Neuromuscular implants: Interfacing with skeletal muscle for improved clinical translation of prosthetic limbs.

After an amputation, advanced prosthetic limbs can be used to interface with the nervous system and restore motor function. Despite numerous breakthroughs in the field, many of the recent research advancements have not been widely integrated into clinical practice. This review highlights recent innovations in neuromuscular implants-specifically those that interface with skeletal muscle-which could improve the clinical translation of prosthetic technologies. Skeletal muscle provides a physiologic gateway to harness and amplify signals from the nervous system. Recent surgical advancements in muscle reinnervation surgeries leverage the "bio-amplification" capabilities of muscle, enabling more intuitive control over a greater number of degrees of freedom in prosthetic limbs than previously achieved. We anticipate that state-of-the-art implantable neuromuscular interfaces that integrate well with skeletal muscle and novel surgical interventions will provide a long-term solution for controlling advanced prostheses. Flexible electrodes are expected to play a crucial role in reducing foreign body responses and improving the longevity of the interface. Additionally, innovations in device miniaturization and ongoing exploration of shape memory polymers could simplify surgical procedures for implanting such interfaces. Once implanted, wireless strategies for powering and transferring data from the interface can eliminate bulky external wires, reduce infection risk, and enhance day-to-day usability. By outlining the current limitations of neuromuscular interfaces along with potential future directions, this review aims to guide continued research efforts and future collaborations between engineers and specialists in the field of neuromuscular and musculoskeletal medicine.

Smart Capsule For Targeted Detection Of Inflammation Levels Inside The Gi Tract.

Effective management of Inflammatory Bowel Disease (IBD) is contingent upon frequent monitoring of inflammation levels at targeted locations within the gastrointestinal (GI) tract. This is crucial for assessing disease progression and detecting potential relapses. To address this need, a novel single-use capsule technology has been devised that enables region-specific inflammation measurement, thereby facilitating repeatable monitoring within the GI tract. The capsule integrates a pH-responsive coating for location-specific activation, a chemiluminescent paper-based myeloperoxidase (MPO) sensor for inflammation detection, and a miniaturized photodetector, complemented by embedded electronics for real-time wireless data transmission. Demonstrating linear sensitivity within the physiological MPO concentration range, the sensor is capable of effectively identifying inflammation risk in the GI fluid. Luminescence emitted by the sensor, proportional to MPO concentration, is converted into an electrical signal by the photodetector, generating a quantifiable energy output with a sensitivity of 6.14 µJ/U.ml-1. The capsule was also tested with GI fluids collected from pig models simulating various inflammation states. Despite the physiological complexities, the capsule consistently activated in the intended region and accurately detected MPO levels with less than a 5% variation between readings in GI fluid and a PBS solution. This study heralds a significant step towards minimally invasive, in situ GI inflammation monitoring, potentially revolutionizing personalized IBD management and patient-specific therapeutic strategies.

Temporal interference current stimulation in peripheral nerves is not driven by envelope extraction.

Background. Electrical neuromodulation remains an effective therapy for multiple neurological disorders. One strategy to electrically stimulate nerves utilizes the interference of multiple high frequency waveforms. This technique, known as temporal interference stimulation or interferential current stimulation, has recently gained significant attention as a method to improve the state-of-the-art in neurostimulation in both animal studies and human clinical trials.Objective.Here we report our investigation into the fundamental properties of the neuronal response to these types of waveforms-the effects of carrier and envelope frequencies, thresholds, firing behavior, and phase and asymmetric interference patterns.Methods.We utilized a cuff electrode on the rat sciatic nerve to apply a variety of interferential signals. We recorded muscle activity in the plantar muscles and biceps femoris, which are proxies for activity on two of the major branches of the sciatic, which are spatially distinct in the target volume. We tested both fundamental recruitment properties as well as spatial techniques to selectively activate either muscle group.Results.Our data suggest, contrary to the currently accepted explanation, that neurons do not extract envelopes at all, and that the response to these signals is well explained by a resistor-capacitor (i.e. integrator) membrane with a fixed firing threshold. Basic interference techniques do not change recruitment far from electrodes. Techniques can produce regions of both phasic activation and tonic activation/conduction block.Conclusions.An integrator model suggests that interference techniques are less capable of minimally invasive stimulation for a subcortical brain target than previously thought. Human clinical trials using these techniques should reevaluate their methods. Interference stimulation allows significant target selectivity in a peripheral cuff electrode with targets near electrodes. These techniques can allow spatially distinct regions of phasic firing, tonic firing, conduction block, and no effect.

