Biology subjects

Viventi, J.

Publications and source records attributed to Viventi, J..

7 recordsLinked to original sources

bioRxiv2025

Shared latent representations of speech production for cross-patient speech decoding

Speech brain-computer interfaces (BCIs) can restore communication in individuals with neuromotor disorders who are unable to speak. However, current speech BCIs limit patient usability and successful deployment by requiring large volumes of patient-specific data collected over long periods of time. A promising solution to facilitate usability and accelerate their successful deployment is to combine data from multiple patients. This has proven difficult, however, due to differences in user neuroanatomy, varied placement of electrode arrays, and sparse sampling of targeted anatomy. Here, by aligning patient-specific neural data to a shared latent space, we show that speech BCIs can be trained on data combined across patients. Using canonical correlation analysis and high-density micro-electrocorticography (ECoG), we uncovered shared neural latent dynamics with preserved micro-scale speech information. This approach enabled cross-patient decoding models to achieve improved performance relative to patient-specific models facilitated by the high resolution and broad coverage of ECoG. Our findings support future speech BCIs that are more accurate and rapidly deployable, ultimately improving the quality of life for people with impaired communication from neuromotor disorders.

neuroscience↗

bioRxiv2025

Distinct cortical encoding of acoustic and electrical cochlear stimulation

Cochlear implants are neuroprosthetic devices that restore hearing and speech comprehension to profoundly deaf humans and represent an exemplar application of biomedical engineering and research to clinical conditions. However, the utility of these devices in many subjects is limited, largely due to lack of information about how neural circuits respond to implant stimulation. Recently we showed that deafened rats can use cochlear implants to recognize sounds, and that this training refined the responses of single neurons in the primary auditory cortex. Here we asked how local populations of cortical neurons represent acute implant stimuli, using electrode arrays we developed for cortical surface recordings for micro-electrocorticography ({micro}ECoG), a form of intracranial electroencephalography (iEEG). We found that there was a coarse, non-random spatial organization with limited evidence for consistent, sharply graded cochleotopy across recording sites, relative to a clearer tonotopic spatial representation in normal-hearing rats. Single-trial iEEG responses to acoustic inputs were more reliable than responses to cochlear implant stimulation, although stimulus identity could be successfully decoded in both cases. However, the spatio-temporal response profiles to acoustic vs cochlear implant stimulation were substantially different. Decoders trained on acoustic responses showed essentially zero information transfer when tested on electrical stimulation responses in the same animals after deafening and cochlear implant stimulation. Thus, while acute cochlear implant stimulation evoked spatially non-random cortical activity with coarse cochleotopic structure, the dynamics of network activity were substantially different from those evoked by acoustic stimulation, with possible implications for perceptual similarity that remain to be tested.

neuroscience↗

bioRxiv2024

Neural mechanisms of the transition from planning to execution in speech production

Speaking is the primary way that humans communicate. This communication is enabled by a production system that can plan and execute unique combinations of speech sounds. Although a distributed network of brain regions has been implicated in speaking, it is unclear how planning and execution of speech are coordinated to produce meaningful sounds. Leveraging the high spatio-temporal resolution of intracranial recordings at different spatial scales, we show distinct neural mechanisms that facilitate speech planning and execution. During planning, different levels of speech units are coded discretely at distinct prefrontal sites. These planned units are then dynamically integrated at various cortical levels to guide subsequent execution. During speech execution, speech motor regions generate continuous sequences that reflect both discrete speech sound units and their transitional properties between units. This rapid neural transition from discrete speech units to motor sequences links speech planning with execution and enables our effortless ability to speak.

neuroscience↗

bioRxiv2023

Cerebellar Activity in Hemi-Parkinsonian Rats during Volitional Gait and Freezing

Parkinsons disease is a neurodegenerative disease characterized by gait dysfunction in the advanced stages of the disease. The unilateral 6-OHDA toxin-induced model is the most studied animal model of Parkinsons disease, which reproduces gait dysfunction after greater than 68% dopamine (DA) loss in the substantia nigra pars compacta (SNc). The extent to which the neural activity in hemi-parkinsonian rats correlates to gait dysfunction and DAergic cell loss is not clear. In this paper we report the effects of unilateral DA depletion on cerebellar vermis activity using micro-electrocorticography (ECoG) during walking and freezing on a runway. Gait and neural activity were measured in 6-OHDA lesioned and sham lesioned rats at 14d, 21d, and 28d after infusion of 6-OHDA or control vehicle into the medial forebrain bundle (MFB) (n=20). Gait deficits in 6-OHDA rats were different from sham rats at 14d (p<0.05). Gait deficits in 6-OHDA rats improved at 21d and 28d except for run speed, which decreased at 28d (p=0.018). No differences in gait deficits were observed in sham lesioned rats at any time points. Hemiparkinsonian rats showed hyperactivity in the cerebellar vermis at 21d (p<0.05), but not at 14d and 28d, and the activity was reduced during freezing epochs in lobules VIa, VIb, and VIc (p<0.05). These results suggest that DAergic cell loss causes pathological cerebellar activity at 21d postlesion and suggests that compensatory mechanisms from the intact hemisphere contribute to normalized cerebellar activity at 28d. The decrease in cerebellar oscillatory activity during freezing may be indicative of neurological changes during freezing of gait in Parkinsons disease patients making this region a potential location for biomarker detection. Although the unilateral 6-OHDA model presents gait deficits that parallel clinical presentations of Parkinsons disease, further studies in animal models of bilateral DA loss are needed to understand the role of the cerebellar vermis in Parkinsons disease.

