Group Differences In Neural Activity Research Articles

State-specific alterations in the neural computations underlying inhibitory control in women remitted from bulimia nervosa.

The neurocomputational processes underlying bulimia nervosa and its primary symptoms, out-of-control overeating and purging, are poorly understood. Research suggests that the brains of healthy individuals form a dynamic internal model to predict whether control is needed in each moment. This study tested the hypothesis that this computational process of inhibitory control is abnormally affected by metabolic state (being fasted or fed) in bulimia nervosa. A Bayesian ideal observer model was fit to behavioral data acquired from 22 women remitted from bulimia nervosa and 20 group-matched controls who completed a stop-signal task during two counterbalanced functional MRI sessions, one after a 16 h fast and one after a meal. This model estimates participants' trial-by-trial updating of the probability of a stop signal based on their experienced trial history. Neural analyses focused on control-related Bayesian prediction errors, which quantify the direction and degree of "surprise" an individual experiences on any given trial. Regardless of group, metabolic state did not affect behavioral performance on the task. However, metabolic state modulated group differences in neural activation. In the fed state, women remitted from bulimia nervosa had attenuated prediction-error-dependent activation in the left dorsal caudate. This fed-state activation was lower among women with more frequent past binge eating and self-induced vomiting. When they are in a fed state, individuals with bulimia nervosa may not effectively process unexpected information needed to engage inhibitory control. This may explain the difficulties these individuals have stopping eating after it begins.

Aberrant reward-related neural activation: Dimensional correlate of binge-eating severity or categorical marker of binge eating?

Binge eating (BE) is characterized by consuming an objectively large amount of food in a short period of time and experiencing loss of control over one's eating. The neural underpinnings of monetary reward anticipation and their association with BE severity remain poorly understood. Fifty-nine women aged 18 to 35 (M = 25.67, SD = 5.11) with a range of average weekly BE frequency (M = 1.96, SD = 1.89, range = 0–7) completed the Monetary Incentive Delay Task during fMRI scanning. Mean percent signal change within the left and right nucleus accumbens (NAc) during anticipation of monetary gain (versus non-gain) was extracted from a priori-defined functional 5 mm spheres and correlated with average weekly BE frequency. Exploratory voxel-wise whole-brain analyses examined the association between neural activation during anticipation of monetary reward and average weekly BE frequency. Body mass index and depression severity were covariates of non-interest in analyses. Mean percent signal change in the left and right NAc inversely correlated with average weekly BE frequency. Whole-brain analysis revealed no significant associations between neural activation during reward anticipation and average weekly BE frequency. In exploratory case-control analyses, mean percent signal change in the right NAc was significantly lower in women with BE (n = 41) versus women without BE (n = 18), but whole-brain analyses revealed no significant group differences in neural activation during reward anticipation. Decreased right NAc activity during monetary reward anticipation may distinguish women with and without BE.

Brain activity during pursuit and goal-conflict threat avoidance in major depressive disorder.

Threat avoidance is a prominent symptom of affective disorders, yet its biological basis remains poorly understood. Here, we used a validated task, the Joystick Operated Runway Task (JORT), combined with fMRI, to explore whether abnormal function in neural circuits responsible for avoidance underlies these symptoms. Eighteen individuals with major depressive disorder (MDD) and 17 unaffected controls underwent the task, which involved using physical effort to avoid threatening stimuli, paired with mild electric shocks on certain trials. Activity during anticipation and avoidance of threats was explored and compared between groups. Anticipation of aversive stimuli was associated with significant activation in the dorsal anterior cingulate cortex, superior frontal gyrus, and striatum, while active avoidance of aversive stimuli was associated with activity in dorsal anterior cingulate cortex, insula, and prefrontal cortex. There were no significant group differences in neural activity or behavioral performance on the JORT; however, participants with depression reported more dread while being chased on the task. The JORT effectively identified neural systems involved in avoidance and anticipation of aversive stimuli. However, the absence of significant differences in behavioral performance and activation between depressed and non-depressed groups suggests that MDD is not associated with abnormal function in these networks. Future research should investigate the basis of passive avoidance in major depression. Further, the JORT should be explored in patients with anxiety disorders, where threat avoidance may be a more prominent characteristic of the disorder.

