BACKGROUND:Deep brain stimulation (DBS) of the thalamus can effectively reduce tics in severely affected patients with Tourette syndrome (TS). Its effect on cortical oscillatory activity is currently unknown.OBJECTIVE:We assessed whether DBS modulates beta activity at fronto-central electrodes. We explored concurrent EEG sources and probabilistic stimulation maps.METHODS:Resting state EEG of TS patients treated with thalamic DBS was recorded in repeated DBS-on and DBS-off states. A mixed linear model was employed for statistical evaluation. EEG sources were estimated with eLORETA. Thalamic probabilistic stimulation maps were obtained by assigning beta power difference scores (DBS-on minus DBS-off) to stimulation sites.RESULTS:We observed increased beta power in DBS-on compared to DBS-off states. Modulation of cortical beta activity was localized to the midcingulate cortex. Beta modulation was more pronounced when stimulating the thalamus posteriorly, peaking in the ventral posterior nucleus.CONCLUSION:Thalamic DBS in TS patients modulates beta frequency oscillations presumably important for sensorimotor function and relevant to TS pathophysiology.

Precision targeting of specific white matter bundles that traverse the subcallosal cingulate (SCC) has been linked to efficacy of deep brain stimulation (DBS) for treatment resistant depression (TRD). Methods to confirm optimal target engagement in this heterogenous region are now critical to establish an objective treatment protocol. As yet unexamined are the time-frequency features of the SCC evoked potential (SCC-EP), including spectral power and phase-clustering. We examined these spectral features—evoked power and phase clustering—in a sample of TRD patients (n = 8) with implanted SCC stimulators. Electroencephalogram (EEG) was recorded during wakeful rest. Location of electrical stimulation in the SCC target region was the experimental manipulation. EEG was analyzed at the surface level with an average reference for a cluster of frontal sensors and at a time window identified by prior study (50–150 ms). Morlet wavelets generated indices of evoked power and inter-trial phase clustering. Enhanced phase clustering at theta frequency (4–7 Hz) was observed in every subject and was significantly correlated with SCC-EP magnitude, but only during left SCC stimulation. Stimulation to dorsal SCC evinced stronger phase clustering than ventral SCC. There was a weak correlation between phase clustering and white matter density. An increase in evoked delta power (2–4 Hz) was also coincident with SCC-EP, but was less consistent across participants. DBS evoked time-frequency features index mm-scale changes to the location of stimulation in the SCC target region and correlate with structural characteristics implicated in treatment optimization. Results also imply a shared generative mechanism (inter-trial phase clustering) between evoked potentials evinced by electrical stimulation and evoked potentials evinced by auditory/visual stimuli and behavioral tasks. Understanding how current injection impacts downstream cortical activity is essential to building new technologies that adapt treatment parameters to individual differences in neurophysiology.

Although conventional averaging across predefined frequency bands reduces the complexity of EEG functional connectivity (FC), it obscures the identification of resting-state brain networks (RSN) and impedes accurate estimation of FC reliability. Extending prior work, we combined scalp current source density (CSD; spherical spline surface Laplacian) and spectral-spatial PCA to identify FC components. Phase-based FC was estimated via debiased weighted phase-locking index from CSD-transformed resting EEGs (71 sensors, 8 min, eyes open/closed, 35 healthy adults, 1-week retest). Spectral PCA extracted 6 robust alpha and theta factors (86.6% variance). Subsequent spatial PCA for each spectral factor revealed seven robust regionally-focused (posterior, central, frontal) and long-range (posterior-anterior) alpha components (peaks at 8, 10 and 13 Hz) and a midfrontal theta (6 Hz) component, accounting for 37.0% of FC variance. These spatial FC components were consistent with well-known networks (e.g., default mode, visual, sensorimotor), and four were sensitive to eyes open/closed conditions. Most FC components had good-to-excellent internal consistency (odd/even epochs, eyes open/closed) and test-retest reliability (ICCs ≥ .8). Moreover, the FC component structure was generally present in subsamples (session × odd/even epoch, or smaller subgroups [n = 7-10]), as indicated by similarity of factor loadings across PCA solutions. Apart from systematically reducing FC dimensionality, our approach avoids arbitrary thresholds and allows quantification of meaningful and reliable network components that may prove to be of high relevance for basic and clinical research applications.

