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Advances in Mobile Brain/Body Imaging (MoBI) technology allows for real-time measurements of human brain dynamics during every day, natural, real-life situations. This special issue Time to Move brings together a collection of experimental papers, targeted reviews and opinion articles that lay out the latest MoBI findings. A wide range of topics across different fields are covered including art, athletics, virtual reality, and mobility. What unites these diverse topics is the common goal to enhance and restore human abilities by reaching a better understanding on how cognition is implemented by the brain-body relationship. The breadth and novelty of paradigms and findings reported here positions MoBI as a new frontier in the field of human cognitive neuroscience.

Behavioral findings suggest that aging alters the involvement of cortical sensorimotor mechanisms in postural control. However, corresponding accounts of the underlying neural mechanisms remain sparse, especially the extent to which these mechanisms are affected during more demanding tasks. Here, we set out to elucidate cortical correlates of altered postural stability in younger and older adults. 3D body motion tracking and high-density electroencephalography (EEG) were measured while 14 young adults (mean age = 24 years, 43% women) and 14 older adults (mean age = 77 years, 50% women) performed a continuous balance task under four different conditions. Manipulations were applied to the base of support (either regular or tandem (heel-to-toe) stance) and visual input (either static visual field or dynamic optic flow). Standing in tandem, the more challenging position, resulted in increased sway for both age groups, but for the older adults, only this effect was exacerbated when combined with optic flow compared to the static visual display. These changes in stability were accompanied by neuro-oscillatory modulations localized to midfrontal and parietal regions. A cluster of electro-cortical sources localized to the supplementary motor area showed a large increase in theta spectral power (4-7 Hz) during tandem stance, and this modulation was much more pronounced for the younger group. Additionally, the older group displayed widespread mu (8-12 Hz) and beta (13-30 Hz) suppression as balance tasks placed more demands on postural control, especially during tandem stance. These findings may have substantial utility in identifying early cortical correlates of balance impairments in otherwise healthy older adults.

The nature and course of limitations in everyday function in the early clinical stages of cognitive decline is not well known.We compared complex everyday functional profiles at baseline in 59 community-dwelling older individuals with normal cognitive performance who went on to develop incident mild cognitive impairment (MCI) ("pre-MCI") with 284 older individuals who remained cognitively normal over follow-up.The mean number of limitations on complex everyday function at baseline was 3.1 ± 3.0 in the 59 pre-MCI cases and 2.0 ± 2.4 in the 284 normal controls (P = .003). Pre-MCI cases had limitations in traveling, entertaining, remembering appointments, and hobbies compared to normal controls. A progressive increase in mild limitations on complex everyday function preceded the incidence of MCI (mean change: pre-MCI 1.9 ± 3.6 vs normal controls 0.5 ± 2.7, P.001).Prodromal stages of MCI are associated with progressive mild limitations in complex activities of daily living.

Assessment of everyday activities is central to the diagnosis of dementia. Yet, little is known about brain processes associated with everyday functional limitations, particularly during early stages of cognitive decline. Twenty-six older adults (mean = 74.9 y) were stratified by risk using the Montreal Cognitive Assessment battery (MoCA, range: 0- 30) to classify individuals as higher (22-26) and lower risk (27+) of cognitive impairment. We investigated everyday function using a gait task designed to destabilize posture and applied Mobile Brain/Body Imaging. We predicted that participants would increase step width to gain stability, yet the underlying neural signatures would be different for lower versus higher risk individuals. Step width and fronto-parietal activation increased during visually perturbed input. Frontomedial theta increased in higher risk individuals during perturbed and unperturbed inputs. Left sensorimotor beta decreased in lower risk individuals during visually perturbed input. Modulations in theta and beta power were associated with MoCA scores. Our findings suggest that older adults at-risk of cognitive impairment can be characterized by a unique neural signature of everyday function.