Carotid body stimulation as a potential intervention in sudden death in epilepsy.

OBJECTIVE: To investigate carotid body (CB) mechanisms related to sudden death during seizure. Ictal activation of oxygen-conserving reflexes (OCRs) can trigger fatal cardiorespiratory collapse in seizing rats, which presents like human sudden unexpected death in epilepsy (SUDEP). The CB is strongly implicated in OCR pathways; we hypothesize that modulating CB activity will provide insight into these mechanisms of death. METHODS: Long-Evans rats were anesthetized with urethane. Recordings included: electrocorticography, electrocardiography, respiration via nasal thermocouple, and blood pressure (BP). The mammalian diving reflex (MDR) was activated by cold water delivered through a nasal cannula. Reflex and stimulation trials were repeated up to 16 times (4 pre-intervention, 12 post-intervention) or until death. In some animals, one or both carotid bodies were denervated. In some animals, the CB was electrically stimulated, both with and without MDR. Seizures were induced with kainic acid (KA). RESULTS: Animals without seizure and with no CB modulation survived all reflexes. Non-seizing animals with CB denervation survived 7.1 ± 5.4 reflexes before death, and only 1 of 7 survived past the 12-trial threshold. Electrical CB stimulation without seizure and without reflex caused significant tachypnea and hypotension. Electrical CB stimulation with seizure and without reflex required higher amplitudes to replicate the physiological responses seen outside seizure. Seizing animals without CB intervention survived 3.2 ± 3.6 trials (per-reflex survival rate 42.0% ± 44.4%), and 0 of 7 survived past the 12-trial threshold. Seizing animals with electrical CB stimulation survived 10.5 ± 4.7 ictal trials (per-reflex survival rate 86.3% ± 35.0%), and 6 of 8 survived past the 12-trial threshold. SIGNIFICANCE: These results suggest that, during seizure, the ability of the CB to stimulate a restart of respiration is impaired. The CB and its afferents may be relevant to fatal ictal apnea and SUDEP in humans, and CB stimulation may be a relevant intervention technique in these deaths.

An ASIC System for Closed-Loop Blood Pressure Modulation Through Right Cervical Vagus Nerve Stimulation.

OBJECTIVE: Heart disease is the leading cause of death worldwide. Hypertension is an important precursor and the most common risk factor to heart failure. While some patients can control their high blood pressure with pharmaceuticals, many suffer from resistant hypertension, where antihypertensive medications do not achieve the desired outcome. Electrical stimulation is an emerging therapy to modulate blood pressure and integrating it with closed-loop feedback can improve blood pressure control. METHODS: We design and fabricate two application-specific integrated circuits (ASICs) for stimulation and pressure sensing using TSMC's 180 nm MS RF G process. We create a closed-loop system by integrating the ASICs with a microscale pressure sensor and a custom-built Python script and test the full system in six Long Evans rats using vagus nerve stimulation. RESULTS: After calibration and benchtop verification, we prove the functionality of the system in lowering, and maintaining a desired blood pressure in vivo. The system effectively monitors pressure and stimulates when that pressure exceeds the user-determined threshold. CONCLUSION: By combining this stimulation therapy with a pressure sensor, we present a novel closed-loop, electroceutical system that has the potential to monitor and modulate blood pressure. SIGNIFICANCE: We present a drug-free, potentially side-effect-free electroceutical therapeutic for managing resistant hypertension.

Clinical Study of the IOPTx™ System - an Electroceutical Wearable to Lower Intraocular Pressure.