Background: Symptoms of obsessive-compulsive disorder (OCD) are partly related to impaired cognitive control processes and theta modulations constitute an important electrophysiological marker for cognitive control processes such as signaling negative performance feedback in a fronto-striatal network. Deep brain stimulation (DBS) targeting the anterior limb of the internal capsule (ALIC)/nucleus accumbens (NAc) shows clinical efficacy in OCD, while the exact influence on the performance monitoring system remains largely unknown. Methods: Seventeen patients with treatment-refractory OCD performed a probabilistic reinforcement learning task. Analyses were focused on 4-8 Hz (theta) power, intertrial phase coherence (ITPC) and debiased weighted Phase-Lag Index (dwPLI) in response to negative performance feedback. Combined EEG and local field potential (LFP) recordings were obtained shortly after DBS electrode implantation to investigate fronto-striatal network modulations. To assess the impact of clinically effective DBS on negative performance feedback modulations, EEG recordings were obtained pre-surgery and at follow-up with DBS on and off. Results: Medial frontal cortex ITPC, striatal ITPC and striato-frontal dwPLI were increased following negative performance feedback. Decreased right-lateralized dwPLI was associated with pre-surgery symptom severity. ITPC was globally decreased during DBS-off. Conclusion: We observed a theta phase coherence mediated fronto-striatal performance monitoring network. Within this network, decreased connectivity was related to increased OCD symptomatology, consistent with the idea of impaired cognitive control in OCD. While ALIC/NAc DBS decreased theta network activity globally, this effect was unrelated to clinical efficacy and performance monitoring.