Assessment of everyday activities are central to the diagnosis of pre-dementia and dementia. Yet, little is known about the brain substrates and processes that contribute to everyday functional impairment, particularly during early stages of cognitive decline. We investigated everyday function using a complex gait task in normal older adults stratified by risk of cognitive impairment. We applied a novel EEG approach, which combines electroencephalographic with 3D-body tracking technology to measure brain-gait dynamics with millisecond precision while participants are in motion. Twenty-six participants (mean age = 74.9 years) with cognitive and everyday functional profiles within the normal range for their age and sex were ranked for risk of cognitive impairment. We used the Montreal Cognitive Assessment battery, a global index of cognition with a range from 0 to 30, to classify individuals as being at higher (22-26) and lower risk (27+). Individuals walking on a treadmill were exposed to visual perturbation designed to destabilize gait. Assuming that brain changes precede behavioral decline, we predicted that older adults increase step width to gain stability, yet the underlying neural signatures would be different for lower versus higher risk individuals. When pooling across risk groups, we found that step width increased and fronto-parietal activation shifted from transient, during swing phases, to sustained across the gait cycle during visually perturbed input. As predicted, step width increased in both groups but underlying neural signatures were different. Fronto-medial theta (3-7Hz) power of gait-related brain oscillations were increased in higher risk individuals during both perturbed and unperturbed inputs. On the other hand, left central gyri beta (13-28Hz) power was decreased in lower risk individuals, specifically during visually perturbed input. Finally, relating MoCA scores to spectral power pooled across fronto-parietal regions, we found associations between increased theta power and worse MoCA scores and between decreased beta power and better MoCA scores.Able-bodied older adults at-risk of cognitive impairment are characterized by unique neural signatures of mobility. Stronger reliance on frontomedial theta activation in at-risk individuals may reflect higher-order compensatory responses for deterioration of basic sensorimotor processes. Region and spectral-specific signatures of mobility may provide brain targets for early intervention against everyday functional decline.

During navigation of complex environments, the brain must continuously adapt to both external demands, such as fluctuating sensory inputs, and internal demands, such as engagement in a cognitively demanding task. Previous studies have demonstrated changes in behavior and gait with increased sensory and cognitive load, but the underlying cortical mechanisms remain largely unknown. In the present study, in a mobile brain/body imaging (MoBI) approach, 16 young adults walked on a treadmill with high-density EEG while 3-dimensional (3D) motion capture tracked kinematics of the head and feet. Visual load was manipulated with the presentation of optic flow with and without continuous mediolateral perturbations. The effects of cognitive load were assessed by the performance of a go/no-go task on half of the blocks. During increased sensory load, participants walked with shorter and wider strides, which may indicate a more restrained pattern of gait. Interestingly, cognitive task engagement attenuated these effects of sensory load on gait. Using an independent component analysis and dipole-fitting approach, we found that cautious gait was accompanied by neuro-oscillatory modulations localized to frontal (supplementary motor area, anterior cingulate cortex) and parietal (inferior parietal lobule, precuneus) areas. Our results show suppression in alpha/mu (8–12 Hz) and beta (13–30 Hz) rhythms, suggesting enhanced activation of these regions with unreliable sensory inputs. These findings provide insight into the neural correlates of gait adaptation and may be particularly relevant to older adults who are less able to adjust to ongoing cognitive and sensory demands while walking. NEW & NOTEWORTHY The neural underpinnings of gait adaptation in humans are poorly understood. To this end, we recorded high-density EEG combined with three-dimensional body motion tracking as participants walked on a treadmill while exposed to full-field optic flow stimulation. Perturbed visual input led to a more cautious gait pattern with neuro-oscillatory modulations localized to premotor and parietal regions. Our findings show a possible brain-behavior link that might further our understanding of gait and mobility impairments.

Individuals with a diagnosis of multiple sclerosis (MS) often present with deficits in the cognitive as well as the motor domain. The ability to perform tasks that rely on both domains may therefore be particularly impaired. Yet, behavioral studies designed to measure costs associated with performing two tasks at the same time such as dual-task walking have yielded mixed results. Patients may mobilize additional brain resources to sustain good levels of performance. To test this hypothesis, we acquired event-related potentials (ERP) in thirteen individuals with MS and fifteen healthy control (HC) participants performing a Go/NoGo response inhibition task while sitting (i.e., single task) or walking on a treadmill (i.e., dual-task). In previous work, we showed that the nogo-N2 elicited by the cognitive task was reduced when healthy adults are also asked to walk, and that nogo-N2 reduction was accompanied by sustained dual-task performance. We predicted that some MS patients, similar to their healthy peers, may mobilize N2-indexed brain resources and thereby reduce costs. Somewhat to our surprise, the HC group performed the Go/NoGo task more accurately while walking, thus showing a dual-task benefit, whereas, in line with expectation, the MS group showed a trend towards dual-task costs. The expected nogo-N2 reduction during dual-task walking was found in the HC group, but was not present at the group level in the MS group, suggesting that this group did not modulate the nogo-N2 process in response to higher task load. Regression analysis for the pooled sample revealed a robust link between nogo-N2 reduction and better dual-task performance. We conclude that impaired nogo-N2 adaptation reflects a neurophysiological marker of cognitive-motor dysfunction in MS.

