Between 1996 and 2009 the annual number of emergency department (ED) visits in the United States increased by 51 percent while the number of EDs nationwide decreased by 6 percent, which placed unprecedented strain on the nation's EDs. To investigate the effects of an ED's closing on surrounding communities, we identified all ED closures in California during the period 1999-2010 and examined their association with inpatient mortality rates at nearby hospitals. We found that one-quarter of hospital admissions in this period occurred near an ED closure and that these admissions had 5 percent higher odds of inpatient mortality than admissions not occurring near a closure. This association persisted whether we considered ED closures as affecting all future nearby admissions or only those occurring in the subsequent two years. These results suggest that ED closures have ripple effects on patient outcomes that should be considered when health systems and policy makers decide how to regulate ED closures.

Current therapies for neurogenic bladder do not allow spinal cord injury patients to regain conscious control of urine storage or voiding. Novel neural technologies may provide means to improve or restore the connection between the brain and the bladder; however, the specific brain areas and their underlying neural activities responsible for micturition must be better understood in order to design such technologies. In this retrospective study, we analyzed electrocorticographic (ECoG) data obtained from epilepsy patients who underwent ECoG grid implantation for epilepsy surgery evaluation, in the hopes of determining specific electrophysiological activity associated with micturition. Our results indicate modulation of the delta (δ, 0.1-4 Hz) and low-gamma (\gamma, 25-50 Hz) activity in the peri-Sylvian area and the inferior temporal lobe. These findings suggest involvement of the insular cortex and the uncinate fasciculus in micturition, important structures related to sensation and decision making. To date, this is the first known study utilizing ECoG data to elucidate the electrophysiological activity of the brain associated with bladder control and sensation.

A fully implantable brain-computer interface (BCI) can be a practical tool to restore independence to those affected by spinal cord injury. We envision that such a BCI system will invasively acquire brain signals (e.g. electrocorticogram) and translate them into control commands for external prostheses. The feasibility of such a system was tested by implementing its benchtop analogue, centered around a commercial, ultra-low power (ULP) digital signal processor (DSP, TMS320C5517, Texas Instruments). A suite of signal processing and BCI algorithms, including (de)multiplexing, Fast Fourier Transform, power spectral density, principal component analysis, linear discriminant analysis, Bayes rule, and finite state machine was implemented and tested in the DSP. The system's signal acquisition fidelity was tested and characterized by acquiring harmonic signals from a function generator. In addition, the BCI decoding performance was tested, first with signals from a function generator, and subsequently using human electroencephalogram (EEG) during eyes opening and closing task. On average, the system spent 322 ms to process and analyze 2 s of data. Crosstalk (<;-65 dB) and harmonic distortion (~1%) were minimal. Timing jitter averaged 49 μs per 1000 ms. The online BCI decoding accuracies were 100% for both function generator and EEG data. These results show that a complex BCI algorithm can be executed on an ULP DSP without compromising performance. This suggests that the proposed hardware platform may be used as a basis for future, fully implantable BCI systems.

Fully-implantable, bi-directional brain-computer interfaces (BCIs) necessitate simultaneous cortical recording and stimulation. This is challenging since electrostimulation of cortical tissue typically causes strong artifacts that may saturate ultra-low power (ULP) analog front-ends of fully-implantable BCIs. To address this problem, we propose an efficient hardware-based method for artifact suppression that employs an auxiliary stimulator with polarity opposite to that of the primary stimulator. The feasibility of this method was explored first in simulations, and then experimentally with brain phantom tissue and electrocorticogram (ECoG) electrode grids. We find that the canceling stimulator can reduce stimulation artifacts below the saturation limit of a typical ULP front-end, while delivering only ~10% of the primary stimulator's voltage.