Deep brain stimulation (DBS) of the ventral capsule/ventral striatum (VC/VS) is a promising neurotherapeutic approach for severe and refractory cases of obsessive-compulsive disorder (OCD). Successful VC/VS-DBS treatment alters function in frontostriatal pathways important for the etiopathogenesis of OCD [1Figee M. Luigjes J. Smolders R. Valencia-Alfonso C.E. van Wingen G. de Kwaasteniet B. et al.Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder.Nat Neurosci. 2013; 16: 386-387Crossref PubMed Scopus (293) Google Scholar, 2Wu H. Miller K.J. Blumenfeld Z. Williams N.R. Ravikumar V.K. Lee K.E. et al.Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man.Proc Natl Acad Sci U S A. 2018; 115: 192-197Crossref PubMed Scopus (54) Google Scholar, 3McCracken C.B. Grace A.A. Nucleus accumbens deep brain stimulation produces region-specific alterations in local field potential oscillations and evoked responses in vivo.J Neurosci. 2009; 29: 5354-5363Crossref PubMed Scopus (97) Google Scholar]. Monitoring changes in frontostriatal functioning resulting from active DBS can reveal signatures of DBS engagement with disease-relevant pathways [[1]Figee M. Luigjes J. Smolders R. Valencia-Alfonso C.E. van Wingen G. de Kwaasteniet B. et al.Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder.Nat Neurosci. 2013; 16: 386-387Crossref PubMed Scopus (293) Google Scholar,[4]Gibson W.S. Cho S. Abulseoud O.A. Gorny K.R. Felmlee J.P. Welker K.M. et al.The impact of mirth-inducing ventral striatal deep brain stimulation on functional and effective connectivity.Cerebr Cortex. 2017; 27: 2183-2194PubMed Google Scholar]. In particular, modulation of the dorsal-medial prefrontal cortex (dmPFC) seems to be crucial for therapeutic success: symptomatic OCD patients demonstrate hyperconnectivity between the VC/VS and dmPFC, which is normalized following successful VC/VS-DBS [[1]Figee M. Luigjes J. Smolders R. Valencia-Alfonso C.E. van Wingen G. de Kwaasteniet B. et al.Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder.Nat Neurosci. 2013; 16: 386-387Crossref PubMed Scopus (293) Google Scholar,[5]Suetens K. Nuttin B. Gabriels L. Van Laere K. Differences in metabolic network modulation between capsulotomy and deep-brain stimulation for refractory obsessive-compulsive disorder.J Nucl Med. 2014; 55: 951-959Crossref PubMed Scopus (39) Google Scholar,[6]Baldermann J.C. Melzer C. Zapf A. Kohl S. Timmermann L. Tittgemeyer M. et al.Connectivity profile predictive of effective deep brain stimulation in obsessive-compulsive disorder.Biol Psychiatry. 2019; 85: 735-743Abstract Full Text Full Text PDF PubMed Scopus (125) Google Scholar]. VC/VS-DBS also alters delta oscillations (1–4 Hz) across frontostriatal regions in rodents and humans, including the dmPFC [1Figee M. Luigjes J. Smolders R. Valencia-Alfonso C.E. van Wingen G. de Kwaasteniet B. et al.Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder.Nat Neurosci. 2013; 16: 386-387Crossref PubMed Scopus (293) Google Scholar, 2Wu H. Miller K.J. Blumenfeld Z. Williams N.R. Ravikumar V.K. Lee K.E. et al.Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man.Proc Natl Acad Sci U S A. 2018; 115: 192-197Crossref PubMed Scopus (54) Google Scholar, 3McCracken C.B. Grace A.A. Nucleus accumbens deep brain stimulation produces region-specific alterations in local field potential oscillations and evoked responses in vivo.J Neurosci. 2009; 29: 5354-5363Crossref PubMed Scopus (97) Google Scholar, 4Gibson W.S. Cho S. Abulseoud O.A. Gorny K.R. Felmlee J.P. Welker K.M. et al.The impact of mirth-inducing ventral striatal deep brain stimulation on functional and effective connectivity.Cerebr Cortex. 2017; 27: 2183-2194PubMed Google Scholar, 5Suetens K. Nuttin B. Gabriels L. Van Laere K. Differences in metabolic network modulation between capsulotomy and deep-brain stimulation for refractory obsessive-compulsive disorder.J Nucl Med. 2014; 55: 951-959Crossref PubMed Scopus (39) Google Scholar]. However, the relationship between dmPFC delta during VC/VS-DBS stimulation and clinical outcome has not been directly tested. We expected that changes in dmPFC delta resulting from active VC/VS-DBS would predict better therapeutic outcomes. This study included data from ten patients (5 females) with refractory and severe (Yale-Brown Obsessive Compulsive Scale [YBOCS] ≥ 25) OCD that were being treated with DBS implants in the VC/VS (for details on study design and recruitment see Ref. [[7]Huys D. Kohl S. Baldermann J.C. Timmermann L. Sturm V. Visser-Vandewalle V. et al.Open-label trial of anterior limb of internal capsule–nucleus accumbens deep brain stimulation for obsessive-compulsive disorder: insights gained.J Neurol Neurosurg Psychiatry. 2019; 90 (jnnp-2018-318996): 805-812Crossref PubMed Scopus (43) Google Scholar]). Patients underwent bilateral stereotactic implantation of quadripolar leads (Model 3387 or 3389 DBS Lead; Medtronic; Minneapolis, MN, USA) with the two most ventral/distal contacts targeting the VS and two most dorsal/proximal contacts located in the VC (Fig. 1A). Stimulated contacts and stimulation parameters were chosen based on the best clinical outcome (Stimulation parameters are reported in Supplementary Table 1). Participants were hospital inpatients for one week during postsurgical follow-ups (6 month and 12 month), and completed electroencephalographic (EEG) recordings and clinical assessments at that time. EEG and clinical data from 6 month follow up were the focus of this report. Total score on the YBOCS at 6 months was the primary measure of treatment success. At 6 months, three participants showed a partial response (25–35% YBOCS reduction) and two participants showed a full response (≥35% YBOCS reduction). Clinical assessments were completed with DBS-ON. EEG (58 electrodes with 10–20 placement sampled at 5000 Hz) was recorded for 10 min consisting of six eyes-closed segments lasting one-minute each, intermitted by 5 eyes-open segments lasting 26 seconds each. Stimulator artifacts were removed using a combination of spectral outlier rejection, zero phase-shift FIR filters (1–45 Hz), semi-automatic ICA-based component subtraction, and spherical-spline interpolation using EEGLAB and custom MATLAB code. Delta amplitude in the dmPFC was calculated using the eLORETA software for inverse modeling (http://www.uzh.ch/keyinst/loreta). In four participants, EEG measurement was first carried out in the DBS-ON, in the other six participants in the DBS-OFF. The DBS device was shut down for at least 12 hours prior to DBS-OFF EEG recordings. Eight of ten participant's EEG recordings were collected during 6 month follow up. One participant's EEG was from 12 month follow-up. Another participant had data from both 6 month and 12 month follow up, and eLORETA delta amplitudes from both recordings were averaged together for this