation was well-tolerated and subjects reported that algorithm decisions generally matched with their perceptions of bladder activity. The custom algorithm automatically, successfully identified bladder contractions to trigger stimulation to inhibit bladder contractions acutely. Closed-loop neuromodulation using our custom algorithm is feasible, but further testing is needed refine this approach for use in a home environment.