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Kurteff, G. L.

Publications and source records attributed to Kurteff, G. L..

4 recordsLinked to original sources

Mapping of critical prosodic and phonetic networks in post-stroke apraxia of speech

PurposeMany have made proposals to better diagnose and/or classify post-stroke apraxia of speech (AOS), with some arguing for the separation of AOS into behavioral subtypes. Recent studies of primary progressive AOS have promoted a separation of prosodic and phonetic subtypes, aligning with a dual-motor coordination model separating the neural substrates of prosodic and phonetic function. Motivated by the limited corroboration of these subtypes in post-stroke AOS, here we present mapping results in a cohort of stroke survivors aiming to identify distinct neural substrates for prosodic and phonetic aspects of speech motor coordination. MethodsLeft-hemisphere stroke survivors (n = 127; 64 with AOS) received speech-language evaluation and neuroimaging at the Center for the Study and Treatment of Aphasia Recovery (C-STAR). AOS severity was quantified via the Apraxia of Speech Rating Scale (ASRS). We utilized a novel lesion-symptom mapping technique with an emphasis on prediction that identifies ensembles of regions supporting performance in the prosodic and phonetic domains. ResultsAn ensemble of networks supporting prosodic function localized to dorsal and ventral (but primarily dorsal) sensorimotor cortex, as well as a distributed network of white matter pathways connecting Rolandic cortex to auditory regions and cerebellum, emphasizing the role of auditory feedback processing and laryngeal control in supporting prosodic function. A separate but partially overlapping network supporting phonetic function localized primarily to ventral Rolandic cortex and the arcuate fasciculus. ConclusionsThis work represents the first mapping of prosodic and phonetic subtypes in post-stroke AOS in a large cohort of individuals. We hope our results motivate the development of assessment and treatment techniques individually targeting prosodic and phonetic functioning to better serve individuals with AOS and facilitate clinical discussion of the disorder.

neuroscience↗

Processing of auditory feedback in perisylvian and insular cortex

When we speak, we not only make movements with our mouth, lips, and tongue, but we also hear the sound of our own voice. Thus, speech production in the brain involves not only controlling the movements we make, but also auditory and sensory feedback. Auditory responses are typically suppressed during speech production compared to perception, but how this manifests across space and time is unclear. Here we recorded intracranial EEG in seventeen pediatric, adolescent, and adult patients with medication-resistant epilepsy who performed a reading/listening task to investigate how other auditory responses are modulated during speech production. We identified onset and sustained responses to speech in bilateral auditory cortex, with a selective suppression of onset responses during speech production. Onset responses provide a temporal landmark during speech perception that is redundant with forward prediction during speech production. Phonological feature tuning in these "onset suppression" electrodes remained stable between perception and production. Notably, the posterior insula responded at sentence onset for both perception and production, suggesting a role in multisensory integration during feedback control.

neuroscience↗

Inhibitory control of speech production in the human premotor frontal cortex

Natural speech is full of starts and stops. Here, we studied the neural mechanisms that underlie the inhibitory control of speech, specifically the ability to stop speaking on demand. We recorded direct cortical activity while participants made continuous speech production and were given a visual cue to stop speaking. Neural recordings revealed activity in the premotor frontal cortex associated with speech stopping. Cortical sites showing stop activity were largely distinct from sites involved in active speech production or, more specifically, encoding articulatory movements. Electrocortical stimulation mapping at many premotor sites with stop activity caused involuntary speech arrest, an immediate inability to speak or vocalize. Furthermore, many speech arrest sites did not co-localize with neural activity correlating with speech motor planning or execution, contrary to this long-assumed function in clinical brain mapping. Together, these results suggest a previously unknown premotor cortical network that underlies the inhibitory control of speech, which has significant implications for understanding the dynamics of normal and altered speech production, as well as clinical brain mapping.

neuroscience↗

Speaker-induced suppression in EEG during a naturalistic reading and listening task

Speaking elicits a suppressed neural response when compared to listening to others speech, a phenomenon known as speaker-induced suppression (SIS). Previous research has focused on investigating SIS at constrained levels of linguistic representation, such as the individual phoneme and word level. Here we present scalp EEG data from a dual speech perception and production task where participants read sentences aloud then listened to playback of themselves reading those sentences. Playback was separated into predictable repetition of the previous trial and unpredictable, randomized repetition of a former trial to investigate the role predictive processing plays in SIS. Concurrent EMG was recorded to control for movement artifact during speech production. In line with previous research, event-related potential analyses at the sentence level demonstrated suppression of early auditory components of the EEG for production compared to perception. To evaluate whether specific neural representations contribute to SIS (in contrast with a global gain change), we fit linear encoding models that predicted scalp EEG based on phonological features, EMG activity, and task condition. We found that phonological features were encoded similarly between production and perception. However, this similarity was only observed when controlling for movement by using the EMG response as an additional regressor. Our results suggest SIS is at the representational level a global gain change between perception and production, not the suppression of specific characteristics of the neural response. We also detail some important considerations when analyzing EEG during continuous speech production.

neuroscience↗