participant. Hypothesis-driven Spearman correlations were calculated between dmPFC delta responsivity (DBS-OFF minus DBS-ON change scores) and OCD symptoms (YBOCS) at 6 months. An exploratory analysis examined correlations between amplitude change and OCD symptoms across canonical frequency bands (1–4 Hz, 4–8 Hz, 8–13 Hz, and 15–25 Hz) and 84 Brodmann areas (42 parcels in each hemisphere from eLORETA software). Exploratory correlations were corrected for multiple comparisons using the False-Discovery Rate (FDR) method. Fig. 1B shows that resting dmPFC delta activity was unchanged at the group-level for DBS-OFF compared to DBS-ON. Notably, there is significant variation in delta band amplitude within individual subjects across the two conditions. Fig. 1C shows that individual variability in responsivity of dmPFC delta correlated significantly with 6 month YBOCS scores (r = 0.809, p = .005): patients with greater dmPFC delta during DBS-ON compared to DBS-OFF had the fewest OCD symptoms. Greater delta responsivity within the dmPFC also predicted relative improvement (i.e., YBOCS change scores) in OCD symptoms from presurgical baseline (r = 0.87, p = .001). Fig. 1D shows the dmPFC ROI used for our primary analysis overlaid on correlations between YBOCS scores and delta responsivity at each voxel. Greater delta oscillations for DBS-ON than DBS-OFF within the right dmPFC (i.e., BA 8) strongly predicted fewer OCD symptoms at 6 months (r = 0.921, FDR-p = .013) in an exploratory/data-driven analysis. There were no other frequency bands or brain regions associated with treatment outcome. In general, delta oscillations are hypothesized to facilitate coordinated activity across frontostriatal regions important for goal-directed activity [[2]Wu H. Miller K.J. Blumenfeld Z. Williams N.R. Ravikumar V.K. Lee K.E. et al.Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man.Proc Natl Acad Sci U S A. 2018; 115: 192-197Crossref PubMed Scopus (54) Google Scholar,[3]McCracken C.B. Grace A.A. Nucleus accumbens deep brain stimulation produces region-specific alterations in local field potential oscillations and evoked responses in vivo.J Neurosci. 2009; 29: 5354-5363Crossref PubMed Scopus (97) Google Scholar,[8]Perera M.P.N. Bailey N.W. Herring S.E. Fitzgerald P.B. Electrophysiology of obsessive compulsive disorder: a systematic review of the electroencephalographic literature.J Anxiety Disord. 2019; 62: 1-14Crossref PubMed Scopus (29) Google Scholar], and delta activity within the dmPFC may have a more specific role in anxiety and compulsive behavior [[1]Figee M. Luigjes J. Smolders R. Valencia-Alfonso C.E. van Wingen G. de Kwaasteniet B. et al.Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder.Nat Neurosci. 2013; 16: 386-387Crossref PubMed Scopus (293) Google Scholar,[8]Perera M.P.N. Bailey N.W. Herring S.E. Fitzgerald P.B. Electrophysiology of obsessive compulsive disorder: a systematic review of the electroencephalographic literature.J Anxiety Disord. 2019; 62: 1-14Crossref PubMed Scopus (29) Google Scholar,[9]Knyazev G.G. EEG delta oscillations as a correlate of basic homeostatic and motivational processes.Neurosci Biobehav Rev. 2012; 36: 677-695Crossref PubMed Scopus (397) Google Scholar]. Mean delta amplitude across the 10 participants was unchanged by DBS (Fig. 1B), but four of five treatment responders had increased dmPFC delta amplitude during DBS-ON. More frontal delta at rest is consistently related to more OCD symptoms in nonsurgical cohorts [reviewed in [8]Perera M.P.N. Bailey N.W. Herring S.E. Fitzgerald P.B. Electrophysiology of obsessive compulsive disorder: a systematic review of the electroencephalographic literature.J Anxiety Disord. 2019; 62: 1-14Crossref PubMed Scopus (29) Google Scholar]. In contrast, EEG studies with VC/VS-DBS cohorts have found stronger [[1]Figee M. Luigjes J. Smolders R. Valencia-Alfonso C.E. van Wingen G. de Kwaasteniet B. et al.Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder.Nat Neurosci. 2013; 16: 386-387Crossref PubMed Scopus (293) Google Scholar] and weaker [[2]Wu H. Miller K.J. Blumenfeld Z. Williams N.R. Ravikumar V.K. Lee K.E. et al.Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man.Proc Natl Acad Sci U S A. 2018; 115: 192-197Crossref PubMed Scopus (54) Google Scholar,[3]McCracken C.B. Grace A.A. Nucleus accumbens deep brain stimulation produces region-specific alterations in local field potential oscillations and evoked responses in vivo.J Neurosci. 2009; 29: 5354-5363Crossref PubMed Scopus (97) Google Scholar] frontostriatal delta oscillations during DBS-ON recordings. Some small neurometabolic studies with VC/VS-DBS patients also implicate the dmPFC, with results showing more dmPFC [[10]Dougherty D.D. Chou T. Corse A.K. Arulpragasam A.R. Widge A.S. Cusin C. et al.Acute deep brain stimulation changes in regional cerebral blood flow in obsessive-compulsive disorder.J Neurosurg. 2016; 125: 1087-1093Crossref PubMed Scopus (22) Google Scholar] and less dmPFC [[4]Gibson W.S. Cho S. Abulseoud O.A. Gorny K.R. Felmlee J.P. Welker K.M. et al.The impact of mirth-inducing ventral striatal deep brain stimulation on functional and effective connectivity.Cerebr Cortex. 2017; 27: 2183-2194PubMed Google Scholar] activity during DBS-ON in treatment responders. In this regard, direction of modification of dmPFC function probably varies with stimulator placement and patient anatomy, insofar as treatment-relevant pathways are highly specific [[4]Gibson W.S. Cho S. Abulseoud O.A. Gorny K.R. Felmlee J.P. Welker K.M. et al.The impact of mirth-inducing ventral striatal deep brain stimulation on functional and effective connectivity.Cerebr Cortex. 2017; 27: 2183-2194PubMed Google Scholar,[6]Baldermann J.C. Melzer C. Zapf A. Kohl S. Timmermann L. Tittgemeyer M. et al.Connectivity profile predictive of effective deep brain stimulation in obsessive-compulsive disorder.Biol Psychiatry. 2019; 85: 735-743Abstract Full Text Full Text PDF PubMed Scopus (125) Google Scholar]. Altogether, these results suggest that monitoring of dmPFC delta may facilitate placement of DBS electrodes into treatment-relevant circuitry and be a promising target for less invasive neuromodulatory treatment of refractory OCD and related diseases. The authors report no biomedical financial interests or potential conflicts of interest. The authors are grateful to the participants of this study. The authors also thank Elena Sildatke for help with EEG data acquisition. Parts of the data presented here were also published in Huys et al., 2019 and Baldermann et al., 2019, but the present study was the first to report EEG data for these patients. This project was funded by the German Research Foundation (KFO-219; KU 2665/1–2). The following is the Supplementary data to this article: Download .docx (.01 MB) Help with docx files Multimedia component 1