Deficits in cognitive control have been considered a core dysfunction of psychopathy, responsible for disrupted self-control. We investigated cognitive control impairments, including difficulties with task switching, failure of response inhibition, and inability to adjust speed of responding. Participants included 16 subjects with psychopathic traits (Ps), and 22 healthy controls (HCs). We recorded behavioral responses during a Task Switching paradigm, a probe of flexible behavioral adaptation to changing contexts; and a Go/NoGo Task, which assesses response inhibition and indexes behavioral impulsivity. During task switching, Ps evidenced impairments shifting set when conflicting (incongruent) information was presented, but performed as well as HCs in the absence of such conflict. In addition, when they encountered these difficulties, they failed to adjust their speed of responding. Ps presented also with deficits in response inhibition, with many commission errors on the Go/NoGo Task. This study identified impairments in response inhibition and in set shifting in psychopathic individuals. When shifting set, they evidenced difficulties refocusing on a new task when it was incongruent with the previous task. These deficits interfere with regulation of ongoing behavior and disrupt self-regulation. Our findings suggest abnormal neural processing during suppression of inappropriate responses in psychopathic individuals.

Advancements in acquisition technology and signal-processing techniques have spurred numerous recent investigations on the electro-cortical signals generated during whole-body motion. This approach, termed Mobile Brain/Body Imaging (MoBI), has the potential to elucidate the neural correlates of perceptual and cognitive processes during real-life activities, such as locomotion. However, as of yet, no one has assessed the long-term stability of event-related potentials (ERPs) recorded under these conditions. Therefore, the objective of the current study was to evaluate the test-retest reliability of cognitive ERPs recorded while walking. High-density EEG was acquired from 12 young adults on two occasions, separated by an average of 2.3 years, as they performed a Go/No-Go response inhibition paradigm. During each testing session, participants performed the task while walking on a treadmill and seated. Using the intraclass correlation coefficient (ICC) as a measure of agreement, we focused on two well-established neurophysiological correlates of cognitive control, the N2 and P3 ERPs. Following ICA-based artifact rejection, the earlier N2 yielded good to excellent levels of reliability for both amplitude and latency, while measurements for the later P3 component were generally less robust but still indicative of adequate to good levels of stability. Interestingly, the N2 was more consistent between walking sessions, compared to sitting, for both hits and correct rejection trials. In contrast, the P3 waveform tended to have a higher degree of consistency during sitting conditions. Overall, these results suggest that the electro-cortical signals obtained during active walking are representative of stable indices of neurophysiological function.

OBJECTIVE: Increased susceptibility to emotional triggers and poor response inhibition are important in the etiology of violence in schizophrenia. Our goal was to evaluate abnormalities in neurophysiological mechanisms underlying response inhibition and emotional processing in violent patients with schizophrenia (VS) and 3 different comparison groups: nonviolent patients (NV), healthy controls (HC) and nonpsychotic violent subjects (NPV). METHODS: We recorded high-density Event-Related Potentials (ERPs) and behavioral responses during an Emotional Go/NoGo Task in 35 VS, 24 NV, 28 HC and 31 NPV subjects. We also evaluated psychiatric symptoms and impulsivity. RESULTS: The neural and behavioral deficits in violent patients were most pronounced when they were presented with negative emotional stimuli: They responded more quickly than NV when they made commission errors (ie, failure of inhibition), and evidenced N2 increases and P3 decreases. In contrast, NVs showed little change in reaction time or ERP amplitude with emotional stimuli. These N2 and P3 amplitude changes in VSs showed a strong association with greater impulsivity. Besides these group specific changes, VSs shared deficits with NV, mostly N2 reduction, and with violent nonpsychotic subjects, particularly P3 reduction. CONCLUSION: Negative affective triggers have a strong impact on violent patients with schizophrenia which may have both behavioral and neural manifestations. The resulting activation could interfere with response inhibition. The affective disruption of response inhibition, identified in this study, may index an important pathway to violence in schizophrenia and suggest new modes of treatment. Language: en