Cortical stimulation via electrocorticography (ECoG) may be an effective method for inducing artificial sensation in bi-directional brain-computer interfaces (BD-BCIs). However, strong electrical artifacts caused by electrostimulation may significantly degrade or obscure neural information. A detailed understanding of stimulation artifact propagation through relevant tissues may improve existing artifact suppression techniques or inspire the development of novel artifact mitigation strategies. Our work thus seeks to comprehensively characterize and model the propagation of artifacts in subdural ECoG stimulation. To this end, we collected and analyzed data from eloquent cortex mapping procedures of four subjects with epilepsy who were implanted with subdural ECoG electrodes. From this data, we observed that artifacts exhibited phase-locking and ratcheting characteristics in the time domain across all subjects. In the frequency domain, stimulation caused broadband power increases, as well as power bursts at the fundamental stimulation frequency and its super-harmonics. The spatial distribution of artifacts followed the potential distribution of an electric dipole with a median goodness-of-fit of R ² = 0.80 across all subjects and stimulation channels. Artifacts as large as ±1,100 μV appeared anywhere from 4.43 to 38.34 mm from the stimulation channel. These temporal, spectral and spatial characteristics can be utilized to improve existing artifact suppression techniques, inspire new strategies for artifact mitigation, and aid in the development of novel cortical stimulation protocols. Taken together, these findings deepen our understanding of cortical electrostimulation and provide critical design specifications for future BD-BCI systems.

INTRODUCTION: Deep brain stimulation (DBS) has shown remarkable success treating neurological and psychiatric disorders including Parkinsons disease, essential tremor, dystonia, epilepsy, and obsessive-compulsive disorder. DBS is now being explored to improve cognitive and functional outcomes in other psychiatric conditions, such as those characterized by reduced N-methyl-D-aspartate (NMDA) function (i.e., schizophrenia). While DBS for movement disorders generally involves high-frequency (>100 Hz) stimulation, there is evidence that low-frequency stimulation may have beneficial and persisting effects when applied to cognitive brain networks. METHODS: In this study, we utilize a novel technology, functional ultrasound imaging (fUSI), to characterize the cerebrovascular impact of medial septal nucleus (MSN) DBS under conditions of NMDA antagonism (pharmacologically using Dizocilpine [MK-801]) in anesthetized male mice. RESULTS: Imaging from a sagittal plane across a variety of brain regions within and outside of the septohippocampal circuit, we find that MSN theta-frequency (7.7 Hz) DBS increases hippocampal cerebral blood volume (CBV) during and after stimulation. This effect was not present using standard high-frequency stimulation parameters [i.e., gamma (100 Hz)]. DISCUSSION: These results indicate the MSN DBS increases circuit-specific hippocampal neurovascular activity in a frequency-dependent manner and does so in a way that continues beyond the period of electrical stimulation.

Electrocorticogram (ECoG) is a promising long-term signal acquisition platform for brain-computer interface (BCI) systems such as upper extremity prostheses. Several studies have demonstrated decoding of arm and finger trajectories from ECoG high-gamma band (80-160 Hz) signals. In this study, we systematically vary the velocity of three elementary movement types (pincer grasp, elbow and shoulder flexion/extension) to test whether the high-gamma band encodes for the entirety of the movements, or merely the movement onset. To this end, linear regression models were created for the durations and amplitudes of high-gamma power bursts and velocity deflections. One subject with 8×8 high-density ECoG grid (4 mm center-to-center electrode spacing) participated in the experiment. The results of the regression models indicated that the power burst durations varied directly with the movement durations (e.g. R(2)=0.71 and slope=1.0 s/s for elbow). The persistence of power bursts for the duration of the movement suggests that the primary motor cortex (M1) is likely active for the entire duration of a movement, instead of providing a marker for the movement onset. On the other hand, the amplitudes were less co-varied. Furthermore, the electrodes of maximum R(2) conformed to somatotopic arrangement of the brain. Also, electrodes responsible for flexion and extension movements could be resolved on the high-density grid. In summary, these findings suggest that M1 may be directly responsible for activating the individual muscle motor units, and future BCI may be able to utilize them for better control of prostheses.

