04343nas a2200433 4500008004100000022001400041245015100055210006900206260001600275490000700291520297600298653001003274653000903284653001903293653002403312653001103336653001503347653001103362653000903373653001603382653002803398653004603426653002803472100001803500700002303518700002103541700002203562700001803584700001403602700001903616700001703635700002603652700002403678700002103702700002303723700001903746700002303765856012103788 2025 eng d a2050-084X00aThe effect of transcutaneous auricular vagus nerve stimulation on cardiovascular function in subarachnoid hemorrhage patients: A randomized trial.0 aeffect of transcutaneous auricular vagus nerve stimulation on ca c2025 Jan 090 v133 a

BACKGROUND: Subarachnoid hemorrhage (SAH) is characterized by intense central inflammation, leading to substantial post-hemorrhagic complications such as vasospasm and delayed cerebral ischemia. Given the anti-inflammatory effect of transcutaneous auricular vagus nerve stimulation (taVNS) and its ability to promote brain plasticity, taVNS has emerged as a promising therapeutic option for SAH patients. However, the effects of taVNS on cardiovascular dynamics in critically ill patients, like those with SAH, have not yet been investigated. Given the association between cardiac complications and elevated risk of poor clinical outcomes after SAH, it is essential to characterize the cardiovascular effects of taVNS to ensure this approach is safe in this fragile population. Therefore, this study assessed the impact of both acute and repetitive taVNS on cardiovascular function.

METHODS: In this randomized clinical trial, 24 SAH patients were assigned to either a taVNS treatment or a sham treatment group. During their stay in the intensive care unit, we monitored patient electrocardiogram readings and vital signs. We compared long-term changes in heart rate, heart rate variability (HRV), QT interval, and blood pressure between the two groups. Additionally, we assessed the effects of acute taVNS by comparing cardiovascular metrics before, during, and after the intervention. We also explored acute cardiovascular biomarkers in patients exhibiting clinical improvement.

RESULTS: We found that repetitive taVNS did not significantly alter heart rate, QT interval, blood pressure, or intracranial pressure (ICP). However, repetitive taVNS increased overall HRV and parasympathetic activity compared to the sham treatment. The increase in parasympathetic activity was most pronounced from 2 to 4 days after initial treatment (Cohen's = 0.50). Acutely, taVNS increased heart rate, blood pressure, and peripheral perfusion index without affecting the corrected QT interval, ICP, or HRV. The acute post-treatment elevation in heart rate was more pronounced in patients who experienced a decrease of more than one point in their modified Rankin Score at the time of discharge.

CONCLUSIONS: Our study found that taVNS treatment did not induce adverse cardiovascular effects, such as bradycardia or QT prolongation, supporting its development as a safe immunomodulatory treatment approach for SAH patients. The observed acute increase in heart rate after taVNS treatment may serve as a biomarker for SAH patients who could derive greater benefit from this treatment.

FUNDING: The American Association of Neurological Surgeons (ALH), The Aneurysm and AVM Foundation (ALH), The National Institutes of Health R01-EB026439, P41-EB018783, U24-NS109103, R21-NS128307 (ECL, PB), McDonnell Center for Systems Neuroscience (ECL, PB), and Fondazione Neurone (PB).

CLINICAL TRIAL NUMBER: NCT04557618.

10aAdult10aAged10aBlood Pressure10aElectrocardiography10aFemale10aHeart Rate10aHumans10aMale10aMiddle Aged10aSubarachnoid Hemorrhage10aTranscutaneous Electric Nerve Stimulation10aVagus Nerve Stimulation1 aTan, Gansheng1 aHuguenard, Anna, L1 aDonovan, Kara, M1 aDemarest, Phillip1 aLiu, Xiaoxuan1 aLi, Ziwei1 aAdamek, Markus1 aLavine, Kory1 aVellimana, Ananthv, K1 aKummer, Terrance, T1 aOsbun, Joshua, W1 aZipfel, Gregory, J1 aBrunner, Peter1 aLeuthardt, Eric, C uhttps://neurotechcenter.org/publications/2025/effect-transcutaneous-auricular-vagus-nerve-stimulation-cardiovascular03671nas a2200265 4500008004100000245014700041210006900188260001600257520272400273100001802997700002303015700002103038700002203059700001803081700001403099700001903113700001703132700002503149700002403174700002103198700002303219700001903242700002303261856012103284 2024 eng d00aThe effect of transcutaneous auricular vagus nerve stimulation on cardiovascular function in subarachnoid hemorrhage patients: a safety study.0 aeffect of transcutaneous auricular vagus nerve stimulation on ca c2024 Sep 083 a