article i nfo Visual processing studies have repeatedly shown impairment in patients with schizophrenia compared to healthy controls. Electroencephalography (EEG) and, specifically, visual evoked potential (VEP) studies have identified an early marker of this impairment in the form of a decrement in the P1 component of the VEP in patients and their clinically unaffected first-degree relatives. Much behavioral and neuroimaging re- search has implicated specific dysfunction of either the subcortical magnocellular pathway or the cortical vi- sual dorsal stream in this impairment. In this study, EEG responses were obtained to the contrast modulation of checkerboard stimuli using the VESPA (Visual Evoked Spread Spectrum Analysis) method. This was done for a high contrast condition and, in order to bias the stimuli towards the magnocellular pathway, a low con- trast condition. Standard VEPs were also obtained using high contrast pattern reversing checkerboards. Re- sponses were measured using high-density electrical scalp recordings in 29 individuals meeting DSM-IV criteria for schizophrenia and in 18 control subjects. Replicating previous research, a large (Cohen's d=1.11) reduction in the P1 component of the VEP was seen in patients when compared with controls with no corresponding difference in the VESPA response to high contrast stimuli. In addition, the low- contrast VESPA displayed no difference between patients and controls. Furthermore, no differences were seen between patients and controls for the C1 components of either the VEP or the high-contrast VESPA. Based on the differing acquisition methods between VEP and VESPA, we discuss these results in terms of con- trast gain control and the possibility of dysfunction at the cortical level with initial afferent activity into V1 along the magnocellular pathway being intact when processing is biased towards that pathway using low contrast stimuli.

Evidence has emerged for age-related amplification of basic sensory processing indexed by early components of the visual evoked potential (VEP). However, since these age-related effects have been incidental to the main focus of these studies, it is unclear whether they are performance dependent or alternately, represent intrinsic sensory processing changes. High-density VEPs were acquired from 19 healthy elderly and 15 young control participants who viewed alphanumeric stimuli in the absence of any active task. The data show both enhanced and delayed neural responses within structures of the ventral visual stream, with reduced hemispheric asymmetry in the elderly that may be indicative of a decline in hemispheric specialization. Additionally, considerably enhanced early frontal cortical activation was observed in the elderly, suggesting frontal hyper-activation. These age-related differences in early sensory processing are discussed in terms of recent proposals that normal aging involves large-scale compensatory reorganization. Our results suggest that such compensatory mechanisms are not restricted to later higher-order cognitive processes but may also be a feature of early sensory-perceptual processes.

PUBLISHED, Mismatch negativity (MMN) is a negative-going event-related potential (ERP) component that occurs in response to intermittent changes in constant auditory backgrounds. A consistent finding across a large number of studies has been impaired MMN generation in schizophrenia, which has been interpreted as evidence for fundamental deficits in automatic auditory sensory processing. The aim of this study was to investigate the extent to which dysfunction in MMN generation might represent an endophenotypic marker for schizophrenia.

Background Variation at the dysbindin gene ( DTNBP1 ) has been associated with increased risk for schizophrenia in numerous independent samples and recently with deficits in general and domain-specific cognitive processing. The relationship between dysbindin risk variants and sensory-level deficits in schizophrenia remains to be explored. We investigated P1 performance, a component of early visual processing on which both patients and their relatives show deficits, in carriers and noncarriers of a known dysbindin risk haplotype. Methods Event-related potential responses to simple visual isolated-check stimuli were measured using high-density electrical scalp recordings in 26 individuals meeting DSM-IV criteria for schizophrenia, comprising 14 patients who were carriers of the dysbindin risk haplotype and 12 patients who were nonrisk haplotype carriers. Results Carriers of the dysbindin risk haplotype demonstrated significantly reduced P1 amplitudes compared with noncarriers. A large effect size of d=.89 was calculated for the difference in P1 amplitude over scalp sites where the deficit was maximal. Conclusions The P1 deficits associated with a dysbindin risk haplotype previously identified in our sample presents functional confirmation of its deleterious effect on brain activity. Building on evidence of dysbindin's role in higher cognitive function, these early visual processing deficits suggest a generalized role for dysbindin in brain function and is likely to be part of the mechanism by which illness susceptibility is mediated.