The goal of this study is to estimate the thermal impact of a titanium skull unit (SU) implanted on the exterior aspect of the human skull. We envision this unit to house the front-end of a fully implantable electrocorticogram (ECoG)-based bi-directional (BD) brain-computer interface (BCI). Starting from the bio-heat transfer equation with physiologically and anatomically constrained tissue parameters, we used the finite element method (FEM) implemented in COMSOL to build a computational model of the SU's thermal impact. Based on our simulations, we predicted that the SU could consume up to 75 mW of power without raising the temperature of surrounding tissues above the safe limits (increase in temperature of 1°C). This power budget by far exceeds the power consumption of our front-end prototypes, suggesting that this design can sustain the SU's ability to record ECoG signals and deliver cortical stimulation. These predictions will be used to further refine the existing SU design and inform the design of future SU prototypes.

Electroencephalographic (EEG) recordings are often contaminated by electromyographic (EMG) artifacts, especially when recording during movement. Existing methods to remove EMG artifacts include independent component analysis (ICA), and other high-order statistical methods. However, these methods can not effectively remove most of EMG artifacts. Here, we proposed a modified ICA model for EMG artifacts removal in the EEG, which is called EMG Removal by Adding Sources of EMG (ERASE). In this new approach, additional channels of real EMG from neck and head muscles (reference artifacts) were added as inputs to ICA in order to "force" the most power from EMG artifacts into a few independent components (ICs). The ICs containing EMG artifacts (the "artifact ICs") were identified and rejected using an automated procedure. ERASE was validated first using both simulated and experimentally-recorded EEG and EMG. Simulation results showed ERASE removed EMG artifacts from EEG significantly more effectively than conventional ICA. Also, it had a low false positive rate and high sensitivity. Subsequently, EEG was collected from 8 healthy participants while they moved their hands to test the realistic efficacy of this approach. Results showed that ERASE successfully removed EMG artifacts (on average, about 75% of EMG artifacts were removed when using real EMGs as reference artifacts) while preserving the expected EEG features related to movement. We also tested the ERASE procedure using simulated EMGs as reference artifacts (about 63% of EMG artifacts removed). Compared to conventional ICA, ERASE removed on average 26% more EMG artifacts from EEG. These findings suggest that ERASE can achieve significant separation of EEG signal and EMG artifacts without a loss of the underlying EEG features. These results indicate that using additional real or simulated EMG sources can increase the effectiveness of ICA in removing EMG artifacts from EEG. Combined with automated artifact IC rejection, ERASE also minimizes potential user bias. Future work will focus on improving ERASE so that it can also be used in real-time applications.

BACKGROUND: Infancy is characterized by rapid neurological transformations leading to consolidation of lifelong function capabilities. Studying the infant brain is crucial for understanding how these mechanisms develop during this sensitive period. We review the neuroimaging modalities used with infants in stimulus-induced activity paradigms specifically, for the unique opportunity the latter provide for assessment of brain function. METHODS: Conducted a systematic review of literature published between 1977-2021, via a comprehensive search of four major databases. Standardized appraisal tools and inclusion/exclusion criteria were set according to the PRISMA guidelines. RESULTS: Two-hundred and thirteen papers met the criteria of the review process. The results show clear evidence of overall cumulative growth in the number of infant functional neuroimaging studies, with electroencephalography (EEG) and functional near-infrared spectroscopy (fNIRS) to be the most utilized and fastest growing modalities with behaving infants. However, there is a high level of exclusion rates associated with technical limitations, leading to limited motor control studies (about 6%) in this population. CONCLUSION: Although the use of functional neuroimaging modalities with infants increases, there are impediments to effective adoption of existing technologies with this population. Developing new imaging modalities and experimental designs to monitor brain activity in awake and behaving infants is vital.