INTRODUCTION: Subarachnoid hemorrhage (SAH) is characterized by intense central inflammation, leading to substantial post-hemorrhagic complications such as vasospasm and delayed cerebral ischemia. Given the anti-inflammatory effect of transcutaneous auricular vagus nerve stimulation (taVNS) and its ability to promote brain plasticity, taVNS has emerged as a promising therapeutic option for SAH patients. However, the effects of taVNS on cardiovascular dynamics in critically ill patients, like those with SAH, have not yet been investigated. Given the association between cardiac complications and elevated risk of poor clinical outcomes after SAH, it is essential to characterize the cardiovascular effects of taVNS to ensure this approach is safe in this fragile population. Therefore, we assessed the impact of both acute taVNS and repetitive taVNS on cardiovascular function in this study.

METHODS: In this randomized clinical trial, 24 SAH patients were assigned to either a taVNS treatment or a Sham treatment group. During their stay in the intensive care unit, we monitored patient electrocardiogram (ECG) readings and vital signs. We compared long-term changes in heart rate, heart rate variability, QT interval, and blood pressure between the two groups. Additionally, we assessed the effects of acute taVNS by comparing cardiovascular metrics before, during, and after the intervention. We also explored acute cardiovascular biomarkers in patients exhibiting clinical improvement.

RESULTS: We found that repetitive taVNS did not significantly alter heart rate, QT interval, blood pressure, or intracranial pressure. However, taVNS increased overall heart rate variability and parasympathetic activity compared to the sham treatment. The increase in parasympathetic activity was most pronounced from 2-4 days after initial treatment (Cohen's d = 0.50). Acutely, taVNS increased heart rate, blood pressure, and peripheral perfusion index without affecting the corrected QT interval, intracranial pressure, or heart rate variability. The acute post-treatment elevation in heart rate was more pronounced in patients who experienced a decrease of more than one point in their Modified Rankin Score at the time of discharge.

CONCLUSIONS: Our study found that taVNS treatment did not induce adverse cardiovascular effects, such as bradycardia or QT prolongation, supporting its development as a safe immunomodulatory treatment approach for SAH patients. The observed acute increase in heart rate after taVNS treatment may serve as a biomarker for SAH patients who could derive greater benefit from this treatment.

TRIAL REGISTRATION: NCT04557618.

1 aTan, Gansheng1 aHuguenard, Anna, L1 aDonovan, Kara, M1 aDemarest, Phillip1 aLiu, Xiaoxuan1 aLi, Ziwei1 aAdamek, Markus1 aLavine, Kory1 aVellimana, Ananth, K1 aKummer, Terrance, T1 aOsbun, Joshua, W1 aZipfel, Gregory, J1 aBrunner, Peter1 aLeuthardt, Eric, C uhttps://neurotechcenter.org/publications/2024/effect-transcutaneous-auricular-vagus-nerve-stimulation-cardiovascular01911nas a2200349 4500008004100000022001400041245004100055210004000096260001600136300000900152490000700161520102100168653001001189653001001199653002001209653002001229653001101249653001101260653000901271653001801280653001601298653001601314100001301330700001901343700001601362700002201378700002501400700001901425700001901444700001701463856008101480 2024 eng d a2041-172300aGraded decisions in the human brain.0 aGraded decisions in the human brain c2024 May 21 a43080 v153 a

Decision-makers objectively commit to a definitive choice, yet at the subjective level, human decisions appear to be associated with a degree of uncertainty. Whether decisions are definitive (i.e., concluding in all-or-none choices), or whether the underlying representations are graded, remains unclear. To answer this question, we recorded intracranial neural signals directly from the brain while human subjects made perceptual decisions. The recordings revealed that broadband gamma activity reflecting each individual's decision-making process, ramped up gradually while being graded by the accumulated decision evidence. Crucially, this grading effect persisted throughout the decision process without ever reaching a definite bound at the time of choice. This effect was most prominent in the parietal cortex, a brain region traditionally implicated in decision-making. These results provide neural evidence for a graded decision process in humans and an analog framework for flexible choice behavior.

