A randomised controlled trial investigating the causal role of the medial prefrontal cortex in mediating self-agency during speech monitoring and reality monitoring.

Self-agency is the awareness of being the agent of one's own thoughts and actions. Self-agency is essential for interacting with the outside world (reality-monitoring). The medial prefrontal cortex (mPFC) is thought to be one neural correlate of self-agency. We investigated whether mPFC activity can causally modulate self-agency on two different tasks of speech-monitoring and reality-monitoring. The experience of self-agency is thought to result from making reliable predictions about the expected outcomes of one's own actions. This self-prediction ability is necessary for the encoding and memory retrieval of one's own thoughts during reality-monitoring to enable accurate judgments of self-agency. This self-prediction ability is also necessary for speech-monitoring where speakers consistently compare auditory feedback (what we hear ourselves say) with what we expect to hear while speaking. In this study, 30 healthy participants are assigned to either 10 Hz repetitive transcranial magnetic stimulation (rTMS) to enhance mPFC excitability (N = 15) or 10 Hz rTMS targeting a distal temporoparietal site (N = 15). High-frequency rTMS to mPFC enhanced self-predictions during speech-monitoring that predicted improved self-agency judgments during reality-monitoring. This is the first study to provide robust evidence for mPFC underlying a causal role in self-agency, that results from the fundamental ability of improving self-predictions across two different tasks.

Neurophysiological evidence of sensory prediction errors driving speech sensorimotor adaptation.

The human sensorimotor system has a remarkable ability to quickly and efficiently learn movements from sensory experience. A prominent example is sensorimotor adaptation, learning that characterizes the sensorimotor system's response to persistent sensory errors by adjusting future movements to compensate for those errors. Despite being essential for maintaining and fine-tuning motor control, mechanisms underlying sensorimotor adaptation remain unclear. A component of sensorimotor adaptation is implicit (i.e., the learner is unaware of the learning process) which has been suggested to result from sensory prediction errors-the discrepancies between predicted sensory consequences of motor commands and actual sensory feedback. However, to date no direct neurophysiological evidence that sensory prediction errors drive adaptation has been demonstrated. Here, we examined prediction errors via magnetoencephalography (MEG) imaging of the auditory cortex during sensorimotor adaptation of speech to altered auditory feedback, an entirely implicit adaptation task. Specifically, we measured how speaking-induced suppression (SIS)--a neural representation of auditory prediction errors--changed over the trials of the adaptation experiment. SIS refers to the suppression of auditory cortical response to speech onset (in particular, the M100 response) to self-produced speech when compared to the response to passive listening to identical playback of that speech. SIS was reduced (reflecting larger prediction errors) during the early learning phase compared to the initial unaltered feedback phase. Furthermore, reduction in SIS positively correlated with behavioral adaptation extents, suggesting that larger prediction errors were associated with more learning. In contrast, such a reduction in SIS was not found in a control experiment in which participants heard unaltered feedback and thus did not adapt. In addition, in some participants who reached a plateau in the late learning phase, SIS increased (reflecting smaller prediction errors), demonstrating that prediction errors were minimal when there was no further adaptation. Together, these findings provide the first neurophysiological evidence for the hypothesis that prediction errors drive human sensorimotor adaptation.

A randomised controlled trial investigating the causal role of the medial prefrontal cortex in mediating self-agency during speech monitoring and reality monitoring.

Self-agency is being aware of oneself as the agent of one's thoughts and actions. Self agency is necessary for successful interactions with the external world (reality-monitoring). The medial prefrontal cortex (mPFC) is considered to represent one neural correlate underlying self-agency. We investigated whether mPFC activity can causally modulate self-agency on two different tasks involving speech-monitoring and reality-monitoring. The experience of self-agency is thought to result from being able to reliably predict the sensory outcomes of one's own actions. This self-prediction ability is necessary for successfully encoding and recalling one's own thoughts to enable accurate self-agency judgments during reality-monitoring tasks. This self-prediction ability is also necessary during speech-monitoring tasks where speakers compare what we hear ourselves say in auditory feedback with what we predict we will hear while speaking. In this randomised-controlled study, heathy controls (HC) are assigned to either high-frequency transcranial magnetic stimulation (TMS) to enhance mPFC excitability or TMS targeting a control site. After TMS to mPFC, HC improved self-predictions during speech-monitoring tasks that predicted improved self-agency judgments during different reality-monitoring tasks. These first-in-kind findings demonstrate the mechanisms of how mPFC plays a causal role in self-agency that results from the fundamental ability of improving self-predictions across two different tasks.

