Semantic Categorization of Naming Responses Based on Prearticulatory Electrical Brain Activity.

PURPOSE: Object naming requires visual decoding, conceptualization, semantic categorization, and phonological encoding, all within 400 to 600 ms of stimulus presentation and before a word is spoken. In this study, we sought to predict semantic categories of naming responses based on prearticulatory brain activity recorded with scalp EEG in healthy individuals. METHODS: We assessed 19 healthy individuals who completed a naming task while undergoing EEG. The naming task consisted of 120 drawings of animate/inanimate objects or abstract drawings. We applied a one-dimensional, two-layer, neural network to predict the semantic categories of naming responses based on prearticulatory brain activity. RESULTS: Classifications of animate, inanimate, and abstract responses had an average accuracy of 80%, sensitivity of 72%, and specificity of 87% across participants. Across participants, time points with the highest average weights were between 470 and 490 milliseconds after stimulus presentation, and electrodes with the highest weights were located over the left and right frontal brain areas. CONCLUSIONS: Scalp EEG can be successfully used in predicting naming responses through prearticulatory brain activity. Interparticipant variability in feature weights suggests that individualized models are necessary for highest accuracy. Our findings may inform future applications of EEG in reconstructing speech for individuals with and without speech impairments.

Impairment of speech auditory feedback error detection and motor correction in post-stroke aphasia.

INTRODUCTION: The present study investigated how damage to left-hemisphere brain networks affects the ability for speech auditory feedback error detection and motor correction in post-stroke aphasia. METHODS: 34 individuals with left-hemisphere stroke and 25 neurologically intact age-matched control participants performed two randomized experimental tasks in which their online speech auditory feedback was altered using externally induced pitch-shift stimuli: 1) vocalization of a steady speech vowel sound /a/, and 2) listening to the playback of the same self-produced vowel vocalizations. Randomized control condition trials were interleaved in between vocalization and listening tasks where no pitch-shift stimuli were delivered. Following each trial, participants pressed a button to indicate whether they detected a pitch-shift error in their speech auditory feedback during vocalization and listening tasks. RESULTS: Our data analysis revealed that speech auditory feedback error detection accuracy rate was significantly lower in the stroke compared with control participants, irrespective of the experimental task (i.e. vocalization vs. listening) and trial condition (i.e. pitch-shifted vs. no-pitch-shift). We found that this effect was associated with the reduced magnitude of speech compensation in the early phase of responses at 150-200 ms following the onset of pitch-shift stimuli in stroke participants. In addition, motor speech compensation deficit in the stroke group was correlated with lower scores on speech repetition tasks as an index of language impairment resulting from aphasia. CONCLUSIONS: These findings provide evidence that left-hemisphere stroke is associated with impaired speech auditory feedback error processing, and such deficits account for specific aspects of language impairment in aphasia.

Slowed Compensation Responses to Altered Auditory Feedback in Post-Stroke Aphasia: Implications for Speech Sensorimotor Integration.

Developing a clearer understanding of impairments that underlie the behavioral characteristics of aphasia is essential for the development of targeted treatments and will help inform theories of speech motor control. Impairments in sensorimotor integration of speech in individuals with conduction aphasia have previously been implicated in their repetition deficits. However, much less is known about the extent to which these integrative deficits occur outside of conduction aphasia and how this manifests behaviorally in areas other than speech repetition. In this study, we aimed to address these issues by examining the behavioral correlates of speech sensorimotor impairment under altered auditory feedback (AAF) and their relationship with the impaired ability to independently correct for online errors during picture naming in people with aphasia. We found that people with aphasia generate slower vocal compensation response to pitch-shift AAF stimuli compared with controls. However, when the timing of responses was controlled for, no significant difference in the magnitude of vocal pitch compensation was observed between aphasia and control groups. Moreover, no relationship was found between self-correction of naming errors and the timing and magnitude of vocal compensation responses to AAF. These findings suggest that slowed compensation is a potential behavioral marker of impaired sensorimotor integration in aphasia.

Neural bases of sensorimotor adaptation in the vocal motor system.