10aAdult10aBrain10aChoice Behavior10aDecision Making10aFemale10aHumans10aMale10aParietal Lobe10aUncertainty10aYoung Adult1 aXie, Tao1 aAdamek, Markus1 aCho, Hohyun1 aAdamo, Matthew, A1 aRitaccio, Anthony, L1 aWillie, Jon, T1 aBrunner, Peter1 aKubanek, Jan uhttps://neurotechcenter.org/publications/2024/graded-decisions-human-brain-000560nas a2200193 4500008004100000245004000041210004000081300000900121490000700130100001300137700001900150700001600169700002200185700002500207700001900232700001900251700001700270856007900287 2024 eng d00aGraded decisions in the human brain0 aGraded decisions in the human brain a43080 v151 aXie, Tao1 aAdamek, Markus1 aCho, Hohyun1 aAdamo, Matthew, A1 aRitaccio, Anthony, L1 aWillie, Jon, T1 aBrunner, Peter1 aKubanek, Jan uhttps://neurotechcenter.org/publications/2024/graded-decisions-human-brain00708nas a2200193 4500008004100000245010200041210006900143300001600212490000600228100002000234700001800254700002400272700001900296700002500315700001900340700001900359700002300378856011300401 2024 eng d00aNeural populations in the language network differ in the size of their temporal receptive windows0 aNeural populations in the language network differ in the size of a1924–19420 v81 aRegev, Tamar, I1 aCasto, Colton1 aHosseini, Eghbal, A1 aAdamek, Markus1 aRitaccio, Anthony, L1 aWillie, Jon, T1 aBrunner, Peter1 aFedorenko, Evelina uhttps://neurotechcenter.org/publications/2024/neural-populations-language-network-differ-size-their-temporal04108nas a2200241 4500008004100000245016200041210006900203260001600272520319000288100002303478700001803501700002603519700001903545700002103564700002403585700002103609700002503630700002303655700002303678700001903701700002303720856012303743 2024 eng d00aNon-invasive Auricular Vagus nerve stimulation for Subarachnoid Hemorrhage (NAVSaH): Protocol for a prospective, triple-blinded, randomized controlled trial.0 aNoninvasive Auricular Vagus nerve stimulation for Subarachnoid H c2024 Mar 193 a

BACKGROUND: Inflammation has been implicated in driving the morbidity associated with subarachnoid hemorrhage (SAH). Despite understanding the important role of inflammation in morbidity following SAH, there is no current effective way to modulate this deleterious response. There is a critical need for a novel approach to immunomodulation that can be safely, rapidly, and effectively deployed in SAH patients. Vagus nerve stimulation (VNS) provides a non-pharmacologic approach to immunomodulation, with prior studies demonstrating VNS can reduce systemic inflammatory markers, and VNS has had early success treating inflammatory conditions such as arthritis, sepsis, and inflammatory bowel diseases. The aim of the Non-invasive Auricular Vagus nerve stimulation for Subarachnoid Hemorrhage (NAVSaH) trial is to translate the use of non-invasive transcutaneous auricular VNS (taVNS) to spontaneous SAH, with our central hypothesis being that implementing taVNS in the acute period following spontaneous SAH attenuates the expected inflammatory response to hemorrhage and curtails morbidity associated with inflammatory-mediated clinical endpoints.