Mechanisms of sensorimotor adaptation in a hierarchical state feedback control model of speech.

Upon perceiving sensory errors during movements, the human sensorimotor system updates future movements to compensate for the errors, a phenomenon called sensorimotor adaptation. One component of this adaptation is thought to be driven by sensory prediction errors-discrepancies between predicted and actual sensory feedback. However, the mechanisms by which prediction errors drive adaptation remain unclear. Here, auditory prediction error-based mechanisms involved in speech auditory-motor adaptation were examined via the feedback aware control of tasks in speech (FACTS) model. Consistent with theoretical perspectives in both non-speech and speech motor control, the hierarchical architecture of FACTS relies on both the higher-level task (vocal tract constrictions) as well as lower-level articulatory state representations. Importantly, FACTS also computes sensory prediction errors as a part of its state feedback control mechanism, a well-established framework in the field of motor control. We explored potential adaptation mechanisms and found that adaptive behavior was present only when prediction errors updated the articulatory-to-task state transformation. In contrast, designs in which prediction errors updated forward sensory prediction models alone did not generate adaptation. Thus, FACTS demonstrated that 1) prediction errors can drive adaptation through task-level updates, and 2) adaptation is likely driven by updates to task-level control rather than (only) to forward predictive models. Additionally, simulating adaptation with FACTS generated a number of important hypotheses regarding previously reported phenomena such as identifying the source(s) of incomplete adaptation and driving factor(s) for changes in the second formant frequency during adaptation to the first formant perturbation. The proposed model design paves the way for a hierarchical state feedback control framework to be examined in the context of sensorimotor adaptation in both speech and non-speech effector systems.

Distinct neurophysiology during nonword repetition in logopenic and non-fluent variants of primary progressive aphasia.

Overlapping clinical presentations in primary progressive aphasia (PPA) variants present challenges for diagnosis and understanding pathophysiology, particularly in the early stages of the disease when behavioral (speech) symptoms are not clearly evident. Divergent atrophy patterns (temporoparietal degeneration in logopenic variant lvPPA, frontal degeneration in nonfluent variant nfvPPA) can partially account for differential speech production errors in the two groups in the later stages of the disease. While the existing dogma states that neurodegeneration is the root cause of compromised behavior and cortical activity in PPA, the extent to which neurophysiological signatures of speech dysfunction manifest independent of their divergent atrophy patterns remain unknown. We test the hypothesis that nonword deficits in lvPPA and nfvPPA arise from distinct patterns of neural oscillations that are unrelated to atrophy. We use a novel structure-function imaging approach integrating magnetoencephalographic imaging of neural oscillations during a non-word repetition task with voxel-based morphometry-derived measures of gray matter volume to isolate neural oscillation abnormalities independent of atrophy. We find reduced beta band neural activity in left temporal regions associated with the late stages of auditory encoding unique to patients with lvPPA and reduced high-gamma neural activity over left frontal regions associated with the early stages of motor preparation in patients with nfvPPA. Neither of these patterns of reduced cortical oscillations was explained by cortical atrophy in our statistical model. These findings highlight the importance of structure-function imaging in revealing neurophysiological sequelae in early stages of dementia when neither structural atrophy nor behavioral deficits are clinically distinct.