The present study used event-related potential (ERP) recordings to investigate the neural mechanisms of sensorimotor adaptation in response to altered auditory feedback (AAF) during vocal production. 12 healthy speakers were tested under a vocal motor adaptation paradigm in which the fundamental frequency (F0) of their voice auditory feedback was pitch-shifted downward by one semi-tone (- 100 cents) during vowel vocalizations. Behavioral results revealed that subjects adapted to AAF by producing opposing (upward) responses to pitch-shift stimuli, and this adaptive behavior persisted after feedback alteration was removed (washout). We found that adaptation to AAF was accompanied by a significant increase in the amplitude of a parietal ERP activity elicited after the onset of vocalization. However, no such effect was observed for pre-motor ERPs elicited before vocalization onset. Moreover, we found that adaptive vocal responses were negatively correlated with ERPs over the parietal and positively correlated with those over the fronto-central areas after vocalization onset. These findings suggest that vocal motor adaptation is mediated by sensorimotor reprogramming of feedforward motor commands through incorporating auditory feedback, which is indexed by modulation of behavioral and ERP responses to AAF. We suggest that modulation of neural activities in the parietal cortex highlights its significance as a neural interface for sensorimotor integration and indicates its critical role in vocal motor adaptation. Our findings support the notion that the parietal mechanisms are involved in driving adaptive motor behavior to cope with unexpected changes in the sensory environment to accomplish communication goals during vocal production and motor control.

A temporal predictive code for voice motor control: Evidence from ERP and behavioral responses to pitch-shifted auditory feedback.

The predictive coding model suggests that voice motor control is regulated by a process in which the mismatch (error) between feedforward predictions and sensory feedback is detected and used to correct vocal motor behavior. In this study, we investigated how predictions about timing of pitch perturbations in voice auditory feedback would modulate ERP and behavioral responses during vocal production. We designed six counterbalanced blocks in which a +100 cents pitch-shift stimulus perturbed voice auditory feedback during vowel sound vocalizations. In three blocks, there was a fixed delay (500, 750 or 1000 ms) between voice and pitch-shift stimulus onset (predictable), whereas in the other three blocks, stimulus onset delay was randomized between 500, 750 and 1000 ms (unpredictable). We found that subjects produced compensatory (opposing) vocal responses that started at 80 ms after the onset of the unpredictable stimuli. However, for predictable stimuli, subjects initiated vocal responses at 20 ms before and followed the direction of pitch shifts in voice feedback. Analysis of ERPs showed that the amplitudes of the N1 and P2 components were significantly reduced in response to predictable compared with unpredictable stimuli. These findings indicate that predictions about temporal features of sensory feedback can modulate vocal motor behavior. In the context of the predictive coding model, temporally-predictable stimuli are learned and reinforced by the internal feedforward system, and as indexed by the ERP suppression, the sensory feedback contribution is reduced for their processing. These findings provide new insights into the neural mechanisms of vocal production and motor control.

Inflammasome activation in airway epithelial cells after multi-walled carbon nanotube exposure mediates a profibrotic response in lung fibroblasts.

BACKGROUND: In vivo studies have demonstrated the ability of multi-walled carbon nanotubes (MWCNT) to induce airway remodeling, a key feature of chronic respiratory diseases like asthma and chronic obstructive pulmonary disease. However, the mechanism leading to remodeling is poorly understood. Particularly, there is limited insight about the role of airway epithelial injury in these changes. OBJECTIVES: We investigated the mechanism of MWCNT-induced primary human bronchial epithelial (HBE) cell injury and its contribution in inducing a profibrotic response. METHODS: Primary HBE cells were exposed to thoroughly characterized MWCNTs (1.5-24 µg/mL equivalent to 0.37-6.0 µg/cm2) and MRC-5 human lung fibroblasts were exposed to 1:4 diluted conditioned medium from these cells. Flow cytometry, ELISA, immunostainings/immunoblots and PCR analyses were employed to study cellular mechanisms. RESULTS: MWCNT induced NLRP3 inflammasome dependent pyroptosis in HBE cells in a time- and dose-dependent manner. Cell death and cytokine production were significantly reduced by antioxidants, siRNA to NLRP3, a caspase-1 inhibitor (z-WEHD-FMK) or a cathepsin B inhibitor (CA-074Me). Conditioned medium from MWCNT-treated HBE cells induced significant increase in mRNA expression of pro-fibrotic markers (TIMP-1, Tenascin-C, Procollagen 1, and Osteopontin) in human lung fibroblasts, without a concomitant change in expression of TGF-beta. Induction of pro-fibrotic markers was significantly reduced when IL-1ß, IL-18 and IL-8 neutralizing antibodies were added to the conditioned medium or when conditioned medium from NLRP3 siRNA transfected HBE cells was used. CONCLUSIONS: Taken together these results demonstrate induction of a NLRP3 inflammasome dependent but TGF-beta independent pro-fibrotic response after MWCNT exposure.