MATERIALS AND METHODS: The overall objectives for the NAHSaH trial are to 1) Define the impact that taVNS has on SAH-induced inflammatory markers in the plasma and cerebrospinal fluid (CSF), 2) Determine whether taVNS following SAH reduces radiographic vasospasm, and 3) Determine whether taVNS following SAH reduces chronic hydrocephalus. Following presentation to a single enrollment site, enrolled SAH patients are randomly assigned twice daily treatment with either taVNS or sham stimulation for the duration of their intensive care unit stay. Blood and CSF are drawn before initiation of treatment sessions, and then every three days during a patient's hospital stay. Primary endpoints include change in the inflammatory cytokine TNF-α in plasma and cerebrospinal fluid between day 1 and day 13, rate of radiographic vasospasm, and rate of requirement for long-term CSF diversion via a ventricular shunt. Secondary outcomes include exploratory analyses of a panel of additional cytokines, number and type of hospitalized acquired infections, duration of external ventricular drain in days, interventions required for vasospasm, continuous physiology data before, during, and after treatment sessions, hospital length of stay, intensive care unit length of stay, and modified Rankin Scale score (mRS) at admission, discharge, and each at follow-up appointment for up to two years following SAH.

DISCUSSION: Inflammation plays a central role in morbidity following SAH. This NAVSaH trial is innovative because it diverges from the pharmacologic status quo by harnessing a novel non-invasive neuromodulatory approach and its known anti-inflammatory effects to alter the pathophysiology of SAH. The investigation of a new, effective, and rapidly deployable intervention in SAH offers a new route to improve outcomes following SAH.

TRIAL REGISTRATION: Clinical Trials Registered, NCT04557618. Registered on September 21, 2020, and the first patient was enrolled on January 4, 2021.

1 aHuguenard, Anna, L1 aTan, Gansheng1 aJohnson, Gabrielle, W1 aAdamek, Markus1 aCoxon, Andrew, T1 aKummer, Terrance, T1 aOsbun, Joshua, W1 aVellimana, Ananth, K1 aLimbrick, David, D1 aZipfel, Gregory, J1 aBrunner, Peter1 aLeuthardt, Eric, C uhttps://neurotechcenter.org/publications/2024/non-invasive-auricular-vagus-nerve-stimulation-subarachnoid-hemorrhage-004492nas a2200409 4500008004100000022001400041245016200055210006900217260000900286300001300295490000700308520319000315653001003505653001103515653001103526653001703537653000903554653001603563653002403579653004203603653002803645653002203673653002803695100002003723700001803743700002303761700001903784700001803803700002103821700001803842700002203860700002003882700002003902700001903922700002003941856012103961 2024 eng d a1932-620300aNon-invasive Auricular Vagus nerve stimulation for Subarachnoid Hemorrhage (NAVSaH): Protocol for a prospective, triple-blinded, randomized controlled trial.0 aNoninvasive Auricular Vagus nerve stimulation for Subarachnoid H c2024 ae03011540 v193 a

BACKGROUND: Inflammation has been implicated in driving the morbidity associated with subarachnoid hemorrhage (SAH). Despite understanding the important role of inflammation in morbidity following SAH, there is no current effective way to modulate this deleterious response. There is a critical need for a novel approach to immunomodulation that can be safely, rapidly, and effectively deployed in SAH patients. Vagus nerve stimulation (VNS) provides a non-pharmacologic approach to immunomodulation, with prior studies demonstrating VNS can reduce systemic inflammatory markers, and VNS has had early success treating inflammatory conditions such as arthritis, sepsis, and inflammatory bowel diseases. The aim of the Non-invasive Auricular Vagus nerve stimulation for Subarachnoid Hemorrhage (NAVSaH) trial is to translate the use of non-invasive transcutaneous auricular VNS (taVNS) to spontaneous SAH, with our central hypothesis being that implementing taVNS in the acute period following spontaneous SAH attenuates the expected inflammatory response to hemorrhage and curtails morbidity associated with inflammatory-mediated clinical endpoints.