Impaired Speaking-Induced Suppression in Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disease involving cognitive impairment and abnormalities in speech and language. Here, we examine how AD affects the fidelity of auditory feedback predictions during speaking. We focus on the phenomenon of speaking-induced suppression (SIS), the auditory cortical responses' suppression during auditory feedback processing. SIS is determined by subtracting the magnitude of auditory cortical responses during speaking from listening to playback of the same speech. Our state feedback control (SFC) model of speech motor control explains SIS as arising from the onset of auditory feedback matching a prediction of that feedback onset during speaking, a prediction that is absent during passive listening to playback of the auditory feedback. Our model hypothesizes that the auditory cortical response to auditory feedback reflects the mismatch with the prediction: small during speaking, large during listening, with the difference being SIS. Normally, during speaking, auditory feedback matches its predictions, then SIS will be large. Any reductions in SIS will indicate inaccuracy in auditory feedback prediction not matching the actual feedback. We investigated SIS in AD patients [n = 20; mean (SD) age, 60.77 (10.04); female (%), 55.00] and healthy controls [n = 12; mean (SD) age, 63.68 (6.07); female (%), 83.33] through magnetoencephalography (MEG)-based functional imaging. We found a significant reduction in SIS at ∼100 ms in AD patients compared with healthy controls (linear mixed effects model, F (1,57.5) = 6.849, p = 0.011). The results suggest that AD patients generate inaccurate auditory feedback predictions, contributing to abnormalities in AD speech.

Auditory Verb Generation Performance Patterns Dissociate Variants of Primary Progressive Aphasia.

Primary progressive aphasia (PPA) is a clinical syndrome in which patients progressively lose speech and language abilities. Three variants are recognized: logopenic (lvPPA), associated with phonology and/or short-term verbal memory deficits accompanied by left temporo-parietal atrophy; semantic (svPPA), associated with semantic deficits and anterior temporal lobe (ATL) atrophy; non-fluent (nfvPPA) associated with grammar and/or speech-motor deficits and inferior frontal gyrus (IFG) atrophy. Here, we set out to investigate whether the three variants of PPA can be dissociated based on error patterns in a single language task. We recruited 21 lvPPA, 28 svPPA, and 24 nfvPPA patients, together with 31 healthy controls, and analyzed their performance on an auditory noun-to-verb generation task, which requires auditory analysis of the input, access to and selection of relevant lexical and semantic knowledge, as well as preparation and execution of speech. Task accuracy differed across the three variants and controls, with lvPPA and nfvPPA having the lowest and highest accuracy, respectively. Critically, machine learning analysis of the different error types yielded above-chance classification of patients into their corresponding group. An analysis of the error types revealed clear variant-specific effects: lvPPA patients produced the highest percentage of "not-a-verb" responses and the highest number of semantically related nouns (production of baseball instead of throw to noun ball); in contrast, svPPA patients produced the highest percentage of "unrelated verb" responses and the highest number of light verbs (production of take instead of throw to noun ball). Taken together, our findings indicate that error patterns in an auditory verb generation task are associated with the breakdown of different neurocognitive mechanisms across PPA variants. Specifically, they corroborate the link between temporo-parietal regions with lexical processing, as well as ATL with semantic processes. These findings illustrate how the analysis of pattern of responses can help PPA phenotyping and heighten diagnostic sensitivity, while providing insights on the neural correlates of different components of language.

Temporal specificity of abnormal neural oscillations during phonatory events in laryngeal dystonia.

Laryngeal dystonia is a debilitating disorder of voicing in which the laryngeal muscles are intermittently in spasm resulting in involuntary interruptions during speech. The central pathophysiology of laryngeal dystonia, underlying computational impairments in vocal motor control, remains poorly understood. Although prior imaging studies have found aberrant activity in the CNS during phonation in patients with laryngeal dystonia, it is not known at what timepoints during phonation these abnormalities emerge and what function may be impaired. To investigate this question, we recruited 22 adductor laryngeal dystonia patients (15 female, age range = 28.83-72.46 years) and 18 controls (eight female, age range = 27.40-71.34 years). We leveraged the fine temporal resolution of magnetoencephalography to monitor neural activity around glottal movement onset, subsequent voice onset and after the onset of pitch feedback perturbations. We examined event-related beta-band (12-30 Hz) and high-gamma-band (65-150 Hz) neural oscillations. Prior to glottal movement onset, we observed abnormal frontoparietal motor preparatory activity. After glottal movement onset, we observed abnormal activity in the somatosensory cortex persisting through voice onset. Prior to voice onset and continuing after, we also observed abnormal activity in the auditory cortex and the cerebellum. After pitch feedback perturbation onset, we observed no differences between controls and patients in their behavioural responses to the perturbation. But in patients, we did find abnormal activity in brain regions thought to be involved in the auditory feedback control of vocal pitch (premotor, motor, somatosensory and auditory cortices). Our study results confirm the abnormal processing of somatosensory feedback that has been seen in other studies. However, there were several remarkable findings in our study. First, patients have impaired vocal motor activity even before glottal movement onset, suggesting abnormal movement preparation. These results are significant because (i) they occur before movement onset, abnormalities in patients cannot be ascribed to deficits in vocal performance and (ii) they show that neural abnormalities in laryngeal dystonia are more than just abnormal responses to sensory feedback during phonation as has been hypothesized in some previous studies. Second, abnormal auditory cortical activity in patients begins even before voice onset, suggesting abnormalities in setting up auditory predictions before the arrival of auditory feedback at voice onset. Generally, activation abnormalities identified in key brain regions within the speech motor network around various phonation events not only provide temporal specificity to neuroimaging phenotypes in laryngeal dystonia but also may serve as potential therapeutic targets for neuromodulation.

