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Stacey, W. C.

Publications and source records attributed to Stacey, W. C..

7 recordsLinked to original sources

Human iEEG recordings during audiovisual speech violations support and extend predictive routing models

Rather than constantly reconstructing the world solely through sensory input, predictive processing theories posit that the brain utilizes predictions maintained as internal representations to guide sensory processing. An emerging model, predictive routing, proposes that an interplay between neuronal gamma (40-150 Hz) and alpha-beta (10-30 Hz) rhythms implements a dynamic mechanism for predictive processing. Namely, predictions enhance alpha-beta oscillations that suppress gamma activity during the processing of predicted inputs. While this model is supported by animal studies, its validity has not been fully explored within the human brain. The present study addresses this by leveraging human intracranial EEG (iEEG) recordings across superior temporal and prefrontal/premotor areas of seven presurgical epilepsy patients during an audiovisual speech paradigm. We calculated iEEG power in the theta, alpha-beta, and high gamma bands during simple auditory deviance, multisensory integration, and a condition where an incongruent visual cue (lip movements) clashed with an auditory stimulus (a syllable), creating audiovisual incongruence that can elicit the McGurk illusion. Results revealed increased high-gamma and decreased alpha-beta power in the superior temporal cortex in response to auditory deviance and the McGurk condition, while frontal areas, despite reflecting a similar decrease in alpha-beta power, did not present this high gamma prediction error signal. Instead, the theta band revealed a strong prediction error signal in the McGurk condition, consistent with theories on the role of theta in reorganizing cortical networks. These results both support and extend existing predictive routing models for human-specific forms of predictive processing.

neuroscience↗

Seizure recruitment properties are dependent upon dynamotype: A modeling study

Seizure propagation - how epileptogenic brain regions recruit less excitable regions - is poorly understood. Previous studies have used dynamical modeling to study seizure propagation and to create patient-specific whole-brain models of seizure spread. However, these studies focused on seizures of a single dynamotype (onset and offset bifurcation pair). Here, we implement a novel coupling method to investigate seizure propagation in a diverse array of dynamotypes. We utilize the Multiclass Epileptor, a recently proposed model that captures a wide range of seizure dynamotypes in a cortical mass ("node"). We consider two nodes: the seizure onset zone (node 1), which bursts autonomously, and the potential propagation zone (node 2), which is not independently epileptogenic but can be recruited by node 1. We examine the impact of intrinsic and coupling factors on the likelihood and speed of recruitment, with particular attention to the onset bifurcation of node 1. We also measure the range of onset behaviors observed in node 2 with respect to the onset behavior of node 1. The model predicted that seizures that display baseline shifts at onset are less likely to spread, and spread more slowly, compared to seizures that do not exhibit baseline shifts at onset. Seizures that present with amplitude scaling at onset were unlikely to propagate. Further, the model predicted the potential for unusual combinations of onset dynamics, such as a baseline shift in node 2 but not node 1. We confirmed the possibility for several of these unusual recruitment behaviors in humans using intracranial electroencephalography data. The results of the study provide a theoretical framework for seizure propagation, establishing a basis for innovations in characterization of patients seizure networks and identification of the seizure onset zone. Author SummaryIn this work, we examined how a seizure spreads from one part of the brain to another using a computational model. We modeled two brain regions using the Multiclass Epileptor, which reproduces a range of brain activity patterns associated with seizures. In the model, the first brain node was able to recruit the second brain node into a seizure. The model predicted that the likelihood and speed of seizure spread differ depending on the pattern of brain activity observed at the start of the seizure. We also found that the pattern of brain activity at seizure onset is not necessarily the same pattern seen when the seizure spreads. We confirmed this possibility for mismatched patterns in recordings from human brain. The findings of the study improve our understanding of seizure spread, which lays the groundwork for development of tools to quantify seizure spread and may inform future work in patient-specific brain modeling.

neuroscience↗

Visual speech enhances auditory onset timing and envelope tracking through distinct mechanisms

Seeing a speakers face facilitates speech recognition in challenging listening environments. Prior work has shown that visual speech contains timing information to aid auditory speech processing, yet how these signals are integrated within the auditory system during audiovisual speech perception remains poorly understood. Observation of preparatory mouth movements may initiate phase reset of intrinsic oscillations, potentially sensitizing the auditory system for receptive speech processing, while observation of mouth movements post speech onset may facilitate entrainment to the speech envelope. Yet, little work has been done to test whether visual speech enhances encoding of auditory speech onset, speech envelope tracking, or both, and through independent or overlapping mechanisms. To investigate this, we examined the ways in which visual speech timing information alters theta band power and phase using human intracranial electroencephalography (iEEG) recordings in a large group of patients with epilepsy (n = 21). Prior to speech onset, preparatory mouth movements elicited theta phase reset (increased inter-trial phase coherence; ITPC) throughout the superior temporal gyrus (STG), which is thought to enhance speech onset encoding. Following speech onset, visual speech modulated theta ITPC only at anterior STG electrodes while theta power was modulated at posterior STG electrodes. Pre- and post-speech onset were spatially and temporally dissociated, consistent with the hypothesis that audiovisual speech onset encoding and envelope tracking mechanisms are partially distinct. Crucially, congruent and incongruent visual speech, designed here to have identical visual timing information about speech onset time, but different visual mouth evolution, produced only a small difference in the phase of theta band oscillations in the anterior STG, highlighting a more restricted role of visual speech in ongoing auditory entrainment. These results support the hypothesis that visual speech improves the precision of auditory speech encoding through two separate mechanisms, with auditory speech onset encoded throughout the entire STG and ongoing speech envelope tracking within anterior STG.

