Kinematic signatures of prosody in Lombard speech

Peer reviewe

Physical mechanisms may be as important as brain mechanisms in evolution of speech [Commentary on Ackerman, Hage, & Ziegler. Brain Mechanisms of acoustic communication in humans and nonhuman primates: an evolutionary perspective]

We present two arguments why physical adaptations for vocalization may be as important as neural adaptations. First, fine control over vocalization is not easy for physical reasons, and modern humans may be exceptional. Second, we present an example of a gorilla that shows rudimentary voluntary control over vocalization, indicating that some neural control is already shared with great apes

Brain mechanisms of acoustic communication in humans and nonhuman primates: An evolutionary perspective

Any account of “what is special about the human brain” (Passingham 2008) must specify the neural basis of our unique ability to produce speech and delineate how these remarkable motor capabilities could have emerged in our hominin ancestors. Clinical data suggest that the basal ganglia provide a platform for the integration of primate-general mechanisms of acoustic communication with the faculty of articulate speech in humans. Furthermore, neurobiological and paleoanthropological data point at a two-stage model of the phylogenetic evolution of this crucial prerequisite of spoken language: (i) monosynaptic refinement of the projections of motor cortex to the brainstem nuclei that steer laryngeal muscles, presumably, as part of a “phylogenetic trend” associated with increasing brain size during hominin evolution; (ii) subsequent vocal-laryngeal elaboration of cortico-basal ganglia circuitries, driven by human-specific FOXP2 mutations.;>This concept implies vocal continuity of spoken language evolution at the motor level, elucidating the deep entrenchment of articulate speech into a “nonverbal matrix” (Ingold 1994), which is not accounted for by gestural-origin theories. Moreover, it provides a solution to the question for the adaptive value of the “first word” (Bickerton 2009) since even the earliest and most simple verbal utterances must have increased the versatility of vocal displays afforded by the preceding elaboration of monosynaptic corticobulbar tracts, giving rise to enhanced social cooperation and prestige. At the ontogenetic level, the proposed model assumes age-dependent interactions between the basal ganglia and their cortical targets, similar to vocal learning in some songbirds. In this view, the emergence of articulate speech builds on the “renaissance” of an ancient organizational principle and, hence, may represent an example of “evolutionary tinkering” (Jacob 1977)

The role of linguistic contrasts in the auditory feedback control of Speech

Thesis (Ph. D. in Speech and Hearing Bioscience and Technology)--Harvard-MIT Division of Health Sciences and Technology, 2010.Cataloged from PDF version of thesis.Includes bibliographical references (p. 165-180).Speakers use auditory feedback to monitor their own speech, ensuring that the intended output matches the observed output. By altering the acoustic feedback signal before it reaches the speaker's ear, we can induce auditory errors: differences between what is expected and what is heard. This dissertation investigates the neural mechanisms responsible for the detection and consequent correction of these auditory errors. Linguistic influences on feedback control were assessed in two experiments employing auditory perturbation. In a behavioral experiment, subjects spoke four-word sentences while the fundamental frequency (FO) of the stressed word was perturbed either upwards or downwards, causing the word to sound more or less stressed. Subjects adapted by altering both the FO and the intensity contrast between stressed and unstressed words, even though intensity remained unperturbed. An integrated model of prosodic control is proposed in which FO and intensity are modulated together to achieve a stress target. In a second experiment, functional magnetic resonance imaging was used to measure neural responses to speech with and without auditory perturbation. Subjects were found to compensate more for formant shifts that resulted in a phonetic category change than for formant shifts that did not, despite the identical magnitudes of the shifts. Furthermore, the extent of neural activation in superior temporal and inferior frontal regions was greater for cross-category than for within-category shifts, evidence that a stronger cortical error signal accompanies a linguistically-relevant acoustic change. Taken together, these results demonstrate that auditory feedback control is sensitive to linguistic contrasts learned through auditory experience.by Caroline A. Niziolek.Ph.D.in Speech and Hearing Bioscience and Technolog