Several structural brain abnormalities have been associated with aggression in patients with schizophrenia. However, little is known about shared and distinct abnormalities underlying aggression in these subjects and non-psychotic violent individuals. We applied a region-of-interest volumetric analysis of the amygdala, hippocampus, and thalamus bilaterally, as well as whole brain and ventricular volumes to investigate violent (n = 37) and non-violent chronic patients (n = 26) with schizophrenia, non-psychotic violent (n = 24) as well as healthy control subjects (n = 24). Shared and distinct volumetric abnormalities were probed by analysis of variance with the factors violence (non-violent versus violent) and diagnosis (non-psychotic versus psychotic), adjusted for substance abuse, age, academic achievement and negative psychotic symptoms. Patients showed elevated vCSF volume, smaller left hippocampus and smaller left thalamus volumes. This was particularly the case for non-violent individuals diagnosed with schizophrenia. Furthermore, patients had reduction in right thalamus size. With regard to left amygdala, we found an interaction between violence and diagnosis. More specifically, we report a double dissociation with smaller amygdala size linked to violence in non-psychotic individuals, while for psychotic patients smaller size was linked to non-violence. Importantly, the double dissociation appeared to be mostly driven by substance abuse. Overall, we found widespread morphometric abnormalities in subcortical regions in schizophrenia. No evidence for shared volumetric abnormalities in individuals with a history of violence was found. Finally, left amygdala abnormalities in non-psychotic violent individuals were largely accounted for by substance abuse. This might be an indication that the association between amygdala reduction and violence is mediated by substance abuse. Our results indicate the importance of structural abnormalities in aggressive individuals.

We investigated anticipatory and consummatory reward processing in cocaine addiction. In addition, we set out to assess whether task-monitoring systems were appropriately recalibrated in light of variable reward schedules. We also examined neural measures of task-monitoring and reward processing as a function of hedonic tone, since anhedonia is a vulnerability marker for addiction that is obviously germane in the context of reward processing.High-density event-related potentials were recorded while participants performed a speeded response task that systematically varied anticipated probabilities of reward receipt. The paradigm dissociated feedback regarding task success (or failure) from feedback regarding the value of reward (or loss), so that task-monitoring and reward processing could be examined in partial isolation. Twenty-three active cocaine abusers and 23 age-matched healthy controls participated.Cocaine abusers showed amplified anticipatory responses to reward predictive cues, but crucially, these responses were not as strongly modulated by reward probability as in controls. Cocaine users also showed blunted responses to feedback about task success or failure and did not use this information to update predictions about reward. In turn, they showed clearly blunted responses to reward feedback. In controls and users, measures of anhedonia were associated with reward motivation. In cocaine users, anhedonia was also associated with diminished monitoring and reward feedback responses.Findings imply that reward anticipation and monitoring deficiencies in addiction are associated with increased responsiveness to reward cues but impaired ability to predict reward in light of task contingencies, compounded by deficits in responding to actual reward outcomes.

Executive function deficits and reward dysregulation, which mainly manifests as anhedonia, are well documented in drug abusers. We investigated specific aspects of executive function (inhibitory control and cognitive control), as well as anhedonia, in a cohort of current cocaine abusers in order to ascertain to what extent these factors are associated with more severe drug dependence. Participants filled out questionnaires relating to anhedonia and their addiction history. Participants also performed a response inhibition task while high-density event-related potentials (ERPs) were recorded. Electrophysiological responses to successful inhibitions (N2/P3 components) and to commission errors (ERN/Pe components) were compared between 23 current users of cocaine and 27 non-using controls. A regression model was performed to determine the association of our measures of reward dysregulation and executive function with addiction severity. As expected, cocaine users performed more poorly than controls on the inhibitory control task and showed significant electrophysiological differences. They were also generally more anhedonic than controls. Higher levels of anhedonia were associated with more severe substance use, whereas the level of executive dysfunction was not associated with more severe substance use. However, N2 amplitude was associated with duration of drug use. Further, inhibitory control and anhedonia were correlated, but only in controls. These data suggest that while executive dysfunction characterizes drug abuse, it is anhedonia, independent of executive dysfunction, that is most strongly associated with more severe use.

