LaDIVA: A neurocomputational model providing laryngeal motor control for speech acquisition and production

Many voice disorders are the result of intricate neural and/or biomechanical impairments that are poorly understood. The limited knowledge of their etiological and pathophysiological mechanisms hampers effective clinical management. Behavioral studies have been used concurrently with computational models to better understand typical and pathological laryngeal motor control. Thus far, however, a unified computational framework that quantitatively integrates physiologically relevant models of phonation with the neural control of speech has not been developed. Here, we introduce LaDIVA, a novel neurocomputational model with physiologically based laryngeal motor control. We combined the DIVA model (an established neural network model of speech motor control) with the extended body-cover model (a physics-based vocal fold model). The resulting integrated model, LaDIVA, was validated by comparing its model simulations with behavioral responses to perturbations of auditory vocal fundamental frequency (fo) feedback in adults with typical speech. LaDIVA demonstrated capability to simulate different modes of laryngeal motor control, ranging from short-term (i.e., reflexive) and long-term (i.e., adaptive) auditory feedback paradigms, to generating prosodic contours in speech. Simulations showed that LaDIVA’s laryngeal motor control displays properties of motor equivalence, i.e., LaDIVA could robustly generate compensatory responses to reflexive vocal fo perturbations with varying initial laryngeal muscle activation levels leading to the same output. The model can also generate prosodic contours for studying laryngeal motor control in running speech. LaDIVA can expand the understanding of the physiology of human phonation to enable, for the first time, the investigation of causal effects of neural motor control in the fine structure of the vocal signal.Fil: Weerathunge, Hasini R.. Boston University; Estados UnidosFil: Alzamendi, Gabriel Alejandro. Universidad Nacional de Entre Ríos. Instituto de Investigación y Desarrollo en Bioingeniería y Bioinformática - Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Investigación y Desarrollo en Bioingeniería y Bioinformática; ArgentinaFil: Cler, Gabriel J.. University of Washington; Estados UnidosFil: Guenther, Frank H.. Boston University; Estados UnidosFil: Stepp, Cara E.. Boston University; Estados UnidosFil: Zañartu, Matías. Universidad Técnica Federico Santa María; Chil

Defective neural motor speech mappings as a source for apraxia of speech : evidence from a quantitative neural model of speech processing

This unique resource reviews research evidence pertaining to best practice in the clinical assessment of established areas such as intelligibility and physiological functioning, as well as introducing recently developed topics such as conversational analysis, participation measures, and telehealth. In addition, new and established research methods from areas such as phonetics, kinematics, imaging, and neural modeling are reviewed in relation to their applicability and value for the study of disordered speech. Based on the broad coverage of topics and methods, the textbook represents a valuable resource for a wide ranging audience, including clinicians, researchers, as well as students with an interest in speech pathology and clinical phonetics

Multi-scale modeling of gene-behavior associations in an artificial neural network model of cognitive development

In the multi-disciplinary field of developmental cognitive neuroscience, statistical associations between levels of description play an increasingly important role. One example of such associations is the observation of correlations between relatively common gene variants and individual differences in behavior. It is perhaps surprising that such associations can be detected despite the remoteness of these levels of description, and the fact that behavior is the outcome of an extended developmental process involving interaction with a variable environment. Given that they have been detected, how do such associations inform cognitive-level theories? To investigate this question, we employed a multi-scale computational model of development, using a sample domain drawn from the field of language acquisition. The model comprised an artificial neural network model of past-tense acquisition trained using the backpropagation learning algorithm, extended to incorporate population modeling and genetic algorithms. It included five levels of description, four internal: genetic, network, neurocomputation, behavior; and one external: environment. Since the mechanistic assumptions of the model were known and its operation was relatively transparent, we could evaluate whether cross-level associations gave an accurate picture of causal processes. We established that associations could be detected between artificial genes and behavioral variation, even under polygenic assumptions of a many-to-one relationship between genes and neurocomputational parameters, and when an experience-dependent developmental process interceded between the action of genes and the emergence of behavior. We evaluated these associations with respect to their specificity (to different behaviors, to function versus structure), to their developmental stability, and to their replicability, as well as considering issues of missing heritability and gene-environment interactions. We argue that gene-behavior associations can inform cognitive theory with respect to effect size, specificity, and timing. The model demonstrates a means by which researchers can undertake modeling multi-scale modeling with respect to cognition, and develop highly specific and complex hypotheses across multiple levels of description