Intact Correction for Self-Produced Vowel Formant Variability in Individuals With Cerebellar Ataxia Regardless of Auditory Feedback Availability.

Purpose Individuals with cerebellar ataxia (CA) caused by cerebellar degeneration exhibit larger reactive compensatory responses to unexpected auditory feedback perturbations than neurobiologically typical speakers, suggesting they may rely more on feedback control during speech. We test this hypothesis by examining variability in unaltered speech. Previous studies of typical speakers have demonstrated a reduction in formant variability (centering) observed during the initial phase of vowel production from vowel onset to vowel midpoint. Centering is hypothesized to reflect feedback-based corrections for self-produced variability and thus may provide a behavioral assay of feedback control in unperturbed speech in the same manner as the compensatory response does for feedback perturbations. Method To comprehensively compare centering in individuals with CA and controls, we examine centering in two vowels (/i/ and /ɛ/) under two contexts (isolated words and connected speech). As a control, we examine speech produced both with and without noise to mask auditory feedback. Results Individuals with CA do not show increased centering compared to age-matched controls, regardless of vowel, context, or masking. Contrary to previous results in neurobiologically typical speakers, centering was not affected by the presence of masking noise in either group. Conclusions The similar magnitude of centering seen with and without masking noise questions whether centering is driven by auditory feedback. However, if centering is at least partially driven by auditory/somatosensory feedback, these results indicate that the larger compensatory response to altered auditory feedback observed in individuals with CA may not reflect typical motor control processes during normal, unaltered speech production.

Laryngeal Dystonia: Multidisciplinary Update on Terminology, Pathophysiology, and Research Priorities.

OBJECTIVE: To delineate research priorities for improving clinical management of laryngeal dystonia, the NIH convened a multidisciplinary panel of experts for a 1-day workshop to examine the current progress in understanding its etiopathophysiology and clinical care. METHODS: The participants reviewed the current terminology of disorder and discussed advances in understanding its pathophysiology since a similar workshop was held in 2005. Clinical and research gaps were identified, and recommendations for future directions were delineated. RESULTS: The panel unanimously agreed to adopt the term "laryngeal dystonia" instead of "spasmodic dysphonia" to reflect the current progress in characterizations of this disorder. Laryngeal dystonia was recognized as a multifactorial, phenotypically heterogeneous form of isolated dystonia. Its etiology remains unknown, whereas the pathophysiology likely involves large-scale functional and structural brain network disorganization. Current challenges include the lack of clinically validated diagnostic markers and outcome measures and the paucity of therapies that address the disorder pathophysiology. CONCLUSION: Research priorities should be guided by challenges in clinical management of laryngeal dystonia. Identification of disorder-specific biomarkers would allow the development of novel diagnostic tools and unified measures of treatment outcome. Elucidation of the critical nodes within neural networks that cause or modulate symptoms would allow the development of targeted therapies that address the underlying pathophysiology. Given the rarity of laryngeal dystonia, future rapid research progress may be facilitated by multicenter, national and international collaborations.