Purpose: To investigate the safety and efficacy of the IOPTx™ system - a novel wearable, electroceutical treatment to lower intraocular pressure. Methods: Patients wear the customized contact lens and spectacles of the IOPTx™ system and undergo three 15-minute randomized stimulation trials at different stimulus amplitudes with 15 minutes of rest in between. The parameters for the stimulation trials include a frequency of 50 Hz, a pulse width of 100 µs, and current amplitudes between 90-150 µA. The optometrist measures the intraocular pressure (IOP) before, immediately after, and 15 minutes after the trial, and performs topography, a slit eye examination, and specular microscopy before and after the entire study to check the health of the eye and confirm the safety of the system. Results: The IOPTx™ system successfully modulates a patient's IOP. By testing various currents, we create individual tuning curves examining the effect of the stimulation amplitude on the change in IOP. Each patient may have an optimal dose-response curve and by normalizing to this value, the IOPTx™ system decreased IOP by an average of 17.7% with fifteen minutes of therapy. No Adverse Events or Adverse Device Effects occurred.Conclusions: The results of this clinical case series provide preliminary evidence of efficacy and safety of the IOPTx™ system and its potential usefulness to lower IOP in glaucoma and ocular hypertension.

Ictal activation of oxygen-conserving reflexes as a mechanism for sudden death in epilepsy.

OBJECTIVE: To test the hypothesis that death with physiological parallels to human cases of sudden unexpected death in epilepsy (SUDEP) can be induced in seizing rats by ictal activation of oxygen-conserving reflexes (OCRs). METHODS: Urethane-anesthetized female Long-Evans rats were implanted with electrodes for electrocardiography (ECG), electrocorticography (ECoG), and respiratory thermocouple; venous and arterial cannulas; and a laryngoscope guide and cannula or nasal cannula for activation of the laryngeal chemoreflex (LCR) or mammalian diving reflex (MDR), respectively. Kainic acid injection, either systemic or into the ventral hippocampus, induced prolonged acute seizures. RESULTS: Reflex challenges during seizures caused sudden death in 18 of 20 rats-all MDR rats (10) and all but two LCR rats (8) failed to recover from ictal activation of OCRs and died within minutes of the reflexes. By comparison, 4 of 4 control (ie, nonseizing) rats recovered from 64 induced diving reflexes (16 per rat), and 4 of 4 controls recovered from 64 induced chemoreflexes (16 per rat). Multiple measures were consistent with reports of human SUDEP. Terminal central apnea preceded terminal asystole in all cases. Heart and respiratory rate fluctuations that paralleled those seen in human SUDEP occurred during OCR-induced sudden death, and mean arterial pressure (MAP) was predictive of death, showing a 17 or 15 mm Hg drop (MDR and LCR, respectively) in the 20 s window centered on the time of brain death. OCR activation was never fatal in nonseizing rats. SIGNIFICANCE: These results present a method of inducing sudden death in two seizure models that show pathophysiology consistent with that observed in human cases of SUDEP. This proposed mechanism directly informs previous findings by our group and others in the field; provides a repeatable, inducible animal model for the study of sudden death; and offers a potential explanation for observations made in cases of human SUDEP.

Mechanisms and prevention of acid reflux induced laryngospasm in seizing rats.

OBJECTIVE: Recent animal work and limited clinical data have suggested that laryngospasm may be involved in the cardiorespiratory collapse seen in sudden unexpected death in epilepsy (SUDEP). In previous work, we demonstrated in an animal model of seizures that laryngospasm and sudden death were always preceded by acid reflux into the esophagus. Here, we expand on that work by testing several techniques to prevent the acid reflux or the subsequent laryngospasm. METHODS: In urethane anesthetized Long Evans rats, we used systemic kainic acid to acutely induce seizure activity. We recorded pH in the esophagus, respiration, electrocorticography activity, and measured the liquid volume in the stomach postmortem. We performed the following three interventions to attempt to prevent acid reflux or laryngospasm and gain insights into mechanisms: fasting animals for 12 h, severing the gastric nerve, and electrical stimulation of either the gastric nerve or the recurrent laryngeal nerve. RESULTS: Seizing animals had significantly more liquid in their stomach. Severing the gastric nerve and fasting animals significantly reduced stomach liquid volume, subsequent acid reflux, and sudden death. Laryngeal nerve stimulation can reverse laryngospasm on demand. Seizing animals are more susceptible to death from stomach acid-induced laryngospasm than nonseizing animals are to artificial acid-induced laryngospasm. SIGNIFICANCE: These results provide insight into the mechanism of acid production and sudden obstructive apnea in this model. These techniques may have clinical relevance if this model is shown to be similar to human SUDEP.