Walking while simultaneously performing cognitively demanding tasks such as talking or texting are typical complex behaviors in our daily routines. Little is known about neural mechanisms underlying cortical resource allocation during such mobile actions, largely due to portability limitations of conventional neuroimaging technologies. We applied an EEG-based Mobile Brain-Body Imaging (MOBI) system that integrates high-density event-related potential (ERP) recordings with simultaneously acquired foot-force sensor data to monitor gait patterns and brain activity. We compared behavioral and ERP measures associated with performing a Go/NoGo response-inhibition task under conditions where participants (N = 18) sat in a stationary way, walked deliberately or walked briskly. This allowed for assessment of effects of increasing dual-task load (i.e. walking speed) on neural indices of inhibitory control. Stride time and variability were also measured during inhibitory task performance and compared to stride parameters without task performance, thereby assessing reciprocal dual-task effects on gait parameters. There were no task performance differences between sitting and either walking condition, indicating that participants could perform both tasks simultaneously without suffering dual-task costs. However, participants took longer strides under dual-task load, likely indicating an adaptive mechanism to reduce inter-task competition for cortical resources. We found robust differences in amplitude, latency and topography of ERP components (N2 and P3) associated with inhibitory control between the sitting and walking conditions. Considering that participants showed no dual-task performance costs, we suggest that observed neural alterations under increasing task-load represent adaptive recalibration of the inhibitory network towards a more controlled and effortful processing mode, thereby optimizing performance under dual-task situations.

We assessed the role of alpha-band oscillatory activity during a task-switching design that required participants to switch between an auditory and a visual task, while task-relevant audio-visual inputs were simultaneously presented. Instructional cues informed participants which task to perform on a given trial and we assessed alpha-band power in the short 1.35-second period intervening between the cue and the task-imperative stimuli, on the premise that attentional biasing mechanisms would be deployed to resolve competition between the auditory and visual inputs. Prior work had shown that alpha-band activity was differentially deployed depending on the modality of the cued task. Here, we asked whether this activity would, in turn, be differentially deployed depending on whether participants had just made a switch of task, or were being asked to simply repeat the task. It is well-established that performance speed and accuracy are poorer on switch than on repeat trials. Here, however, the use of instructional cues completely mitigated these classic switch-costs. Measures of alpha-band synchronization/desynchronization showed that there was indeed greater and earlier differential deployment of alpha-band activity on switch versus repeat trials. Contrary to our hypothesis, this differential effect was entirely due to changes in the amount of desynchronization observed during switch and repeat trials of the visual task, with more desynchronization over both posterior and frontal scalp regions during switch-visual trials. These data imply that particularly vigorous, and essentially fully effective, anticipatory biasing mechanisms resolved the competition between competing auditory and visual inputs when a rapid switch of task was required.

The auditory system is organized such that progressively more complex features are represented across successive cortical hierarchical stages. Just when and where the processing of phonemes, fundamental elements of the speech signal, is achieved in this hierarchy remains a matter of vigorous debate. Non-invasive measures of phonemic representation have been somewhat equivocal. While some studies point to a primary role for middle/anterior regions of the superior temporal gyrus (STG), others implicate the posterior STG. Differences in stimulation, task and inter-individual anatomical/functional variability may account for these discrepant findings. Here, we sought to clarify this issue by mapping phonemic representation across left perisylvian cortex, taking advantage of the excellent sampling density afforded by intracranial recordings in humans. We asked whether one or both major divisions of the STG were sensitive to phonemic transitions. The high signal-to-noise characteristics of direct intracranial recordings allowed for analysis at the individual participant level, circumventing issues of inter-individual anatomic and functional variability that may have obscured previous findings at the group level of analysis. The mismatch negativity (MMN), an electro-physiological response elicited by changes in repetitive streams of stimulation, served as our primary dependent measure. Oddball configurations of pairs of phonemes, spectro-temporally matched non-phonemes, and simple tones were presented. The loci of the MMN clearly differed as a function of stimulus type. Phoneme representation was most robust over middle/anterior STG/STS, but was also observed over posterior STG/SMG. These data point to multiple phonemic processing zones along perisylvian cortex, both anterior and posterior to primary auditory cortex. This finding is considered within the context of a dual stream model of auditory processing in which functionally distinct ventral and dorsal auditory processing pathways may be engaged by speech stimuli.