Closed-loop neuromodulation is presumed to be the logical evolution for improving the effectiveness of deep brain stimulation (DBS) treatment protocols (Widge et al., 2018). Identifying symptom-relevant biomarkers that provide meaningful feedback to stimulator devices is an important initial step in this direction. This report demonstrates a technique for assaying neural circuitry hypothesized to contribute to OCD and DBS treatment outcomes. We computed phase-lag connectivity between LFPs and EEGs in thirteen treatment-refractory OCD patients. Simultaneous recordings from scalp EEG and externalized DBS electrodes in the ventral capsule/ventral striatum (VC/VS) were collected at rest during the perioperative treatment stage. Connectivity strength between midfrontal EEG sensors and VC/VS electrodes correlated with baseline OCD symptoms and 12-month posttreatment OCD symptoms. Results are qualified by a relatively small sample size, and limitations regarding the conclusiveness of VS and mPFC as neural generators given some concerns about volume conduction. Nonetheless, findings are consistent with treatment-relevant tractography findings and theories that link frontostriatal hyperconnectivity to the etiopathogenesis of OCD. Findings support the continued investigation of connectivity-based assays for aiding in determination of optimal stimulation location, and are an initial step towards the identification of biomarkers that can guide closed-loop neuromodulation systems.

Transcranial focused ultrasound (tFUS) is an emerging method for non-invasive neuromodulation akin to transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). tFUS offers several advantages over electromagnetic methods including high spatial resolution and the ability to reach deep brain targets. Here we describe two experiments assessing whether tFUS could modulate mood in healthy human volunteers by targeting the right inferior frontal gyrus (rIFG), an area implicated in mood and emotional regulation. In a randomized, placebo-controlled, double-blind study, participants received 30 s of 500 kHz tFUS or a placebo control. Visual Analog Mood Scales (VAMS) assessed mood four times within an hour (baseline and three times after tFUS). Participants who received tFUS reported an overall increase in Global Affect (GA), an aggregate score from the VAMS scale, indicating a positive shift in mood. Experiment 2 examined resting-state functional (FC) connectivity using functional magnetic resonance imaging (fMRI) following 2 min of 500 kHz tFUS at the rIFG. As in Experiment 1, tFUS enhanced self-reported mood states and also decreased FC in resting state networks related to emotion and mood regulation. These results suggest that tFUS can be used to modulate mood and emotional regulation networks in the prefrontal cortex.