Brainstem activity, apnea, and death during seizures induced by intrahippocampal kainic acid in anaesthetized rats.

OBJECTIVE: To investigate how prolonged seizure activity affects cardiorespiratory function and activity of pre-Bötzinger complex, leading to sudden death. METHODS: Urethane-anesthetized female Long-Evans rats were implanted with nasal thermocouple; venous and arterial cannulae; and electrodes for electrocardiography (ECG) and hippocampal, cortical, and brainstem recording. Kainic acid injection into the ventral hippocampus induced status epilepticus. RESULTS: Seizures caused hypertension, tachycardia, and tachypnea punctuated by recurrent transient apneas. Salivation increased considerably: in 11 of 12 rats, liquid with alkaline pH consistent with saliva was expelled from the mouth. Most transient apneas were obstructive: nasal airflow ceased, while, in 83%, efforts to breathe persisted as continued rhythmic activity of respiratory pre-Bötzinger neurons, inspiratory electromyography (EMG), and excursions of the chest wall and abdomen. Blood pressure oscillated in time with respiratory efforts. This pattern also occurred in a minority of cases (16%) of incomplete apnea, but not in rare cases (1%) of transient central apneas. During transient obstructive apneas, the frequency of all inspiratory efforts decreased abruptly by ~30%, suggesting a resetting of the central respiratory rhythm generator. Twenty-two of thirty-one rats died, due either to obstructive apnea (12) or central apnea following progressive slowing of respiration (10). Most rats dying of central apnea had experienced several transient obstructive apneas. Negative DC field potential shifts of the brainstem followed the final breath, consistent with previous reports on spreading depolarization in mouse models. Timing suggests that the DC shift is a consequence rather than cause of respiratory collapse. Cardiac activity continued for tens of seconds. SIGNIFICANCE: Seizure activity in forebrain induces pronounced autonomic activation and disrupts activity in medullary respiratory centers, resulting in death from either obstructive or central apnea. These results directly inform mechanisms of death in status epilepticus, and indirectly provide clues to mechanisms of sudden unexpected death in epilepsy (SUDEP).

A Method of Flexible Micro-Wire Electrode Insertion in Rodent for Chronic Neural Recording and a Device for Electrode Insertion.

Reliable chronic neural recording from focal deep brain structures is impeded by insertion injury and foreign body response, the magnitude of which is correlated with the mechanical mismatch between the electrode and tissue. Thin and flexible electrodes cause less glial scarring and record longer than stiff electrodes. However, the insertion of flexible microelectrodes in brain has been a challenge. Here, a novel insertion method is proposed, and demonstrated, for precise targeting deep brain structures using flexible micro-wire electrodes. The microelectrode is spun and slowly inserted in brain through an appropriate electrode guide. The electrode guide does not penetrate into cortex. Based on two new mechanisms, namely spinning and guided insertion, we have demonstrated successful insertion of 25-micron platinum flexible electrodes about 10-mm deep in rat brains without buckling. We present an electrode insertion device based on the proposed method and demonstrate its use to implant flexible microelectrodes in rat brains. The step-by-step insertion process is described. Microelectrodes were inserted in the Bötzinger complex and respiratory neural activity was recorded acutely in nine rats and chronically in two rats for 50 days.

Characterization of plasma cytokine response to intraperitoneally administered LPS & subdiaphragmatic branch vagus nerve stimulation in rat model.