Speech compensation responses and sensorimotor adaptation to formant feedback perturbations.

Control of speech formants is important for the production of distinguishable speech sounds and is achieved with both feedback and learned feedforward control. However, it is unclear whether the learning of feedforward control involves the mechanisms of feedback control. Speakers have been shown to compensate for unpredictable transient mid-utterance perturbations of pitch and loudness feedback, demonstrating online feedback control of these speech features. To determine whether similar feedback control mechanisms exist in the production of formants, responses to unpredictable vowel formant feedback perturbations were examined. Results showed similar within-trial compensatory responses to formant perturbations that were presented at utterance onset and mid-utterance. The relationship between online feedback compensation to unpredictable formant perturbations and sensorimotor adaptation to consistent formant perturbations was further examined. Within-trial online compensation responses were not correlated with across-trial sensorimotor adaptation. A detailed analysis of within-trial time course dynamics across trials during sensorimotor adaptation revealed that across-trial sensorimotor adaptation responses did not result from an incorporation of within-trial compensation response. These findings suggest that online feedback compensation and sensorimotor adaptation are governed by distinct neural mechanisms. These findings have important implications for models of speech motor control in terms of how feedback and feedforward control mechanisms are implemented.

Discrete constriction locations describe a comprehensive range of vocal tract shapes in the Maeda model.

The Maeda model was used to generate a large set of vocoid-producing vocal tract configurations. The resulting dataset (a) produced a comprehensive range of formant frequencies and (b) displayed discrete tongue body constriction locations (palatal, velar/uvular, and lower pharyngeal). The discrete parameterization of constriction location across the vowel space suggests this is likely a fundamental characteristic of the human vocal tract, and not limited to any specific set of vowel contrasts. These findings suggest that in addition to established articulatory-acoustic constraints, fundamental biomechanical constraints of the vocal tract may also explain such discreteness.

Sensorimotor adaptation of speech depends on the direction of auditory feedback alteration.

A hallmark feature of speech motor control is its ability to learn to anticipate and compensate for persistent feedback alterations, a process referred to as sensorimotor adaptation. Because this process involves adjusting articulation to counter the perceived effects of altering acoustic feedback, there are a number of factors that affect it, including the complex relationship between acoustics and articulation and non-uniformities of speech perception. As a consequence, sensorimotor adaptation is hypothesised to vary as a function of the direction of the applied auditory feedback alteration in vowel formant space. This hypothesis was tested in two experiments where auditory feedback was altered in real time, shifting the frequency values of the first and second formants (F1 and F2) of participants' speech. Shifts were designed on a subject-by-subject basis and sensorimotor adaptation was quantified with respect to the direction of applied shift, normalised for individual speakers. Adaptation was indeed found to depend on the direction of the applied shift in vowel formant space, independent of shift magnitude. These findings have implications for models of sensorimotor adaptation of speech.

Taking the sublexical route: brain dynamics of reading in the semantic variant of primary progressive aphasia.

Reading aloud requires mapping an orthographic form to a phonological one. The mapping process relies on sublexical statistical regularities (e.g. 'oo' to |uː|) or on learned lexical associations between a specific visual form and a series of sounds (e.g. yacht to/jɑt/). Computational, neuroimaging, and neuropsychological evidence suggest that sublexical, phonological and lexico-semantic processes rely on partially distinct neural substrates: a dorsal (occipito-parietal) and a ventral (occipito-temporal) route, respectively. Here, we investigated the spatiotemporal features of orthography-to-phonology mapping, capitalizing on the time resolution of magnetoencephalography and the unique clinical model offered by patients with semantic variant of primary progressive aphasia (svPPA). Behaviourally, patients with svPPA manifest marked lexico-semantic impairments including difficulties in reading words with exceptional orthographic to phonological correspondence (irregular words). Moreover, they present with focal neurodegeneration in the anterior temporal lobe, affecting primarily the ventral, occipito-temporal, lexical route. Therefore, this clinical population allows for testing of specific hypotheses on the neural implementation of the dual-route model for reading, such as whether damage to one route can be compensated by over-reliance on the other. To this end, we reconstructed and analysed time-resolved whole-brain activity in 12 svPPA patients and 12 healthy age-matched control subjects while reading irregular words (e.g. yacht) and pseudowords (e.g. pook). Consistent with previous findings that the dorsal route is involved in sublexical, phonological processes, in control participants we observed enhanced neural activity over dorsal occipito-parietal cortices for pseudowords, when compared to irregular words. This activation was manifested in the beta-band (12-30 Hz), ramping up slowly over 500 ms after stimulus onset and peaking at ∼800 ms, around response selection and production. Consistent with our prediction, svPPA patients did not exhibit this temporal pattern of neural activity observed in controls this contrast. Furthermore, a direct comparison of neural activity between patients and controls revealed a dorsal spatiotemporal cluster during irregular word reading. These findings suggest that the sublexical/phonological route is involved in processing both irregular and pseudowords in svPPA. Together these results provide further evidence supporting a dual-route model for reading aloud mediated by the interplay between lexico-semantic and sublexical/phonological neurocognitive systems. When the ventral route is damaged, as in the case of neurodegeneration affecting the anterior temporal lobe, partial compensation appears to be possible by over-recruitment of the slower, serial attention-dependent, dorsal one.