MATERIALS AND METHODS: The overall objectives for the NAHSaH trial are to 1) Define the impact that taVNS has on SAH-induced inflammatory markers in the plasma and cerebrospinal fluid (CSF), 2) Determine whether taVNS following SAH reduces radiographic vasospasm, and 3) Determine whether taVNS following SAH reduces chronic hydrocephalus. Following presentation to a single enrollment site, enrolled SAH patients are randomly assigned twice daily treatment with either taVNS or sham stimulation for the duration of their intensive care unit stay. Blood and CSF are drawn before initiation of treatment sessions, and then every three days during a patient's hospital stay. Primary endpoints include change in the inflammatory cytokine TNF-α in plasma and cerebrospinal fluid between day 1 and day 13, rate of radiographic vasospasm, and rate of requirement for long-term CSF diversion via a ventricular shunt. Secondary outcomes include exploratory analyses of a panel of additional cytokines, number and type of hospitalized acquired infections, duration of external ventricular drain in days, interventions required for vasospasm, continuous physiology data before, during, and after treatment sessions, hospital length of stay, intensive care unit length of stay, and modified Rankin Scale score (mRS) at admission, discharge, and each at follow-up appointment for up to two years following SAH.

DISCUSSION: Inflammation plays a central role in morbidity following SAH. This NAVSaH trial is innovative because it diverges from the pharmacologic status quo by harnessing a novel non-invasive neuromodulatory approach and its known anti-inflammatory effects to alter the pathophysiology of SAH. The investigation of a new, effective, and rapidly deployable intervention in SAH offers a new route to improve outcomes following SAH.

TRIAL REGISTRATION: Clinical Trials Registered, NCT04557618. Registered on September 21, 2020, and the first patient was enrolled on January 4, 2021.

10aAdult10aFemale10aHumans10aInflammation10aMale10aMiddle Aged10aProspective Studies10aRandomized Controlled Trials as Topic10aSubarachnoid Hemorrhage10aTreatment Outcome10aVagus Nerve Stimulation1 aHuguenard, Anna1 aTan, Gansheng1 aJohnson, Gabrielle1 aAdamek, Markus1 aCoxon, Andrew1 aKummer, Terrance1 aOsbun, Joshua1 aVellimana, Ananth1 aLimbrick, David1 aZipfel, Gregory1 aBrunner, Peter1 aLeuthardt, Eric uhttps://neurotechcenter.org/publications/2024/non-invasive-auricular-vagus-nerve-stimulation-subarachnoid-hemorrhage03041nas a2200157 4500008004100000022001400041245012600055210006900181260001600250520242400266100001602690700001902706700001902725700001902744856012002763 2024 eng d a2692-820500aNovel Cyclic Homogeneous Oscillation Detection Method for High Accuracy and Specific Characterization of Neural Dynamics.0 aNovel Cyclic Homogeneous Oscillation Detection Method for High A c2024 Mar 233 a

Detecting temporal and spectral features of neural oscillations is essential to understanding dynamic brain function. Traditionally, the presence and frequency of neural oscillations are determined by identifying peaks over 1/f noise within the power spectrum. However, this approach solely operates within the frequency domain and thus cannot adequately distinguish between the fundamental frequency of a non-sinusoidal oscillation and its harmonics. Non-sinusoidal signals generate harmonics, significantly increasing the false-positive detection rate - a confounding factor in the analysis of neural oscillations. To overcome these limitations, we define the fundamental criteria that characterize a neural oscillation and introduce the Cyclic Homogeneous Oscillation (CHO) detection method that implements these criteria based on an auto-correlation approach that determines the oscillation's periodicity and fundamental frequency. We evaluated CHO by verifying its performance on simulated sinusoidal and non-sinusoidal oscillatory bursts convolved with 1/f noise. Our results demonstrate that CHO outperforms conventional techniques in accurately detecting oscillations. Specifically, we determined the sensitivity and specificity of CHO as a function of signal-to-noise ratio (SNR). We further assessed CHO by testing it on electrocorticographic (ECoG, 8 subjects) and electroencephalographic (EEG, 7 subjects) signals recorded during the pre-stimulus period of an auditory reaction time task and on electrocorticographic signals (6 SEEG subjects and 6 ECoG subjects) collected during resting state. In the reaction time task, the CHO method detected auditory alpha and pre-motor beta oscillations in ECoG signals and occipital alpha and pre-motor beta oscillations in EEG signals. Moreover, CHO determined the fundamental frequency of hippocampal oscillations in the human hippocampus during the resting state (6 SEEG subjects). In summary, CHO demonstrates high precision and specificity in detecting neural oscillations in time and frequency domains. The method's specificity enables the detailed study of non-sinusoidal characteristics of oscillations, such as the degree of asymmetry and waveform of an oscillation. Furthermore, CHO can be applied to identify how neural oscillations govern interactions throughout the brain and to determine oscillatory biomarkers that index abnormal brain function.

