scholarly journals Language prediction mechanisms in human auditory cortex

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
K. J. Forseth ◽  
G. Hickok ◽  
P. S. Rollo ◽  
N. Tandon

Abstract Spoken language, both perception and production, is thought to be facilitated by an ensemble of predictive mechanisms. We obtain intracranial recordings in 37 patients using depth probes implanted along the anteroposterior extent of the supratemporal plane during rhythm listening, speech perception, and speech production. These reveal two predictive mechanisms in early auditory cortex with distinct anatomical and functional characteristics. The first, localized to bilateral Heschl’s gyri and indexed by low-frequency phase, predicts the timing of acoustic events. The second, localized to planum temporale only in language-dominant cortex and indexed by high-gamma power, shows a transient response to acoustic stimuli that is uniquely suppressed during speech production. Chronometric stimulation of Heschl’s gyrus selectively disrupts speech perception, while stimulation of planum temporale selectively disrupts speech production. This work illuminates the fundamental acoustic infrastructure—both architecture and function—for spoken language, grounding cognitive models of speech perception and production in human neurobiology.

2018 ◽  
Author(s):  
KJ Forseth ◽  
G Hickok ◽  
Patrick Rollo ◽  
N Tandon

AbstractSpoken language is thought to be facilitated by an ensemble of predictive mechanisms, yet the neurobiology of prediction for both speech perception and production remains unknown. We used intracranial recordings (31 patients, 6580 electrodes) from depth probes implanted along the anteroposterior extent of the supratemporal plane during rhythm listening, speech perception, and speech production. This revealed a frequency-multiplexed encoding of sublexical features during entrainment and a traveling wave of high-frequency activity across Heschl’s gyrus. Critically, we isolated two predictive mechanisms in early auditory cortex with distinct anatomical and functional characteristics. The first mechanism, localized to bilateral Heschl’s gyrus and indexed by low-frequency phase, predicts the timing of acoustic events (“when”). The second mechanism, localized to planum temporale in the language-dominant hemisphere and indexed by gamma power, predicts the acoustic consequence of speech motor plans (“what”). This work grounds cognitive models of speech perception and production in human neurobiology, illuminating the fundamental acoustic infrastructure – both architecture and function – for spoken language.


2014 ◽  
Vol 369 (1651) ◽  
pp. 20130297 ◽  
Author(s):  
Jeremy I. Skipper

What do we hear when someone speaks and what does auditory cortex (AC) do with that sound? Given how meaningful speech is, it might be hypothesized that AC is most active when other people talk so that their productions get decoded. Here, neuroimaging meta-analyses show the opposite: AC is least active and sometimes deactivated when participants listened to meaningful speech compared to less meaningful sounds. Results are explained by an active hypothesis-and-test mechanism where speech production (SP) regions are neurally re-used to predict auditory objects associated with available context. By this model, more AC activity for less meaningful sounds occurs because predictions are less successful from context, requiring further hypotheses be tested. This also explains the large overlap of AC co-activity for less meaningful sounds with meta-analyses of SP. An experiment showed a similar pattern of results for non-verbal context. Specifically, words produced less activity in AC and SP regions when preceded by co-speech gestures that visually described those words compared to those words without gestures. Results collectively suggest that what we ‘hear’ during real-world speech perception may come more from the brain than our ears and that the function of AC is to confirm or deny internal predictions about the identity of sounds.


2019 ◽  
Vol 45 (7) ◽  
pp. 1252-1270
Author(s):  
Wouter P. J. Broos ◽  
Aster Dijkgraaf ◽  
Eva Van Assche ◽  
Heleen Vander Beken ◽  
Nicolas Dirix ◽  
...  

2019 ◽  
Author(s):  
Lílian Rodrigues de Almeida ◽  
Paul A. Pope ◽  
Peter Hansen

In our previous studies we supported the claim that the motor theory is modulated by task load. Motoric participation in phonological processing increases from speech perception to speech production, with the endpoints of the dorsal stream having changing and complementary weightings for processing: the left inferior frontal gyrus (LIFG) being increasingly relevant and the left superior temporal gyrus (LSTG) being decreasingly relevant. Our previous results for neurostimulation of the LIFG support this model. In this study we investigated whether our claim that the motor theory is modulated by task load holds in (frontal) aphasia. Person(s) with aphasia (PWA) after stroke typically have damage on brain areas responsible for phonological processing. They may present variable patterns of recovery and, consequently, variable strategies of phonological processing. Here these strategies were investigated in two PWA with simultaneous fMRI and tDCS of the LIFG during speech perception and speech production tasks. Anodal tDCS excitation and cathodal tDCS inhibition should increase with the relevance of the target for the task. Cathodal tDCS over a target of low relevance could also induce compensation by the remaining nodes. Responses of PWA to tDCS would further depend on their pattern of recovery. Responses would depend on the responsiveness of the perilesional area, and could be weaker than in controls due to an overall hypoactivation of the cortex. Results suggest that the analysis of motor codes for articulation during phonological processing remains in frontal aphasia and that tDCS is a promising diagnostic tool to investigate the individual processing strategies.


2008 ◽  
Vol 28 (52) ◽  
pp. 14301-14310 ◽  
Author(s):  
J. Besle ◽  
C. Fischer ◽  
A. Bidet-Caulet ◽  
F. Lecaignard ◽  
O. Bertrand ◽  
...  

2021 ◽  
Vol 11 (5) ◽  
pp. 639
Author(s):  
David Bergeron ◽  
Sami Obaid ◽  
Marie-Pierre Fournier-Gosselin ◽  
Alain Bouthillier ◽  
Dang Khoa Nguyen

Introduction: To date, clinical trials of deep brain stimulation (DBS) for refractory chronic pain have yielded unsatisfying results. Recent evidence suggests that the posterior insula may represent a promising DBS target for this indication. Methods: We present a narrative review highlighting the theoretical basis of posterior insula DBS in patients with chronic pain. Results: Neuroanatomical studies identified the posterior insula as an important cortical relay center for pain and interoception. Intracranial neuronal recordings showed that the earliest response to painful laser stimulation occurs in the posterior insula. The posterior insula is one of the only regions in the brain whose low-frequency electrical stimulation can elicit painful sensations. Most chronic pain syndromes, such as fibromyalgia, had abnormal functional connectivity of the posterior insula on functional imaging. Finally, preliminary results indicated that high-frequency electrical stimulation of the posterior insula can acutely increase pain thresholds. Conclusion: In light of the converging evidence from neuroanatomical, brain lesion, neuroimaging, and intracranial recording and stimulation as well as non-invasive stimulation studies, it appears that the insula is a critical hub for central integration and processing of painful stimuli, whose high-frequency electrical stimulation has the potential to relieve patients from the sensory and affective burden of chronic pain.


1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.


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