The Visual Word Form Area compensates for auditory working memory dysfunction in schizophrenia.

Auditory working memory impairments feature prominently in schizophrenia. However, the existence of altered and perhaps compensatory neural dynamics, sub-serving auditory working memory, remains largely unexplored. We compared the dynamics of induced high gamma power (iHGP) across cortex in humans during speech-sound working memory in individuals with schizophrenia (SZ) and healthy comparison subjects (HC) using magnetoencephalography (MEG). SZ showed similar task performance to HC while utilizing different brain regions. During encoding of speech sounds, SZ lacked the correlation of iHGP with task performance in posterior superior temporal gyrus (STGp) that was observed in healthy subjects. Instead, SZ recruited the visual word form area (VWFA) during both stimulus encoding and response preparation. Importantly, VWFA activity during encoding correlated with the magnitude of SZ hallucinations, task performance and an independent measure of verbal working memory. These findings suggest that VWFA plasticity is harnessed to compensate for STGp dysfunction in schizophrenia patients with hallucinations.

Optimizing Magnetoencephalographic Imaging Estimation of Language Lateralization for Simpler Language Tasks.

Magnetoencephalographic imaging (MEGI) offers a non-invasive alternative for defining preoperative language lateralization in neurosurgery patients. MEGI indeed can be used for accurate estimation of language lateralization with a complex language task - auditory verb generation. However, since language function may vary considerably in patients with focal lesions, it is important to optimize MEGI for estimation of language function with other simpler language tasks. The goal of this study was to optimize MEGI laterality analyses for two such simpler language tasks that can have compliance from those with impaired language function: a non-word repetition (NWR) task and a picture naming (PN) task. Language lateralization results for these two tasks were compared to the verb-generation (VG) task. MEGI reconstruction parameters (regions and time windows) for NWR and PN were first defined in a presurgical training cohort by benchmarking these against laterality indices for VG. Optimized time windows and regions of interest (ROIs) for NWR and PN were determined by examining oscillations in the beta band (12-30 Hz) a marker of neural activity known to be concordant with the VG laterality index (LI). For NWR, additional ROIs include areas MTG/ITG and for both NWR and PN, the postcentral gyrus was included in analyses. Optimal time windows for NWR were defined as 650-850 ms (stimulus-locked) and -350 to -150 ms (response-locked) and for PN -450 to -250 ms (response-locked). To verify the optimal parameters defined in our training cohort for NWR and PN, we examined an independent validation cohort (n = 30 for NWR, n = 28 for PN) and found high concordance between VG laterality and PN laterality (82%) and between VG laterality and NWR laterality (87%). Finally, in a test cohort (n = 8) that underwent both the intracarotid amobarbital procedure (IAP) test and MEG for VG, NWR, and PN, we identified excellent concordance (100%) with IAP for VG + NWR + PN composite LI, high concordance for PN alone (87.5%), and moderate concordance for NWR alone (66.7%). These findings provide task options for non-invasive language mapping with MEGI that can be calibrated for language abilities of individual patients. Results also demonstrate that more accurate estimates can be obtained by combining laterality estimates obtained from multiple tasks. MEGI.