Mechanisms of auditory signal decoding in the progressive aphasias

The primary progressive aphasias (PPA) are a diverse group of neurodegenerative disorders that selectively target brain networks mediating language. The pathophysiology of PPA remains poorly understood, but emerging evidence suggests that deficits in auditory processing accompany and may precede language symptoms in these patients. In four studies, I have probed the pathophysiology of auditory signal decoding in patient cohorts representing all major PPA syndromes – nonfluent variant PPA (nfvPPA), semantic variant PPA (svPPA), and logopenic variant PPA (lvPPA) – in relation to healthy age-matched controls. In my first experiment, I presented sequences of spoken syllables manipulated for temporal regularity, spectrotemporal structure and entropy. I used voxel-based morphometry to define critical brain substrates for the processing of these attributes, identifying correlates of behavioural performance within a cortico-subcortical network extending beyond canonical language areas. In my second experiment, I used activation functional magnetic resonance imaging (fMRI) with the same stimuli. I identified network signatures of particular signal attributes: nfvPPA was associated with reduced activity in anterior cingulate for processing temporal irregularity; lvPPA with reduced activation of posterior superior temporal cortex for processing spectrotemporal structure; and svPPA with reduced activation of caudate and anterior cingulate for processing signal entropy. In my third experiment, I manipulated the auditory feedback via which participants heard their own voices during speech production. Healthy control participants spoke significantly less fluently under delayed auditory feedback, but patients with nfvPPA and lvPPA were affected significantly less. In my final experiment, I probed residual capacity for dynamic auditory signal processing and perceptual learning in PPA, using sinewave speech. Patients with nfvPPA and lvPPA showed severely attenuated learning to the degraded stimuli, while patients with svPPA showed intact early perceptual processing, but deficient integration of semantic knowledge. Together, these experiments represent the most concerted and comprehensive attempt to date to define the pathophysiology of auditory signal decoding in PPA

Cognitive Phonetics: The Transduction of Distinctive Features at the Phonology-Phonetics Interface

We propose that the interface between phonology and phonetics is mediated by a transduction process that converts elementary units of phonological computation, features, into temporally coordinated neuromuscular patterns, called ‘True Phonetic Representations’, which are directly interpretable by the motor system of speech production. Our view of the interface is constrained by substance-free generative phonological assumptions and by insights gained from psycholinguistic and phonetic models of speech production. To distinguish transduction of abstract phonological units into planned neuromuscular patterns from the biomechanics of speech production usually associated with physiological phonetics, we have termed this interface theory ‘Cognitive Phonetics’ (CP). The inner workings of CP are described in terms of Marr’s (1982/2010) tri-level approach, which we used to construct a linking hypothesis relating formal phonology to neurobiological activity. Potential neurobiological correlates supporting various parts of CP are presented. We also argue that CP augments the study of certain phonetic phenomena, most notably coarticulation, and suggest that some phenomena usually considered phonological (e.g., naturalness and gradience) receive better explanations within CP

Effects of deep brain stimulation on speech in patients with Parkinson’s disease and dystonia

Disorders affecting the basal ganglia can have a severe effect on speech motor control. The effect can vary depending on the pathophysiology of the basal ganglia disease but in general terms it can be classified as hypokinetic or hyperkinetic dysarthria. Despite the role of basal ganglia on speech, there is a marked discrepancy between the effect of medical and surgical treatments on limb and speech motor control. This is compounded by the complex nature of speech and communication in general, and the lack of animal models of speech motor control. The emergence of deep brain stimulation of basal ganglia structures gives us the opportunity to record systematically the effects on speech and attempt some assumptions on the role of basal ganglia on speech motor control. The aim of the present work was to examine the impact of bilateral subthalamic nucleus deep brain stimulation (STN-DBS) for Parkinson’s disease (PD) and globus pallidus internus (GPi-DBS) for dystonia on speech motor control. A consecutive series of PD and dystonia patients who underwent DBS was evaluated. Patients were studied in a prospective longitudinal manner with both clinical assessment of their speech intelligibility and acoustical analysis of their speech. The role of pre-operative clinical factors and electrical parameters of stimulation, mainly electrode positioning and voltage amplitude was systematically examined. In addition, for selected patients, tongue movements were studied using electropalatography. Aerodynamic aspects of speech were also studied. The impact of speech therapy was assessed in a subgroup of patients. The clinical evaluation of speech intelligibility one and three years post STN-DBS in PD patients showed a deterioration of speech, partly related to medially placed electrodes and high amplitude of stimulation. Pre-operative predictive factors included low speech intelligibility before surgery and longer disease duration. Articulation rather than voice was most frequently affected with a distinct dysarthria type emerging, mainly hyperkinetic-dystonic, rather than hypokinetic. Traditionally effective therapy for PD dysarthria had little to no benefit following STN-DBS. Speech following GPi-DBS for dystonia did not significantly change after one year of stimulation. A subgroup of patients showed hypokinetic features, mainly reduced voice volume and fast rate of speech more typical of Parkinsonian speech. Speech changes in both STN-DBS and GPi-DBS were apparent after six months of stimulation. This progressive deterioration of speech and the critical role of the electrical parameters of stimulation suggest a long-term effect of electrical stimulation of basal ganglia on speech motor control