Vagus nerve stimulation (VNS) has been on the forefront of inflammatory disorder research and has yielded many promising results. Questions remain, however, about the biological mechanisms of such treatments and the inconsistencies in the methods used in research efforts. Here, we aimed to clarify the inflammatory response to intraperitoneal (IP) injections of lipopolysaccharide (LPS) in rats, while analyzing corresponding effects of electrical stimulation to subdiaphragmatic branches (anterior gastric, accessory celiac, and hepatic) of the left vagus nerve. We accomplished an in-depth characterization of the time-varying cytokine cascade response in the serum of 58 rats to an acute IP LPS challenge over a 330-minute period by utilizing curve-fitting and starting point-alignment methods. We then explored the post-LPS neuromodulation effects of electrically stimulating individually cuffed subdiaphragmatic branches. Through our analysis, we found there to be a consistent order of IP LPS cytokine response (IL-10, TNF-α, GM-CSF, IL-17F, IL-6, IL-22, INF-γ). Apart from IL-10, the IP cytokine cascade was more variable in starting time and occurred later than in previously recorded intravenous (IV) challenges. We also found distinct regulatory effects on multiple cytokine levels by each of the three subdiaphragmatic stimulation subsets. While the time-variability of IP LPS use in rats complicates its utility, we have shown it to be a practical, arguably more physiologically relevant method than IV in rats when our methods are used. More importantly, we have shown that selective subdiaphragmatic neurostimulation can be utilized to selectively induce specific effects on inflammation in the body.

Modulating the Inflammatory Reflex in Rats Using Low-Intensity Focused Ultrasound Stimulation of the Vagus Nerve.

Tumor necrosis factor α (TNF-α) is linked to several chronic inflammatory diseases. Electrical vagus nerve stimulation reduces serum TNF-α levels but may cause chronic nerve damage and requires surgery. Alternatively, we proposed focused ultrasound stimulation of the vagus nerve (uVNS), which can be applied non-invasively. In this study, we induced an inflammatory response in rats using lipopolysaccharides (LPS) and collected blood to analyze the effects of uVNS on cytokine concentrations. We applied one or three 5-min pulsed focused ultrasound stimulation treatments to the vagus nerve (250 kHz, ISPPA = 3 W/cm2). Animals receiving a single ultrasound application had an average reduction in TNF-α levels of 19%, similar to the 16% reduction observed in electrically stimulated animals. With multiple applications, uVNS therapy statistically reduced serum TNF-α levels by 73% compared with control animals without any observed damage to the nerve. These findings suggest that uVNS is a suitable way to attenuate TNF-α levels.

Acid reflux induced laryngospasm as a potential mechanism of sudden death in epilepsy.

OBJECTIVE: Recent research suggests that obstructive laryngospasm and consequent respiratory arrest may be a mechanism in sudden unexpected death in epilepsy. We sought to test a new hypothesis that this laryngospasm is caused by seizures driving reflux of stomach acid into the larynx, rather than spontaneous pathological activity in the recurrent laryngeal nerve. APPROACH: We used an acute kainic acid model under urethane anesthesia to observe seizure activity in Long-Evans rats. We measured the pH in the esophagus and respiratory activity. In a subset of experiments, we blocked acid movement up the esophagus with a balloon catheter. MAIN RESULTS: In all cases of sudden death, terminal apnea was preceded by a large pH drop from 7 to 2 in the esophagus. In several animals we observed acidic fluid exiting the mouth, sometimes in large quantities. In animals where acid movement was blocked, sudden deaths did not occur. No acid was detected in controls. SIGNIFICANCE: The results suggest that acid movement up the esophagus is a trigger for sudden death in KA induced seizures. The fact that blocking acid also eliminates sudden death implies causation. These results may provide insight to the mechanism of SUDEP in humans.

Wafer-recyclable, environment-friendly transfer printing for large-scale thin-film nanoelectronics.

Transfer printing of thin-film nanoelectronics from their fabrication wafer commonly requires chemical etching on the sacrifice of wafer but is also limited by defects with a low yield. Here, we introduce a wafer-recyclable, environment-friendly transfer printing process that enables the wafer-scale separation of high-performance thin-film nanoelectronics from their fabrication wafer in a defect-free manner that enables multiple reuses of the wafer. The interfacial delamination is enabled through a controllable cracking phenomenon in a water environment at room temperature. The physically liberated thin-film nanoelectronics can be then pasted onto arbitrary places of interest, thereby endowing the particular surface with desirable add-on electronic features. Systematic experimental, theoretical, and computational studies reveal the underlying mechanics mechanism and guide manufacturability for the transfer printing process in terms of scalability, controllability, and reproducibility.

Suppression of Urinary Voiding by Conditional High Frequency Stimulation of the Pelvic Nerve in Conscious Rats.

