Psychologists have identified multiple different forms of conflict, such as information processing conflict and goal conflict. As such, there is a need to examine the similarities and differences in neurology between each form of conflict. To address this, we conducted a comprehensive electroencephalogram (EEG) analysis of Shadli, Glue, McIntosh, and McNaughton’s calibrated stop-signal task (SST) goal-conflict task. Specifically, we examined changes in scalp-wide current source density (CSD) power and coherence across a wide range of frequency bands during the calibrated SST (n = 34). We assessed differences in EEG between the high and low goal-conflict conditions using hierarchical analyses of variance (ANOVAs). We also related goal-conflict EEG to trait anxiety, neuroticism, Behavioural Inhibition System (BIS)-anxiety and revised BIS (rBIS) using regression analyses. We found that changes in CSD power during goal conflict were limited to increased midfrontocentral theta. Conversely, coherence increased across 23 scalp-wide theta region pairs and one frontal delta region pair. Finally, scalp-wide theta significantly predicted trait neuroticism but not trait anxiety, BIS-anxiety or rBIS. We conclude that goal conflict involves increased midfrontocentral CSD theta power and scalp-wide theta-dominated coherence. Therefore, compared with information processing conflict, goal conflict displays a similar EEG power profile of midfrontocentral theta but a much wider coherence profile. Furthermore, the increases in theta during goal conflict are the characteristic of BIS-driven activity. Therefore, future research should confirm whether these goal-conflict effects are driven by the BIS by examining whether the effects are attenuated by anxiolytic drugs. Overall, we have identified a unique network of goal-conflict EEG during the calibrated SST.

Despite the critical role of working memory (WM) in neuropsychiatric conditions, there remains a dearth of available WM-targeted interventions. Gamma and theta oscillations as measured with electroencephalography (EEG) or magnetoencephalography (MEG) reflect the neural underpinnings of WM. The WM processes that fluctuate in conjunction with WM demands are closely correlated with WM test performance, and their EEG signatures are abnormal in several clinical populations. Novel interventions such as transcranial magnetic stimulation (TMS) have been shown to modulate these oscillations and subsequently improve WM performance and clinical symptoms. Systematically identifying pathological WM-related gamma/theta oscillatory patterns with EEG/MEG and developing ways to target them with interventions such as TMS is an active area of clinical research. Results hold promise for enhancing the outcomes of our patients with WM deficits and for moving the field of clinical neuropsychology towards a mechanism-based approach.

Background: Although current pain-evoked electroencephalographic (EEG) studies provide valuable information regarding human brain regions involved in pain, they have mostly considered neuronal responses which oscillate in phase following a painful event. In many instances, cortical neurons respond by generating bursts of activity that are slightly out of phase from trial-to-trial. These types of activity bursts are known as induced brain responses. The significance of induced brain responses to pain is still unknown. Methods: In this study, 23 healthy subjects were given both non-painful and painful transcutaneous electrical stimulations in separate testing blocks (stimulation strength was kept constant within blocks). Subjective intensity was rated using a numerical rating scale, while cerebral activity tied to each stimulation was measured using EEG recordings. Induced brain responses were identified using a time frequency wavelet transform applied to average-removed single trials. Results: Results showed a pain-specific burst of induced theta activity occurring between 180 and 500 ms post-shock onset. Source current density estimations located this activity within the dorsolateral prefrontal cortex (DLPFC, bilaterally), however, only right DLPFC activity predicted a decrease in subjective pain as testing progressed. Conclusion: This finding suggests that non-phase locked neuronal responses in the right DLPFC contribute to the endogenous attenuation of pain through time. Perspective: This article presents neuroimaging findings demonstrating that, in response to pain, non-phase locked bursts of theta activity located in the right dorsolateral prefrontal cortex are associated with a progressive decrease in subjective pain intensity, which has potentially important implications regarding how humans endogenously control their experiences of pain.

As established in early studies, the basalo-cortical system serves as an extra-thalamic relay from the brainstem reticular activating system to the cerebral cortex. As Mircea Steriade documented, activating impulses are transmitted through either the nonspecific thalamo-cortical projection system or the basalo-cortical projection system to stimulate widespread, fast, cortical activity that is characteristic of the activation that occurs naturally during waking (W) and paradoxical sleep (PS) states. However, basal forebrain (BF) neurons are different from thalamic neurons in several ways. First, many cortically projecting BF neurons utilize acetylcholine (ACh), which has a crucial role in stimulating fast cortical activity. Second, ACh-releasing neurons discharge selectively during W and PS and cease firing during slow-wave sleep (SWS). Third, ACh-releasing neurons discharge rhythmically in bursts during cortical activation and can, thus, modulate the cortex in a slow rhythmic manner to facilitate coherent activity across broad cortical networks. Fourth, the rhythmic discharge by BF neurons that release ACh, GABA or glutamate and project to the cortex occurs at respiratory or theta frequencies of the olfactory and limbic cortices, which reveals the particular importance of these inputs as well as outputs within basalo-cortico-basalo circuits. Fifth, other noncholinergic BF neurons, including GABA-releasing neurons, are active selectively during sleep: some of these potentially promote slow-wave activity during SWS through cortical projections; and others might promote behavioral quiescence during SWS and PS through descending projections. Finally, BF neurons also project to the thalamus and might, thus, either recruit or join thalamic neurons in modulating cortical activity across the sleep–waking cycle.

Abnormal thalamocortical dynamics have been proposed as the underlying mechanism for a subset of neurological and psychiatric disorders that include centrally generated pain. Spectral analysis and independent component-based localization of neuromagnetic signals reveal ongoing theta-range activity localized to physiologically significant cortical regions in a group of subjects with well-characterized central and peripheral lesions. In addition, recordings from subjects who failed to obtain relief from spinal cord stimulation (SCS) and from those in whom SCS was successful further delineate thalamocortical dysrhythmias as a mechanism that underlies chronic pain.