neuroscience↗

bioRxiv2023

Cerebellar Activity in PINK1 Knockout Rats during Volitional Gait

Preclinical models of Parkinsons disease are imperative to gain insight into the neural circuits that contribute to gait dysfunction in advanced stages of the disease. The PTEN-induced putative kinase 1 (P1) knockout (KO) early onset model of Parkinsons disease may be a useful rodent model to study the effects of neurotransmitter degeneration caused by loss of P1 function on brain activity during volitional gait. The goal of this study was to measure changes in neural activity at the cerebellar vermis (CBLv) at 8 months of age. Gait deficits, except run speed, were not significantly different from age-matched wild-type (WT) controls as previously reported. P1KO (n=4) and WT (n=4) rats were implanted with a micro-electrocorticographic array placed over CBLv lobules VI (a, b, and c) and VII. Local field potential recordings were obtained during volitional gait across a runway. Power spectral analysis and coherence analysis were used to quantify network oscillatory activity in frequency bands of interest. CBLv power was hypoactive in the beta (VIb, VIc, and VII) and alpha (VII) bands at CBLv lobules VIb, VIc, and VII in P1KO rats compared to WT controls during gait (p<0.05). These results suggest that gait improvement in P1KO rats at 8 months may be a compensatory mechanism attributed to movement corrections caused by decreased inhibition of the alpha band of CBLv lobule VII and beta band of lobules VIb, VIc, and VII. The P1KO model may be a valuable tool for understanding the circuit mechanisms underlying gait dysfunction in early-onset Parkinsons disease patients with functional loss of P1. Future studies investigating the CBLv as a potential biomarker and therapeutic target for the treatment of gait dysfunction in Parkinsons disease are warranted.

neuroscience↗

bioRxiv2022

Accurate speech decoding requires high-resolution neural interfaces

Patients suffering from debilitating neurodegenerative diseases often lose the ability to communicate, detrimentally affecting their quality of life. One promising solution to restore communication is to decode signals directly from the brain to enable neural speech prostheses. However, decoding has been limited by coarse neural recordings which inadequately capture the rich spatio-temporal structure of human brain signals. To resolve this limitation, we performed novel, high-resolution, micro-electrocorticographic (ECoG) neural recordings during intra-operative speech production. We obtained neural signals with 57x higher spatial resolution and 48% higher signal-to-noise ratio compared to standard invasive recordings. This increased signal quality improved phoneme decoding by 35% compared to standard intracranial signals. Accurate decoding was dependent on the high-spatial resolution of the neural interface. Non-linear decoding models designed to utilize enhanced spatio-temporal neural information produced better results than linear techniques. We show for the first time that ECoG can enable high-quality speech decoding, demonstrating its ability to improve neural interfaces for neural speech prostheses.

neuroscience↗

bioRxiv2019

A modular high-density 294-channel μECoG system on macaque vlPFC for auditory cognitive decoding

OBJECTIVEA fundamental goal of the auditory system is to parse the auditory environment into distinct perceptual representations. Auditory perception is mediated by the ventral auditory pathway, which includes the ventrolateral prefrontal cortex (vlPFC) late. Because large-scale recordings of auditory signals are quite rare, the spatiotemporal resolution of the neuronal code that underlies vlPFCs contribution to auditory perception has not been fully elucidated. Therefore, we developed a modular, chronic, high-resolution, multi-electrode array system with long-term viability.\n\nAPPROACHWe molded three separate ECoG arrays into one and implanted this system in a non-human primate. A custom 3D-printed titanium chamber was mounted on left hemisphere. The molded 294-contact ECoG array was implanted subdurally over vlPFC. ECoG activity was recorded while the monkey participated in a \"hearing-in-noise\" task in which they reported hearing a \"target\" vocalization from a background \"chorus\" of vocalizations. We titrated task difficulty by varying the sound level of the target vocalization, relative to the chorus (target-to-chorus ratio, TCr).\n\nMAIN RESULTSWe decoded the TCr and the monkeys behavioral choices from the ECoG signal. We analyzed decoding capacity as a function of neuronal frequency band, spatial resolution, and time from implantation. Over a one-year period, we were successfully able to record ECoG signals. Although we found significant decoding with as few as two electrodes, we found near-perfect decoding with [~]16 electrodes. Decoding further improved when we included more electrodes. Finally, because the decoding capacity of individual electrodes varied on a day-by-day basis, high-density electrode arrays ensure robust decoding in the long term.\n\nSIGNIFICANCEOur results demonstrate the utility and robustness of high-resolution chronic {micro}ECoG recording. We developed a new high-resolution surface electrode array that can be scaled to cover larger cortical areas without increasing the chamber footprint.

neuroscience↗