Female Wistar rats were instrumented to record bladder pressure and to stimulate the left pelvic nerve. Repeated voids were induced by continuous infusion of saline into the bladder (11.2 ml/h) via a T-piece in the line to the bladder catheter. In each animal tested (n = 6) high frequency pelvic nerve stimulation (1-3 kHz, 1-2 mA sinusoidal waveform for 60 s) applied within 2 s of the onset of a sharp rise in bladder pressure signaling an imminent void was able to inhibit micturition. Voiding was modulated in three ways: (1) Suppression of voiding (four rats, n = 13 trials). No fluid output or a very small volume of fluid expelled (<15% of the volume expected based on the mean of the previous 2 or 3 voids). Voiding suppressed for the entirety of the stimulation period (60 s) and resumed within 37 s of stopping stimulation. (2) Void deferred (four rats, n = 6 trials). The imminent void was suppressed (no fluid expelled) but a void occurred later in the stimulation period (12-44 s, mean 24.5 ± 5.2 s after the onset of the stimulation). (3) Reduction in voided volume (five rats, n = 20 trials). Voiding took place but the volume of fluid voided was 15-80% (range 21.8-77.8%, mean 45.3 ± 3.6%) of the volume expected from the mean of the preceding two or three voids. Spontaneous voiding resumed within 5 min of stopping stimulation. Stimulation during the filling phase in between voids had no effect. The experiments demonstrate that conditional high frequency stimulation of the pelvic nerve started at the onset of an imminent void can inhibit voiding. The effect was rapidly reversible and was not accompanied by any adverse behavioral side effects.

B fibers are the best predictors of cardiac activity during Vagus nerve stimulation: Qing, vagal B fiber activation and cardiac effects.

BACKGROUND: Vagus nerve stimulation (VNS) is a promising therapy for many neurologic and psychiatric conditions. However, determining stimulus parameters for individual patients is a major challenge. The traditional method of titrating stimulus intensity based on patient perception produces highly variable responses. This study explores using the vagal response to measure stimulation dose and predict physiological effect. Clinicians are investigating the use of VNS for heart failure management, and this work aims to correlate cardiac measures with vagal fiber activity. RESULTS: By recording vagal activity during VNS in rats and using regression analysis, we found that cardiac activity across all animals was best correlated to the activation of a specific vagal fiber group. With conduction velocities ranging from 5 to 10 m/s, these fibers are classified as B fibers (using the Erlanger-Gasser system) and correspond to vagal parasympathetic efferents. CONCLUSIONS: B fiber activation can serve as a standardized, objective measure of stimulus dose across all subjects. Tracking fiber activation provides a more systematic way to study the effects of VNS and in the future, may lead to a more consistent method of therapy delivery.

Chronic cuffing of cervical vagus nerve inhibits efferent fiber integrity in rat model.

OBJECTIVE: Numerous studies of vagal nerve stimulation (VNS) have been published showing it to be a potential treatment for chronic inflammation and other related diseases and disorders. Studies in recent years have shown that electrical stimulation of the vagal efferent fibers can artificially modulate cytokine levels and reduce systematic inflammation. Most VNS research in the treatment of inflammation have been acute studies on rodent subjects. Our study tested VNS on freely moving animals by stimulating and recording from the cervical vagus with nerve cuff electrodes over an extended period of time. APPROACH: We used methods of electrical stimulation, retrograde tracing (using Fluorogold) and post necropsy histological analysis of nerve tissue, flow cytometry to measure plasma cytokine levels, and MRI scanning of gastric emptying. This novel combination of methods allowed examination of physiological aspects of VNS previously unexplored. MAIN RESULTS: Through our study of 53 rat subjects, we found that chronically cuffing the left cervical vagus nerve suppressed efferent Fluorogold transport in 43 of 44 animals (36 showed complete suppression). Measured cytokine levels and gastric emptying rates concurrently showed nominal differences between chronically cuffed rats and those tested with similar acute methods. Meanwhile, results of electrophysiological and histological tests of the cuffed nerves revealed them to be otherwise healthy, consistent with previous literature. SIGNIFICANCE: We hypothesize that due to these unforeseen and unexplored physiological consequences of the chronically cuffed vagus nerve in a rat, that inflammatory modulation and other vagal effects by VNS may become unreliable in chronic studies. Given our findings, we submit that it would benefit the VNS community to re-examine methods used in previous literature to verify the efficacy of the rat model for chronic VNS studies.