neuroscience↗

Using compartmental models to understand excitation-inhibition imbalance in epilepsy

Epileptic seizures are characterized by abnormal synchronous bursting of neurons. This is commonly attributed to an imbalance between excitatory and inhibitory neurotransmission. We introduce compartmental models from epidemiology to study this interaction between excitatory and inhibitory populations of neurons in the context of epilepsy. Neurons could either be bursting or susceptible, and the propagation of action potentials within the brain through the bursting of neurons is considered as an infection spreading through a population. We model the recruitment of neurons into bursting and their subsequent decay to susceptibility to be influenced by the proportion of excitatory and inhibitory neurons bursting, resulting in a two population Susceptible - Infected - Susceptible (SIS) model. This approach provides a tractable framework to inspect the mechanisms behind seizure generation and termination. Considering the excitatory neurotransmission as an epidemic spreading through the neuronal population and the inhibitory neurotransmission as a competing epidemic that stops the spread of excitation, we establish the conditions for a seizure-like state to be stable. Subsequently, we show how an activity-dependent dysfunction of inhibitory mechanisms such as impaired GABAergic inhibition or inhibitory-inhibitory interactions could result in a seizure even when the above conditions are not satisfied.

neuroscience↗

Visual speech differentially modulates beta, theta, and high gamma bands in auditory cortex

Speech perception is a central component of social communication. While principally an auditory process, accurate speech perception in everyday settings is supported by meaningful information extracted from visual cues (e.g., speech content, timing, and speaker identity). Previous research has shown that visual speech modulates activity in cortical areas subserving auditory speech perception, including the superior temporal gyrus (STG), potentially through feedback connections from the multisensory posterior superior temporal sulcus (pSTS). However, it is unknown whether visual modulation of auditory processing in the STG is a unitary phenomenon or, rather, consists of multiple temporally, spatially, or functionally distinct processes. To explore these questions, we examined neural responses to audiovisual speech measured from intracranially implanted electrodes within the temporal cortex of 21 patients undergoing clinical monitoring for epilepsy. We found that visual speech modulates auditory processes in the STG in multiple ways, eliciting temporally and spatially distinct patterns of activity that differ across theta, beta, and high-gamma frequency bands. Before speech onset, visual information increased high-gamma power in the posterior STG and suppressed beta power in mid-STG regions, suggesting crossmodal prediction of speech signals in these areas. After sound onset, visual speech decreased theta power in the middle and posterior STG, potentially reflecting a decrease in sustained feedforward auditory activity. These results are consistent with models that posit multiple distinct mechanisms supporting audiovisual speech perception and provide a crucial map for subsequent studies to identify the types of visual features that are encoded by these separate mechanisms.

neuroscience↗

Carbamazepine and GABA have distinct effects on seizure onset dynamics in mouse brain slices

Optimizing antiepileptic drug therapy is very challenging due to the absence of a reliable method to assess how brain activity changes between seizures. This work uses the Taxonomy of Seizure Dynamics (Saggio et al., 2020) to investigate how anticonvulsants influence seizure onset dynamotypes. The no Mg2+ /high K+ mouse brain-slice seizure model (N = 92) was used to generate consistent epileptiform onsets. We compared the onset bifurcations of controls with slices treated with either GABA or carbamazepine. Each anticonvulsant uniquely changed the types of bifurcations in the slices. This experiment provides proof-of-concept evidence that brain states exist on a "map" of seizure dynamics, and that antiepileptic drugs with different mechanisms can change the positioning of the brain states on the map. Impact statementAntiepileptic drugs modify underlying brain states and influence the pathway into seizure onset in brain slices.

bioinformatics↗

Epidynamics characterize and navigate the map of seizure dynamics

Seizures are a disruption of normal brain activity present across a vast range of species, diseases, and conditions. Here we introduce an organizing principle that leads to the first objective Taxonomy of Seizure Dynamics (TSD) based on bifurcation theory, and applied it to the analysis of EEG data. The "dynamotype" of a seizure is the part of its dynamic composition that defines its observable characteristics, including how it starts, evolves and terminates. Analyzing over 2000 focal-onset seizures recorded from 7 epilepsy centers on five continents, we find evidence of all 16 dynamotypes predicted in TSD. We demonstrate that patients dynamotypes evolve during their lifetime and display complex but systematic variations including hierarchy (certain dynamotypes are more common), non-bijectivity (a patient may display multiple dynamotypes) and pairing preference (multiple dynamotypes may occur during one seizure). TSD not only provides a way to stratify patients in complement to present practical classifications but also guides biophysically based mechanistic approaches and provides a language to describe the most critical features of seizure dynamics. Impact statementTaxonomy of Seizure Dynamics (TSD) provides a rigorous method for classifying and quantifying seizures and a principled framework for understanding seizure initiation and propagation.

bioinformatics↗