EEG-informed fMRI reveals spatiotemporal characteristics of perceptual decision making

Single-unit and multiunit recordings in primates have already established that decision making involves at least two general stages of neural processing: representation of evidence from early sensory areas and accumulation of evidence to a decision threshold from decision-related regions. However, the relay of information from early sensory to decision areas, such that the accumulation process is instigated, is not well understood. Using a cued paradigm and single-trial analysis of electroencephalography (EEG), we previously reported on temporally specific components related to perceptual decision making. Here, we use information derived from our previous EEG recordings to inform the analysis of fMRI data collected for the same behavioral task to ascertain the cortical origins of each of these EEG components. We demonstrate that a cascade of events associated with perceptual decision making takes place in a highly distributed neural network. Of particular importance is an activation in the lateral occipital complex implicating perceptual persistence as a mechanism by which object decision making in the human brain is instigated

The cognitive neuroscience of visual working memory

Visual working memory allows us to temporarily maintain and manipulate visual information in order to solve a task. The study of the brain mechanisms underlying this function began more than half a century ago, with Scoville and Milner’s (1957) seminal discoveries with amnesic patients. This timely collection of papers brings together diverse perspectives on the cognitive neuroscience of visual working memory from multiple fields that have traditionally been fairly disjointed: human neuroimaging, electrophysiological, behavioural and animal lesion studies, investigating both the developing and the adult brain

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 297)

This bibliography lists 89 reports, articles and other documents introduced into the NASA scientific and technical information system in April, 1987

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 349)

This bibliography lists 149 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during April, 1991. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

Investigating the Primate Prefrontal Cortex Correlates of Cognitive Deficits In the Ketamine Model of Schizophrenia

The World Health Organization has classified schizophrenia as one of the five leading causes of disability worldwide. Afflicting almost 1% of the world’s population, the disease’s greatest impact stems from its reduction in patients’ cognitive faculties. In order to better study these impairments, a pharmacological model has been developed using the NMDA antagonist, ketamine. This disease model successfully recreates the cognitive dysfunction of schizophrenia, allowing researchers to search for associated electrophysiological changes. In this project I examined the behavioural and neurophysiological effects of ketamine on non-human primates performing the anti-saccade task. Success in this task requires a degree of cognitive control over behaviour and previous studies have described poor performance in both patients with schizophrenia and healthy controls administered ketamine. Our intracranial recordings are localized in the prefrontal cortex (PFC), a region associated with many of the cognitive functions impaired in schizophrenia. The first study shows that neurons in the PFC exhibit selectivity for the task rule. This rule selectivity is lost after ketamine administration due to an indiscriminate increase in the neuronal firing rate. These changes were also associated with an increased error rate and longer reaction times. The second study shows that neurons in the PFC are also sensitive to the outcome of the trial, firing more for either correct or erroneous responses. Once again, selectivity is lost following ketamine administration and the neurons show increased, nonspecific activity. Lastly, we recorded the local field potential of the PFC and found changes in the oscillatory patterns during the anti-saccade task. Prior to ketamine there was a significantly stronger beta-band activity after correct trials compared to error trials, but this selective activity was lost due to an overall decrease in the outcome selective oscillatory events. These findings show that ketamine’s effect on the PFC is one of selectivity reduction. Patients with schizophrenia have been shown to require increased PFC activity but only reach moderate performance levels in cognitive challenges. It is possible that their brains suffer the same changes highlighted in this research. Although the signals are still present in their PFC, they are being lost amongst the noise

The Simon Effect in Rats: A Comparative Study on Conflict and Error Processing Using Electrophysiology and Functional µPET Imaging

Both humans and animals have the ability to learn from past experience and to adapt their behavior to resolve future conflicts faster or avoid them entirely. Conflicts in spatial stimulus–response tasks occur when the origin of the stimulus and the response area differ in location. Those conflicts lead to increased error rates, reaction times (RT) and movement time (MT) which has been termed Simon effect. A model of dual route processing (automatic and intentional) of stimulus features has been proposed, predicting response conflicts if the two routes are incongruent. Although there are various theories related to underlying neuronal mechanisms, it is commonly assumed that the anterior cingulate cortex (ACC) plays a crucial role in conflict and error processing. The Simon task is a neuropsychological interference task commonly used to study performance monitoring. Interestingly, the resulting conflict is far from uniquely human, as it has also been observed in pigeons, rats, and monkeys. On a neural level, the on-going monitoring of correct and incorrect behavior appears in the form of eventrelated potentials (ERPs). More precisely, the error-related negativity (ERN/Ne) component of the resulting ERP, assumed to be generated in the ACC, is suggested to reflect conflict and error monitoring. Unfortunately, there is often little correspondence between human and animal studies. On this account the present study uses a modified auditory Simon task to investigate a) the anatomical basis, b) the conflict- and errorrelated electrophysiological correlates and c) the performance monitoring from a crossspecies point of view. By using positron emission tomography (PET) in combination with the metabolic tracer [18F]fluorodeoxyglucose, which accumulates in metabolically active brain cells during the behavioral task, we first aim at identifying relevant brain areas in a rat model of the Simon task. According to the dual route model, brain areas involved in conflict processing are supposed to be activated when automatic and intentional route lead to different responses (dual route model). Results show specific activation patterns for different task settings coherent with the dual route model. Our data suggest that the rat motor cortex (M1) may be part of the automatic route or involved in its facilitation, while premotor (M2) and prelimbic areas, as well as the ACC appear to be essential for inhibiting the incorrect, automatic response, indicating conflict monitoring functions. Interestingly, our findings remarkably fit the pattern of activated regions reported during conflict processing in humans. To further support our findings, we measured local field potentials (LFP) from electrodes centered in the rat ACC. LFPs showed a negative slow wave less pronounced for errors at about 250-400 ms after reaction. Stimulus-locked data revealed a compatibility effect in rats, with a negative slow wave with onset in the latency range of the reaction. To finally compare these results with a human setup, we also developed a translational task for humans. In both species, similar behavioral effects were found, including an increase in error rate, RT and MT. In humans, although no difference in EEG amplitude between errors and hits in the ERN latency range was found, a pronounced error positivity between 250 and 350 ms after reaction was seen. Humans surprisingly demonstrated a stronger negativity for compatible compared to incompatible trials. Similarly to rats, this effect started at about the time of reaction time. Thus, both species (i) showed electrophysiological responses differentiating between errors and correct in a similar latency range, (ii) demonstrated a valid occurrence of the Simon effect and seem to pursue similar response strategies, both in terms of RT and MT and (iii) displayed sustained differences in the modulation of the ERP depending on correct or incorrect responses starting at the time of response and prior to reward/no reward. It is thus tempting to speculate that the underlying cognitive error processing mechanisms are highly similar across species. In conclusion, we found remarkable behavioral, electrophysiological and functional similarities between rat and human conflict and error processing. Our paradigm offers a new approach in integrative, cross-species research and provides a useful rodent model for investigating performance monitoring