The *subjectivity* of subjective experience - A representationalist analysis of the first-person perspective

This is a brief and accessible English summary of the "Self-model Theory of Subjectivity" (SMT), which is only available as German book in this archive. It introduces two new theoretical entities, the "phenomenal self-model" (PSM) and the "phenomenal model of the intentionality-relation" PMIR. A representationalist analysis of the phenomenal first-person persepctive is offered. This is a revised version, including two pictures

The over-pruning hypothesis of autism

This article outlines the over-pruning hypothesis of autism. The hypothesis originates in a neurocomputational model of the regressive sub-type (Thomas, Knowland & Karmiloff-Smith, 2011a,b). Here we develop a more general version of the over-pruning hypothesis to address heterogeneity in the timing of manifestation of ASD, including new computer simulations which can reconcile the different observed developmental trajectories (early onset, late onset, regression) via a single underlying atypical mechanism; and which show how unaffected siblings of individuals with ASD may differ from controls either by inheriting a milder version of the pathological mechanism or by co-inheriting the risk factors without the pathological mechanism. The proposed atypical mechanism involves overly aggressive synaptic pruning in infancy and early childhood, an exaggeration of a normal phase of brain development. We show how the hypothesis generates novel predictions that differ from existing theories, including that (1) the first few months of development in ASD will be indistinguishable from typical, and (2) the earliest atypicalities in ASD will be sensory and motor rather than social. Both predictions gain cautious support from emerging longitudinal studies of infants at risk of ASD. We review evidence consistent with the over-pruning hypothesis, its relation to other current theories (including C. Frith’s under-pruning proposal; C. Frith, 2003, 2004), as well as inconsistent data and current limitations. The hypothesis situates causal accounts of ASD within a framework of protective and risk factors (Newschaffer et al., 2012); clarifies different versions of the broader autism phenotype (i.e., the implication of observed similarities between individuals with autism and their family members); and integrates data from multiple disciplines, including behavioural studies, neuroscience studies, genetics, and intervention studies

A neural model of hippocampalstriatal interactions in associative learningand transfer generalization in various neurological and psychiatric patients

Building on our previous neurocomputational models of basal ganglia and hippocampal region function (and their modulation by dopamine and acetylcholine, respectively), we show here how an integration of these models can inform our understanding of the interaction between the basal ganglia and hippocampal region in associative learning and transfer generalization across various patient populations. As a common test bed for exploring interactions between these brain regions and neuromodulators, we focus on the acquired equivalence task, an associative learning paradigm in which stimuli that have been associated with the same outcome acquire a functional similarity such that subsequent generalization between these stimuli increases. This task has been used to test cognitive dysfunction in various patient populations with damages to the hippocampal region and basal ganglia, including studies of patients with Parkinson’s disease (PD), schizophrenia, basal forebrain amnesia, and hippocampal atrophy. Simulation results show that damage to the hippocampal region—as in patients with hippocampal atrophy (HA), hypoxia, mild Alzheimer’s (AD), or schizophrenia—leads to intact associative learning but impaired transfer generalization performance. Moreover, the model demonstrates how PD and anterior communicating artery (ACoA) aneurysm—two very different brain disorders that affect different neural mechanisms— can have similar effects on acquired equivalence performance. In particular, the model shows that simulating a loss of dopamine function in the basal ganglia module (as in PD) leads to slow acquisition learning but intact transfer generalization. Similarly, the model shows that simulating the loss of acetylcholine in the hippocampal region (as in ACoA aneurysm) also results in slower acquisition learning. We argue from this that changes in associative learning of stimulus–action pathways (in the basal ganglia) or changes in the learning of stimulus representations (in the hippocampal region) can have similar functional effects.Portions of this work were funded by the NSF/NIH Collaborative Research in Computational Neuroscience (CRCNS) Program and by NIAAA R01 AA018737 (CEM)