Cortical-Basal Ganglia-Cerebellar Networks in Unilateral Vocal Fold Paralysis: A Pilot Study.

OBJECTIVES/HYPOTHESIS: To evaluate differences in cortical-basal ganglia-cerebellar functional connectivity between treated unilateral vocal fold paralysis (UVFP) and healthy control cohorts using resting-state functional magnetic resonance imaging (RS-fMRI). STUDY DESIGN: Cross-sectional. METHODS: Ten UVFP study patients treated by type I thyroplasty and 12 control subjects underwent RS-fMRI on a 3-Tesla scanner to evaluate differences in functional connectivity of whole-brain networks. Spontaneous RS-fMRI data were collected using a gradient echo planar pulse sequence, preprocessed, and analyzed to compare seed-to-voxel maps between the two cohorts. Seeds were placed in the caudate, putamen, and globus pallidus divisions of the basal ganglia in both hemispheres. Group contrasts were tested for statistical significance using two-tailed unpaired t tests corrected for multiple comparisons with a cluster false discovery rate threshold of P < .05. RESULTS: UVFP patients demonstrated increased connectivity between both caudate nuclei and the precuneus, a node of the default mode network, compared to healthy controls. Both caudate nuclei also showed decreased connectivity with the left cerebellar hemisphere. The putamen and globus pallidus divisions of the basal ganglia were not abnormally connected to other brain structures. CONCLUSIONS: UVFP patients treated by type I thyroplasty exhibited long-term alterations of cortical-basal ganglia-cerebellar networks thought to be important for self-referential voice quality awareness and learning processes that compensate for changes to the paralyzed hemilarynx. This pilot study on relatively small cohorts adds to growing evidence for persistent central nervous system changes in treated UVFP. Replication studies with larger numbers of subjects will be essential to validate and extend findings. LEVEL OF EVIDENCE: 3b Laryngoscope, 130:460-464, 2020.

Learning and adaptation in speech production without a vocal tract.

How is the complex audiomotor skill of speaking learned? To what extent does it depend on the specific characteristics of the vocal tract? Here, we developed a touchscreen-based speech synthesizer to examine learning of speech production independent of the vocal tract. Participants were trained to reproduce heard vowel targets by reaching to locations on the screen without visual feedback and receiving endpoint vowel sound auditory feedback that depended continuously on touch location. Participants demonstrated learning as evidenced by rapid increases in accuracy and consistency in the production of trained targets. This learning generalized to productions of novel vowel targets. Subsequent to learning, sensorimotor adaptation was observed in response to changes in the location-sound mapping. These findings suggest that participants learned adaptable sensorimotor maps allowing them to produce desired vowel sounds. These results have broad implications for understanding the acquisition of speech motor control.

The FACTS model of speech motor control: Fusing state estimation and task-based control.

We present a new computational model of speech motor control: the Feedback-Aware Control of Tasks in Speech or FACTS model. FACTS employs a hierarchical state feedback control architecture to control simulated vocal tract and produce intelligible speech. The model includes higher-level control of speech tasks and lower-level control of speech articulators. The task controller is modeled as a dynamical system governing the creation of desired constrictions in the vocal tract, after Task Dynamics. Both the task and articulatory controllers rely on an internal estimate of the current state of the vocal tract to generate motor commands. This estimate is derived, based on efference copy of applied controls, from a forward model that predicts both the next vocal tract state as well as expected auditory and somatosensory feedback. A comparison between predicted feedback and actual feedback is then used to update the internal state prediction. FACTS is able to qualitatively replicate many characteristics of the human speech system: the model is robust to noise in both the sensory and motor pathways, is relatively unaffected by a loss of auditory feedback but is more significantly impacted by the loss of somatosensory feedback, and responds appropriately to externally-imposed alterations of auditory and somatosensory feedback. The model also replicates previously hypothesized trade-offs between reliance on auditory and somatosensory feedback and shows for the first time how this relationship may be mediated by acuity in each sensory domain. These results have important implications for our understanding of the speech motor control system in humans.