Role of N-methyl-D-aspartate receptors in action-based predictive coding deficits in schizophrenia

Published in final edited form as:Biol Psychiatry. 2017 March 15; 81(6): 514–524. doi:10.1016/j.biopsych.2016.06.019.BACKGROUND: Recent theoretical models of schizophrenia posit that dysfunction of the neural mechanisms subserving predictive coding contributes to symptoms and cognitive deficits, and this dysfunction is further posited to result from N-methyl-D-aspartate glutamate receptor (NMDAR) hypofunction. Previously, by examining auditory cortical responses to self-generated speech sounds, we demonstrated that predictive coding during vocalization is disrupted in schizophrenia. To test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the effects of the NMDAR antagonist, ketamine, on predictive coding during vocalization in healthy volunteers and compared them with the effects of schizophrenia. METHODS: In two separate studies, the N1 component of the event-related potential elicited by speech sounds during vocalization (talk) and passive playback (listen) were compared to assess the degree of N1 suppression during vocalization, a putative measure of auditory predictive coding. In the crossover study, 31 healthy volunteers completed two randomly ordered test days, a saline day and a ketamine day. Event-related potentials during the talk/listen task were obtained before infusion and during infusion on both days, and N1 amplitudes were compared across days. In the case-control study, N1 amplitudes from 34 schizophrenia patients and 33 healthy control volunteers were compared. RESULTS: N1 suppression to self-produced vocalizations was significantly and similarly diminished by ketamine (Cohen’s d = 1.14) and schizophrenia (Cohen’s d = .85). CONCLUSIONS: Disruption of NMDARs causes dysfunction in predictive coding during vocalization in a manner similar to the dysfunction observed in schizophrenia patients, consistent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schizophrenia.This work was supported by AstraZeneca for an investigator-initiated study (DHM) and the National Institute of Mental Health Grant Nos. R01 MH-58262 (to JMF) and T32 MH089920 (to NSK). JHK was supported by the Yale Center for Clinical Investigation Grant No. UL1RR024139 and the US National Institute on Alcohol Abuse and Alcoholism Grant No. P50AA012879. (AstraZeneca for an investigator-initiated study (DHM); R01 MH-58262 - National Institute of Mental Health; T32 MH089920 - National Institute of Mental Health; UL1RR024139 - Yale Center for Clinical Investigation; P50AA012879 - US National Institute on Alcohol Abuse and Alcoholism)Accepted manuscrip

Midfrontal theta transcranial alternating current stimulation modulates behavioural adjustment after error execution

Cognitive control during conflict monitoring, error processing, and post-error adjustment appear to be associated with the occurrence of midfrontal theta (MFϴ). While this association is supported by correlational EEG studies, much less is known about the possible causal link between MFϴ and error and conflict processing. In the present study, we aimed to explore the role of band-specific effects in modulating the error system during a conflict resolution. In turn, we delivered transcranial alternating current stimulation (tACS) at different frequency bands (delta δ, theta θ, alpha α, beta β, gamma γ) and sham stimulation over the medial frontal cortex (MFC) in 36 healthy participants performing a modified version of the Flanker task. Task performance and reports about the sensations (e.g. visual flickering, cutaneous burning) induced by the different frequency bands, were also recorded. We found that online θ-tACS increased the response speed to congruent stimuli after error execution with respect to sham stimulation. Importantly, the accuracy following the errors did not decrease because of speed-accuracy trade off. Moreover, tACS evoked visual and somatosensory sensations were significantly stronger at α-tACS and β-tACS compared to other frequencies. Our findings suggest that theta activity plays a causative role in modulating behavioural adjustments during perceptual choices in a stimulus-response conflict task. © 2018 Federation of European Neuroscience Societies and John Wiley & Sons Lt

Top-down effects on early visual processing in humans: a predictive coding framework

An increasing number of human electroencephalography (EEG) studies examining the earliest component of the visual evoked potential, the so-called C1, have cast doubts on the previously prevalent notion that this component is impermeable to top-down effects. This article reviews the original studies that (i) described the C1, (ii) linked it to primary visual cortex (V1) activity, and (iii) suggested that its electrophysiological characteristics are exclusively determined by low-level stimulus attributes, particularly the spatial position of the stimulus within the visual field. We then describe conflicting evidence from animal studies and human neuroimaging experiments and provide an overview of recent EEG and magnetoencephalography (MEG) work showing that initial V1 activity in humans may be strongly modulated by higher-level cognitive factors. Finally, we formulate a theoretical framework for understanding top-down effects on early visual processing in terms of predictive coding