Sigma-lognormal modeling of speech

Human movement studies and analyses have been fundamental in many scientific domains, ranging from neuroscience to education, pattern recognition to robotics, health care to sports, and beyond. Previous speech motor models were proposed to understand how speech movement is produced and how the resulting speech varies when some parameters are changed. However, the inverse approach, in which the muscular response parameters and the subject's age are derived from real continuous speech, is not possible with such models. Instead, in the handwriting field, the kinematic theory of rapid human movements and its associated Sigma-lognormal model have been applied successfully to obtain the muscular response parameters. This work presents a speech kinematics based model that can be used to study, analyze, and reconstruct complex speech kinematics in a simplified manner. A method based on the kinematic theory of rapid human movements and its associated Sigma lognormal model are applied to describe and to parameterize the asymptotic impulse response of the neuromuscular networks involved in speech as a response to a neuromotor command. The method used to carry out transformations from formants to a movement observation is also presented. Experiments carried out with the (English) VTR TIMIT database and the (German) Saarbrucken Voice Database, including people of different ages, with and without laryngeal pathologies, corroborate the link between the extracted parameters and aging, on the one hand, and the proportion between the first and second formants required in applying the kinematic theory of rapid human movements, on the other. The results should drive innovative developments in the modeling and understanding of speech kinematics.Comment: Published in Open Acce

Comorbidity of Motor and Sensory Functions in Childhood Motor Speech Disorders

Subtypes of speech sound disorders (SSDs) with a sensorimotor origin are known as motor speech disorders (MSDs). The symptoms can be diverse, and the causes of the disorders in children are in many cases unknown. Examples of MSD are childhood apraxia of speech and dysarthria. MSD is often seen in neurodevelopmental disorders such as cerebral palsy, developmental coordination disorder (DCD) or autism spectrum disorders (ASD), or it is seen with no obvious diagnosis but usually with comorbid problems. Within all existing comorbidity dysfunctions, the motor and sensory systems are of interest for identifying possible underlying mechanisms of MSD. Namely, soft neurological signs such as hypotonia, decreased speed and low accuracy of motor skills and delayed motor development are given consideration by many researchers for better understanding of underlying motor mechanisms of MSD. Results from comorbidity studies highlight the relationship of MSD with complex sensorimotor tasks and sequential motor tasks. In this chapter, our aim is to frame findings from studies about comorbidity of sensory and motor dysfunctions in MSD in order to theorise affected mechanisms and propose an underlying global motor deficit. We will conclude with implications for therapy models

Precis of neuroconstructivism: how the brain constructs cognition

Neuroconstructivism: How the Brain Constructs Cognition proposes a unifying framework for the study of cognitive development that brings together (1) constructivism (which views development as the progressive elaboration of increasingly complex structures), (2) cognitive neuroscience (which aims to understand the neural mechanisms underlying behavior), and (3) computational modeling (which proposes formal and explicit specifications of information processing). The guiding principle of our approach is context dependence, within and (in contrast to Marr [1982]) between levels of organization. We propose that three mechanisms guide the emergence of representations: competition, cooperation, and chronotopy; which themselves allow for two central processes: proactivity and progressive specialization. We suggest that the main outcome of development is partial representations, distributed across distinct functional circuits. This framework is derived by examining development at the level of single neurons, brain systems, and whole organisms. We use the terms encellment, embrainment, and embodiment to describe the higher-level contextual influences that act at each of these levels of organization. To illustrate these mechanisms in operation we provide case studies in early visual perception, infant habituation, phonological development, and object representations in infancy. Three further case studies are concerned with interactions between levels of explanation: social development, atypical development and within that, developmental dyslexia. We conclude that cognitive development arises from a dynamic, contextual change in embodied neural structures leading to partial representations across multiple brain regions and timescales, in response to proactively specified physical and social environment