Perturbation-based mapping is an emerging approach to the study of circuit dynamics in the living human brain. Pulses of deep brain stimulation (DBS) to the subcallosal cingulate (SCC) evoke a coherent and reliable cortical response, recorded on the scalp surface with dense array EEG, that may reflect endogenous network dynamics. As precision targeting within the SCC region has been linked to DBS treatment efficacy, we examined features of the cortical perturbation map that change when stimulation is delivered to different locations within the surgical target region.

Improving patient-treatment matching can relieve patient suffering, lower healthcare costs, and also reveal psychiatric subtypes.

Prior research has identified two resting EEG biomarkers with potential for predicting functional outcomes in depression: theta current density in frontal brain regions (especially rostral anterior cingulate cortex) and alpha power over posterior scalp regions. As little is known about the discriminant and convergent validity of these putative biomarkers, a thorough evaluation of these psychometric properties was conducted toward the goal of improving clinical utility of these markers. Resting 71-channel EEG recorded from 35 healthy adults at two sessions (1-week retest) were used to systematically compare different quantification techniques for theta and alpha sources at scalp (surface Laplacian or current source density [CSD]) and brain (distributed inverse; exact low resolution electromagnetic tomography [eLORETA]) level. Signal quality was evaluated with signal-to-noise ratio, participant-level spectra, and frequency PCA covariance decomposition. Convergent and discriminant validity were assessed within a multitrait-multimethod framework. Posterior alpha was reliably identified as two spectral components, each with unique spatial patterns and condition effects (eyes open/closed), high signal quality, and good convergent and discriminant validity. In contrast, frontal theta was characterized by one low-variance component, low signal quality, lack of a distinct spectral peak, and mixed validity. Correlations between candidate biomarkers suggest that posterior alpha components constitute reliable, convergent, and discriminant biometrics in healthy adults. Component-based identification of spectral activity (CSD/eLORETA-fPCA) was superior to fixed, a priori frequency bands. Improved quantification and conceptualization of frontal theta is necessary to determine clinical utility.