The present study investigated the feasibility of acquiring high-density event-related brain potential (ERP) recordings during treadmill walking in human subjects. The work builds upon recent studies testing the applicability of real-world tasks while obtaining electroencephalographic (EEG) recordings. Participants performed a response inhibition GO/NOGO task - designed to evoke a P3 component for correct response inhibitions and an error-related negativity (ERN) for incorrect commission errors - while speed of walking was experimentally manipulated. Robust P3 and ERN components were obtained under all experimental conditions - while participants were sitting, walking at moderate speed (2.4 km/hour), or walking rapidly (5 km/hour). Signal-to-noise ratios were remarkably similar across conditions, pointing to the feasibility of high-fidelity ERP recordings under relatively vigorous activity regimens. There is considerable research and clinical motivation to obtain high quality neurophysiological measures under more naturalistic environmental settings such as these. Strong links between cognitive load and gait abnormalities are seen in a number of clinical populations and these MoBI technologies provide highly promising methods for gaining insights into the underlying pathophysiology.

Response inhibition deficits are well-documented in drug users, and are related to the impulsive tendencies characteristic of the addictive phenotype. Addicts also show significant motivational issues that may accentuate these inhibitory deficits. We investigated the extent to which these inhibitory deficits are present in abstinence. Salience of the task stimuli was also manipulated on the premise that emotionally-valenced inputs might impact inhibitory efficacy by overcoming the blunted responses to everyday environmental inputs characteristic of this population. Participants performed response inhibition tasks consisting of both neutral and emotionally valenced stimuli while high-density event-related potentials (ERPs) were recorded. Electrophysiological responses (N2/P3 components) to successful inhibitions in abstinent abusers (N = 20) and non-using participants (N = 21) were compared. In contrast to previous work in current users, our abstinent cohort showed no detectable behavioral or electrophysiological differences in their inhibitory responses, and no differences on self-reports of impulsivity, despite their long histories of chronic use (mean = 10.3 years). The current findings are consistent with a recovery of inhibitory control processes as a function of abstinence. Abstinent former users, however, did show a reduced modulation, relative to controls, of their ERPs to valenced input while performing successful inhibitions, although contrary to our hypothesis, the use of valenced inputs had no impact on inhibitory performance. Reduced ERP modulation to emotionally valenced inputs may have implications for relapse in emotional contexts outside the treatment center.

Individuals with schizophrenia are more prone to violent behaviors than the general population. It is increasingly recognized that processing of emotionally valenced stimuli is impaired in schizophrenia, a deficit that may play a role in aggressive behavior. Our goal was to establish whether patients with a history of violence would show more severe deficits in processing emotionally valenced inputs than non-violent patients. Using event-related potentials, we measured how early during processing of emotional valence, evidence of aberrant function was observed. A total of 42 schizophrenia patients (21 with history of violence; 21 without) and 28 healthy controls were tested. Participants performed an inhibitory control task, making speeded responses to pictorial stimuli. Pictures occasionally repeated twice and participants withheld responses to these repeats. Valenced pictures from the International Affective Picture System were presented. Results in controls showed modulations during the earliest phases of sensory processing (

Objectives Geriatric depression is associated with frontolimbic functional deficits, and this frontal dysfunction may underlie the marked executive control deficits often seen in this population. The authors' goal was to assess the integrity of frontal cortical functioning in geriatric depression, while these individuals performed a standard cognitive control task. The N2 component of the event-related potential (ERP), an evoked response generated within the anterior cingulate cortex (ACC), is significantly enhanced when nondepressed individuals successfully inhibit a response, providing an excellent metric of frontal inhibitory function. Design The authors used a variant of a demanding Go/NoGo task-switching paradigm that required participants to inhibit response execution during NoGo trials by overcoming a potent response tendency established by frequent Go trials. Participants The authors compared a cohort of depressed geriatric outpatients (N = 11) with a similarly aged group of nondepressed participants (N = 11). Measurements Reaction times, accuracy, and high-density event-related potential recordings from a 64-channel electrode montage were obtained. Results A significantly enhanced N2 to NoGo trials was observed in nondepressed elderly participants, with generators localized to the ACC. In contrast, this enhancement was strongly reduced in the depressed sample. Source analysis and topographic mapping pointed to a displacement of N2 generators toward more posterior areas of the middle frontal gyrus in depressed subjects. Conclusions Findings confirm previous reports of an inhibitory control deficit in depressed elderly who show significantly increased rates of commission errors (i.e., failures to inhibit responses on NoGo trials). Electrophysiologic data suggest underlying dysfunction in ACC as the basis for this deficit.