1 aCho, Hohyun1 aAdamek, Markus1 aWillie, Jon, T1 aBrunner, Peter uhttps://neurotechcenter.org/publications/2024/novel-cyclic-homogeneous-oscillation-detection-method-high-accuracy-100591nas a2200145 4500008004100000245012500041210006900166300001200235490000700247100001600254700001900270700001900289700001900308856011800327 2024 eng d00aNovel cyclic homogeneous oscillation detection method for high accuracy and specific characterization of neural dynamics0 aNovel cyclic homogeneous oscillation detection method for high a aRP916050 v121 aCho, Hohyun1 aAdamek, Markus1 aWillie, Jon, T1 aBrunner, Peter uhttps://neurotechcenter.org/publications/2024/novel-cyclic-homogeneous-oscillation-detection-method-high-accuracy02336nas a2200229 4500008004100000022001400041245012600055210006900181260001600250490000700266520152600273653001001799653002501809653002701834653001101861653004101872100001601913700001901929700001901948700001901967856012001986 2024 eng d a2050-084X00aNovel cyclic homogeneous oscillation detection method for high accuracy and specific characterization of neural dynamics.0 aNovel cyclic homogeneous oscillation detection method for high a c2024 Sep 060 v123 a

Determining the presence and frequency of neural oscillations is essential to understanding dynamic brain function. Traditional methods that detect peaks over 1/ noise within the power spectrum fail to distinguish between the fundamental frequency and harmonics of often highly non-sinusoidal neural oscillations. To overcome this limitation, we define fundamental criteria that characterize neural oscillations and introduce the cyclic homogeneous oscillation (CHO) detection method. We implemented these criteria based on an autocorrelation approach to determine an oscillation's fundamental frequency. We evaluated CHO by verifying its performance on simulated non-sinusoidal oscillatory bursts and validated its ability to determine the fundamental frequency of neural oscillations in electrocorticographic (ECoG), electroencephalographic (EEG), and stereoelectroencephalographic (SEEG) signals recorded from 27 human subjects. Our results demonstrate that CHO outperforms conventional techniques in accurately detecting oscillations. In summary, CHO demonstrates high precision and specificity in detecting neural oscillations in time and frequency domains. The method's specificity enables the detailed study of non-sinusoidal characteristics of oscillations, such as the degree of asymmetry and waveform of an oscillation. Furthermore, CHO can be applied to identify how neural oscillations govern interactions throughout the brain and to determine oscillatory biomarkers that index abnormal brain function.

10aBrain10aElectrocorticography10aElectroencephalography10aHumans10aSignal Processing, Computer-Assisted1 aCho, Hohyun1 aAdamek, Markus1 aWillie, Jon, T1 aBrunner, Peter uhttps://neurotechcenter.org/publications/2024/novel-cyclic-homogeneous-oscillation-detection-method-high-accuracy-002500nas a2200385 4500008004100000022001400041245010500055210006900160260001600229300000900245490000700254520128700261653003001548653001701578653002701595653001101622653002501633653001801658653004601676653001901722100002201741700001901763700001701782700001301799700001901812700001601831700002201847700001801869700002301887700002101910700001901931700002401950700002301974856011701997 2024 eng d a2045-232200aA novel theta-controlled vibrotactile brain-computer interface to treat chronic pain: a pilot study.0 anovel thetacontrolled vibrotactile braincomputer interface to tr c2024 Feb 10 a34330 v143 a