Objectives: This report examined theta-band neurodynamics for potential biomarkers of brain health in athletes with concussion. Methods: Participants included college-age contact/collision athletes with (N=24) and without a history of concussion (N=16) in Study 1. Study 2 (N=10) examined changes over time in contact/collision athletes. There were two primary dependent variables: (1) theta-band phase-synchronization (e.g., functional connectivity) between medial and right-lateral electrodes; and (2) the within-subject correlation between synchronization strength on error trials and post-error reaction time (i.e., operationalization of cognitive control). Results: Head injury history was inversely related with medial-lateral connectivity. Head injury was also related to declines in a neurobehavioral measure of cognitive control (i.e., the single-trial relationship between connectivity and post-error slowing). Conclusions: Results align with a theory of connectivity-mediated cognitive control. Mild injuries undetectable by behavioral measures may still be apparent on direct measures of neural functioning. This report demonstrates that connectivity and cognitive control measures may be useful for tracking recovery from concussion. Theoretically relevant neuroscientific findings in healthy adults may have applications in patient populations, especially with regard to monitoring brain health. (JINS 2019, 25, 314-323)

Background: Despite its designation as a 'dissociative anaesthetic,' the dissociative and psychoactive effects of ketamine remain incompletely understood. The goal of this study was to characterise the subjective experiences and accompanying EEG changes with subanaesthetic doses of ketamine. Methods: High-density EEG was recorded in 15 human volunteers before, during, and after subanaesthetic ketamine infusion (0.5 mg kg(-1) over 40 min), with self-reported measures of altered states of consciousness obtained after ketamine exposure. Sensor- and source-level EEG changes were analysed with a focus on spectral power and regional changes. Results: Ketamine-induced altered states were characterised predominantly by dissociative experiences such as disembodiment and ego transcendence; sensory disturbances were also common. Ketamine broadly decreased low-frequency power, with mean reductions largest at alpha (8-12 Hz) in parietal ( 0.94 dB, P<0.001) and occipital ( 1.8 dB, P<0.001) channel clusters. Significant decreases in alpha were identified in the precuneus and temporal-parietal junction. Conclusions: Ketamine induces altered states of consciousness during periods of reduced alpha power in the precuneus and temporal-parietal junction. Modulation of these temporal-parietal loci are candidate mechanisms of the psychoactive effects of ketamine, given that this region is involved in multisensory integration, body representation, and consciousness.

Frontal EEG alpha asymmetry provides a promising index of depression risk, yet very little is known about the neural sources of alpha asymmetry. To identify these sources, this study examined alpha asymmetry using a distributed inverse solution: exact low resolution brain electromagnetic tomography (eLORETA). Findings implicated a generator in lateral midfrontal regions that contributed to both surface asymmetry and depression risk. Participants with any lifetime history of depressive episodes were characterized by less left than right activity in the precentral gyrus and midfrontal gyrus. Anhedonia accounted for a significant portion of the relationship between alpha asymmetry and lifetime major depressive disorder. Results are suggestive of convergence between motivational and capability models of asymmetry and replicate results from experimental studies in a large resting-state data set. The capability model of frontal alpha asymmetry is contextualized in terms of motor preparedness following emotional mobilization.

Frontal electroencephalographic (EEG) alpha asymmetry is widely researched in studies of emotion, motivation, and psychopathology, yet it is a metric that has been quantified and analyzed using diverse procedures, and diversity in procedures muddles cross-study interpretation. The aim of this article is to provide an updated tutorial for EEG alpha asymmetry recording, processing, analysis, and interpretation, with an eye towards improving consistency of results across studies. First, a brief background in alpha asymmetry findings is provided. Then, some guidelines for recording, processing, and analyzing alpha asymmetry are presented with an emphasis on the creation of asymmetry scores, referencing choices, and artifact removal. Processing steps are explained in detail, and references to MATLAB-based toolboxes that are helpful for creating and investigating alpha asymmetry are noted. Then, conceptual challenges and interpretative issues are reviewed, including a discussion of alpha asymmetry as a mediator/moderator of emotion and psychopathology. Finally, the effects of two automated component-based artifact correction algorithms—MARA and ADJUST—on frontal alpha asymmetry are evaluated.