Cavity Resonator Wireless Power Transfer System for Freely Moving Animal Experiments.

OBJECTIVE: The goal of this paper is to create a large wireless powering arena for powering small devices implanted in freely behaving rodents. METHODS: We design a cavity resonator based wireless power transfer (WPT) system and utilize our previously developed optimal impedance matching methodology to achieve effective WPT performance for operating sophisticated implantable devices, made with miniature receive coils (<8 mm in diameter), within a large volume (dimensions: 60.96 cm × 60.96 cm × 30 cm). We provide unique cavity design and construction methods which maintains electromagnetic performance of the cavity while promoting its utility as a large animal husbandry environment. In addition, we develop a biaxial receive resonator system to address device orientation insensitivity within the cavity environment. Functionality is demonstrated with chronic experiments involving rats implanted with our custom designed bioelectric recording device. RESULTS: We demonstrate an average powering fidelity of 93.53% over nine recording sessions across nine weeks, indicating nearly continuous device operation for a freely behaving rat within the large cavity resonator space. CONCLUSION: We have developed and demonstrated a cavity resonator based WPT system for long term experiments involving freely behaving small animals. SIGNIFICANCE: This cavity resonator based WPT system offers an effective and simple method for wirelessly powering miniaturized devices implanted in freely moving small animals within the largest space.

Enhancing the versatility of wireless biopotential acquisition for myoelectric prosthetic control.

OBJECTIVE: A significant challenge in rehabilitating upper-limb amputees with sophisticated, electric-powered prostheses is sourcing reliable and independent channels of motor control information sufficient to precisely direct multiple degrees of freedom simultaneously. APPROACH: In response to the expressed needs of clinicians, we have developed a miniature, batteryless recording device that utilizes emerging integrated circuit technology and optimal impedance matching for magnetic resonantly coupled (MRC) wireless power transfer to improve the performance and versatility of wireless electrode interfaces with muscle. MAIN RESULTS: In this work we describe the fabrication and performance of a fully wireless and batteryless EMG recording system and use of this system to direct virtual and electric-powered limbs in real-time. The advantage of using MRC to optimize power transfer to a network of wireless devices is exhibited by EMG collected from an array of eight devices placed circumferentially around a human subject's forearm. SIGNIFICANCE: This is a comprehensive, low-cost, and non-proprietary solution that provides unprecedented versatility of configuration to direct myoelectric prostheses without wired connections to the body. The amenability of MRC to varied coil geometries and arrangements has the potential to improve the efficiency and robustness of wireless power transfer links at all levels of upper-limb amputation. Additionally, the wireless recording device's programmable flash memory and selectable features will grant clinicians the unique ability to adapt and personalize the recording system's functional protocol for patient- or algorithm-specific needs.

Three-Dimensional Microcavity Array Electrodes for High-Capacitance All-Solid-State Flexible Microsupercapacitors.

We report novel three-dimensional (3D) microcavity array electrodes for high-capacitance all-solid-state microsupercapactiors. The microcavity arrays are formed in a polymer substrate via a plasma-assisted reactive ion etching (RIE) process and provide extra sidewall surface areas on which the active materials are grown in the form of nanofibers. This 3D structure leads to an increase in the areal capacitance by a factor of 2.56 for a 15-µm-deep cavity etching, agreeing well with the prediction. The fabricated microsupercapactiors exhibit a maximum areal capacitance of 65.1 mF cm(-2) (a volumetric capacitance of 93.0 F cm(-3)) and an energy density of 0.011 mWh cm(-2) (a volumetric energy density of 16.4 mWh cm(-3)) which substantially surpass previously reported values for all-solid-state flexible microsupercapacitors. The devices show good electrochemical stability under extended voltammetry cycles and bending cycles. It is demonstrated that they can sustain a radio frequency (rf) microsystem in a temporary absence of a power supply. These results suggest the potential utility of our 3D microsupercapactiors as miniaturized power sources in wearable and implantable medical devices.