Important evidence about the information flow between perceptual and motor processes has been obtained from the lateralized readiness potential (LRP) recorded in two-choice go/nogo tasks. Here, we investigated the effect of time pressure on information transmission for one-dimensional stimuli (four squares differing in size). In between- and within-subject designs, respectively, Experiments 1 and 2 showed that under time pressure partial information initiates hand decision and response preparation before complete size information is available. These findings appear to be at odds with the asynchronous discrete coding model. Experiment 3 assessed the mechanisms behind these effects by manipulating the relative difficulty of extracting hand- and go/nogo-specific information from the size of the stimuli. Consistent with asynchronous coding, our results suggest that serial-consecutive processes in extracting partial and full size information may occur also for one-dimensional stimuli. Our data are inconclusive as to the question of discreteness or continuity of information transmission. On a more general level, our data support the notion of flexibility in the coding of perceptual dimensions to adapt performance to environmental conditions.

Segregation of auditory inputs into meaningful acoustic groups is a key element of auditory scene analysis. Previously, we showed that two interwoven sets of tones differing widely along multiple feature dimensions (duration, pitch and location) were pre-attentively separated into different groups, and that tones separated in this manner did not elicit the mismatch negativity component with respect to each other. Grouping was studied with human subjects using a stimulus rate too slow to induce streaming. Here, we varied the separation of tone sequences along a single feature dimension, i.e. frequency. Frequency differences were either 24 Hz (small) or 1054 Hz (large). Two relatively slow stimulus rates were used (2.7 or 1 tone/s) to explicitly investigate grouping outside the so-called 'streaming effect', which requires rates of about 4 tones/s or faster. Two tones were presented in a quasi-random manner with embedded trains of one to four identical tones in a row. Deviants were defined as frequency switches after trains of four identical tones. Mismatch negativity was only elicited for small frequency switches at the slower stimulation rate. The data indicate that pre-attentive grouping of tones occurred when the frequency difference that separated them was large, regardless of stimulation rate. For small frequency differences, inputs were only grouped separately when the stimulation rate was relatively fast.

In order to promote preattenive grouping of two sets of tones, one set of tones with a combination of frequency and ear of delivery was intermixed with another set of tones with a different combination of frequency and ear of delivery. The ERPs elicited by tones delivered to one ear that were preceded by three or four tones delivered in a row to the other ear were associated with an enhanced N1, due to the changes in frequency and ear of delivery with respect to the immediately preceding tones. However, no mismatch negativity (MMN) was obtained, even though these tones differed from the previious tones on the two dimensions of frequency and ear of delivery. The data were interpreted to signify that preattentively grouped sets of tones do not elicit MMN with respect to one another. This implies that once acoustic input has been preattentively grouped, the MMN system is dedicated to detecting changes that occur within but not between preattentively grouped stimuli

Seeing a speaker's facial articulatory gestures powerfully affects speech perception, helping us overcome noisy acoustical environments. One particularly dramatic illustration of visual influences on speech perception is the "McGurk illusion", where dubbing an auditory phoneme onto video of an incongruent articulatory movement can often lead to illusory auditory percepts. This illusion is so strong that even in the absence of any real change in auditory stimulation, it activates the automatic auditory change-detection system, as indexed by the mismatch negativity (MMN) component of the auditory event-related potential (ERP). We investigated the putative left hemispheric dominance of McGurk-MMN using high-density ERPs in an oddball paradigm. Topographic mapping of the initial McGurk-MMN response showed a highly lateralized left hemisphere distribution, beginning at 175 ms. Subsequently, scalp activity was also observed over bilateral fronto-central scalp with a maximal amplitude at approximately 290 ms, suggesting later recruitment of right temporal cortices. Strong left hemisphere dominance was again observed during the last phase of the McGurk-MMN waveform (350-400 ms). Source analysis indicated bilateral sources in the temporal lobe just posterior to primary auditory cortex. While a single source in the right superior temporal gyrus (STG) accounted for the right hemisphere activity, two separate sources were required, one in the left transverse gyrus and the other in STG, to account for left hemisphere activity. These findings support the notion that visually driven multisensory illusory phonetic percepts produce an auditory-MMN cortical response and that left hemisphere temporal cortex plays a crucial role in this process.