Limitations in chronic pain therapies necessitate novel interventions that are effective, accessible, and safe. Brain-computer interfaces (BCIs) provide a promising modality for targeting neuropathology underlying chronic pain by converting recorded neural activity into perceivable outputs. Recent evidence suggests that increased frontal theta power (4-7 Hz) reflects pain relief from chronic and acute pain. Further studies have suggested that vibrotactile stimulation decreases pain intensity in experimental and clinical models. This longitudinal, non-randomized, open-label pilot study's objective was to reinforce frontal theta activity in six patients with chronic upper extremity pain using a novel vibrotactile neurofeedback BCI system. Patients increased their BCI performance, reflecting thought-driven control of neurofeedback, and showed a significant decrease in pain severity (1.29 ± 0.25 MAD, p = 0.03, q = 0.05) and pain interference (1.79 ± 1.10 MAD p = 0.03, q = 0.05) scores without any adverse events. Pain relief significantly correlated with frontal theta modulation. These findings highlight the potential of BCI-mediated cortico-sensory coupling of frontal theta with vibrotactile stimulation for alleviating chronic pain.

10abrain-computer interfaces10aChronic Pain10aElectroencephalography10aHumans10aLongitudinal Studies10aNeurofeedback10aNon-Randomized Controlled Trials as Topic10aPilot Projects1 aDemarest, Phillip1 aRustamov, Nabi1 aSwift, James1 aXie, Tao1 aAdamek, Markus1 aCho, Hohyun1 aWilson, Elizabeth1 aHan, Zhuangyu1 aBelsten, Alexander1 aLuczak, Nicholas1 aBrunner, Peter1 aHaroutounian, Simon1 aLeuthardt, Eric, C uhttps://neurotechcenter.org/publications/2024/novel-theta-controlled-vibrotactile-brain-computer-interface-treat00790nas a2200229 4500008004100000245010600041210007100147300000900218490000700227100002200234700001900256700001700275700001300292700001900305700001600324700002200340700001800362700002300380700002100403700001100424856012500435 2024 eng d00aA novel theta-controlled vibrotactile brain–computer interface to treat chronic pain: a pilot study0 anovel thetacontrolled vibrotactile brain–computer interface to t a34330 v141 aDemarest, Phillip1 aRustamov, Nabi1 aSwift, James1 aXie, Tao1 aAdamek, Markus1 aCho, Hohyun1 aWilson, Elizabeth1 aHan, Zhuangyu1 aBelsten, Alexander1 aLuczak, Nicholas1 aothers uhttps://neurotechcenter.org/publications/2024/novel-theta-controlled-vibrotactile-brain%E2%80%93computer-interface-treat02268nas a2200337 4500008004100000022001400041245011100055210006900166260001200235300001100247490000800258520124200266653002501508653001001533653000901543653001701552653002001569653001801589653002601607653002501633653001101658653001101669653000901680653001601689100002301705700003201728700001901760700001901779700001901798856011301817 2021 eng d a1095-957200aModulation in cortical excitability disrupts information transfer in perceptual-level stimulus processing.0 aModulation in cortical excitability disrupts information transfe c11/2021 a1184980 v2433 a

Despite significant interest in the neural underpinnings of behavioral variability, little light has been shed on the cortical mechanism underlying the failure to respond to perceptual-level stimuli. We hypothesized that cortical activity resulting from perceptual-level stimuli is sensitive to the moment-to-moment fluctuations in cortical excitability, and thus may not suffice to produce a behavioral response. We tested this hypothesis using electrocorticographic recordings to follow the propagation of cortical activity in six human subjects that responded to perceptual-level auditory stimuli. Here we show that for presentations that did not result in a behavioral response, the likelihood of cortical activity decreased from auditory cortex to motor cortex, and was related to reduced local cortical excitability. Cortical excitability was quantified using instantaneous voltage during a short window prior to cortical activity onset. Therefore, when humans are presented with an auditory stimulus close to perceptual-level threshold, moment-by-moment fluctuations in cortical excitability determine whether cortical responses to sensory stimulation successfully connect auditory input to a resultant behavioral response.

10aAcoustic Stimulation10aAdult10aAged10aAlpha Rhythm10aAuditory Cortex10aBrain Mapping10aCortical Excitability10aElectrocorticography10aFemale10aHumans10aMale10aMiddle Aged1 aMoheimanian, Ladan1 aParaskevopoulou, Sivylla, E1 aAdamek, Markus1 aSchalk, Gerwin1 aBrunner, Peter uhttps://neurotechcenter.org/publications/2021/modulation-cortical-excitability-disrupts-information-transfer