Electroencephalograph (EEG) has been widely applied for brain-computer interface (BCI) which enables paralyzed people to directly communicate with and control external devices, due to its portability, high temporal resolution, ease of use and low cost. Of various EEG paradigms, steady-state visual evoked potential (SSVEP)-based BCI system which uses multiple visual stimuli (such as LEDs or boxes on a computer screen) flickering at different frequencies has been widely explored in the past decades due to its fast communication rate and high signal-to-noise ratio. In this article, we review the current research in SSVEP-based BCI, focusing on the data analytics that enables continuous, accurate detection of SSVEPs and thus high information transfer rate. The main technical challenges, including signal pre-processing, spectrum analysis, signal decomposition, spatial filtering in particular canonical correlation analysis and its variations, and classification techniques are described in this article. Research challenges and opportunities in spontaneous brain activities, mental fatigue, transfer learning as well as hybrid BCI are also discussed.

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Data Analytics in Steady-State Visual Evoked Potential-Based Brain–Computer Interface: A Review

Slower Binocular Rivalry in the Autistic Brain.

Binocular rivalry is a classic experimental tool to probe the neural machinery of perceptual awareness. During rivalry, perception alternates between the two eyes, and the ebb and flow of perception is modeled to rely on the strength of inhibitory interactions between competitive neuronal populations in visual cortex. As a result, rivalry has been suggested as a noninvasive perceptual marker of inhibitory signaling in visual cortex, and its putative disturbance in psychiatric conditions, including autism. Yet, direct evidence causally implicating inhibitory signaling in the dynamics of binocular rivalry is currently lacking. We previously found that people with higher GABA levels in visual cortex, measured using magnetic resonance spectroscopy, have stronger perceptual suppression during rivalry. Here, we present direct causal tests of the impact of GABAergic inhibition on rivalry dynamics, and the contribution of specific GABA receptors to these dynamics. In a crossover pharmacological design with male and female adult participants, we found that drugs that modulate the two dominant GABA receptor types in the brain, GABAA (clobazam) and GABAB (arbaclofen), increase perceptual suppression during rivalry relative to a placebo. Crucially, these results could not be explained by changes in reaction times or response criteria, as determined through rivalry simulation trials, suggesting a direct and specific influence of GABA on perceptual suppression. A full replication study of the GABAB modulator reinforces these findings. These results provide causal evidence for a link between the strength of inhibition in the brain and perceptual suppression during rivalry and have implications for psychiatric conditions including autism.SIGNIFICANCE STATEMENT How does the brain accomplish perceptual gating? Here we use a direct and causal pharmacological manipulation to present insight into the neural machinery of a classic illusion of perceptual awareness: binocular rivalry. We show that drugs that increase GABAergic inhibition in the brain, clobazam (GABAA modulator) and arbaclofen (GABAB modulator), increase perceptual suppression during rivalry relative to a placebo. These results present the first causal link between GABAergic inhibition and binocular rivalry in humans, complementing classic models of binocular rivalry, and have implications for our understanding of psychiatric conditions, such as autism, where binocular rivalry is posited as a behavioral marker of disruptions in inhibitory signaling in the brain.

https://www.jneurosci.org/content/jneuro/39/42/8398.full.pdf

GABAergic Inhibition Gates Perceptual Awareness During Binocular Rivalry

Altered Visual Plasticity in Morbidly Obese Subjects.

Disturbances in the glutamatergic system have been increasingly documented in several neuropsychiatric disorders, including autism spectrum disorder (ASD). Glutamate-centered theories of ASD are based on evidence from patient samples and postmortem studies, as well as from studies documenting abnormalities in glutamatergic gene expression and metabolic pathways, including changes in the gut microbiota glutamate metabolism in patients with ASD. In addition, preclinical studies on animal models have demonstrated glutamatergic neurotransmission deficits and altered expression of glutamate synaptic proteins. At present, there are no approved glutamatergic drugs for ASD, but several ongoing clinical trials are currently focusing on evaluating in autistic patients glutamatergic pharmaceuticals already approved for other conditions. In this review, we provide an overview of the literature concerning the role of glutamatergic neurotransmission in the pathophysiology of ASD and as a potential target for novel treatments.

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Autism Spectrum Disorder: Focus on Glutamatergic Neurotransmission

Introduction While medical school curricula increasingly address health disparities, content regarding health care for persons impacted by incarceration is a persistent and notable gap. There is a ...

https://www.mededportal.org/doi/pdf/10.15766/mep_2374-8265.11014

Health Care in the Age of Mass Incarceration: A Selective Course for Medical Students in Their Preclinical Years.

Bumetanide has received much interest as a potential pharmacological modulator of the putative imbalance in excitatory/inhibitory (E/I) signaling that is thought to characterize autism spectrum conditions. Yet, currently, no studies of bumetanide efficacy have used an outcome measure that is modeled to depend on E/I balance in the brain. In this manuscript, we present the first causal study of the effect of bumetanide on an objective marker of E/I balance in the brain, binocular rivalry, which we have previously shown to be sensitive to pharmacological manipulation of GABA. Using a within-subjects placebo-control crossover design study, we show that, contrary to expectation, acute administration of bumetanide does not alter binocular rivalry dynamics in neurotypical adult individuals. Neither changes in response times nor response criteria can account for these results. These results raise important questions about the efficacy of acute bumetanide administration for altering E/I balance in the human brain, and highlight the importance of studies using objective markers of the underlying neural processes that drugs hope to target.

/pdf/a-causal-study-of-bumetanide-on-a-marker-of-excitatory-15a8bmwpdj.pdf

Alina Spiegel

Papers

Slower Binocular Rivalry in the Autistic Brain.

GABAergic Inhibition Gates Perceptual Awareness During Binocular Rivalry

Health Care in the Age of Mass Incarceration: A Selective Course for Medical Students in Their Preclinical Years.

A causal study of bumetanide on a marker of excitatory-inhibitory balance in the human brain

Causal Push-and-Pull Modulation of Binocular Rivalry Dynamics using GABAergic Drugs