Neural Correlates of Successful Memory Encoding in Kindergarten and Early Elementary School Children: Longitudinal Trends and Effects of Schooling.

From age 5 to 7, there are remarkable improvements in children's cognitive abilities ("5-7 shift"). In many countries, including Germany, formal schooling begins in this age range. It is, thus, unclear to what extent exposure to formal schooling contributes to the "5-7 shift." In this longitudinal study, we investigated if schooling acts as a catalyst of maturation. We tested 5-year-old children who were born close to the official cutoff date for school entry and who were still attending a play-oriented kindergarten. One year later, the children were tested again. Some of the children had experienced their first year of schooling whereas the others had remained in kindergarten. Using 2 functional magnetic resonance imaging tasks that assessed episodic memory formation (i.e., subsequent memory effect), we found that children relied strongly on the medial temporal lobe (MTL) at both time points but not on the prefrontal cortex (PFC). In contrast, older children and adults typically show subsequent memory effects in both MTL and PFC. Both children groups improved in their memory performance, but there were no longitudinal changes nor group differences in neural activation. We conclude that successful memory formation in this age group relies more heavily on the MTL than in older age groups.

Neural Correlates of Theory of Mind Are Preserved in Young Women With Anorexia Nervosa.

People with anorexia nervosa (AN) commonly exhibit social difficulties, which may be related to problems with understanding the perspectives of others, commonly known as Theory of Mind (ToM) processing. However, there is a dearth of literature investigating the neural basis of these differences in ToM and at what age they emerge. This study aimed to test for differences in the neural correlates of ToM processes in young women with AN, and young women weight-restored (WR) from AN, as compared to healthy control participants (HC). Based on previous findings in AN, we hypothesized that young women with current or prior AN, as compared to HCs, would exhibit a reduced neural response in the medial prefrontal cortex (mPFC), the inferior frontal gyrus, and the temporo-parietal junction (TPJ) whilst completing a ToM task. We recruited 73 young women with AN, 45 WR young women, and 70 young women without a history of AN to take part in the current study. Whilst undergoing a functional magnetic resonance imaging (fMRI) scan, participants completed the Frith-Happé task, which is a commonly used measure of ToM with demonstrated reliability and validity in adult populations. In this task, participants viewed the movements of triangles, which depicted either action movements, simple interactions, or complex social interactions. Viewing trials with more complex social interactions in the Frith-Happé task was associated with increased brain activation in regions including the right TPJ, the bilateral mPFC, the cerebellum, and the dorsolateral prefrontal cortex. There were no group differences in neural activation in response to the ToM contrast. Overall, these results suggest that the neural basis of spontaneous mentalizing is preserved in most young women with AN.

The Influence of Subclinical Neck Pain on Neurophysiological and Behavioral Measures of Multisensory Integration.

Multisensory integration (MSI) is necessary for the efficient execution of many everyday tasks. Alterations in sensorimotor integration (SMI) have been observed in individuals with subclinical neck pain (SCNP). Altered audiovisual MSI has previously been demonstrated in this population using performance measures, such as reaction time. However, neurophysiological techniques have not been combined with performance measures in the SCNP population to determine differences in neural processing that may contribute to these behavioral characteristics. Electroencephalography (EEG) event-related potentials (ERPs) have been successfully used in recent MSI studies to show differences in neural processing between different clinical populations. This study combined behavioral and ERP measures to characterize MSI differences between healthy and SCNP groups. EEG was recorded as 24 participants performed 8 blocks of a simple reaction time (RT) MSI task, with each block consisting of 34 auditory (A), visual (V), and audiovisual (AV) trials. Participants responded to the stimuli by pressing a response key. Both groups responded fastest to the AV condition. The healthy group demonstrated significantly faster RTs for the AV and V conditions. There were significant group differences in neural activity from 100–140 ms post-stimulus onset, with the control group demonstrating greater MSI. Differences in brain activity and RT between individuals with SCNP and a control group indicate neurophysiological alterations in how individuals with SCNP process audiovisual stimuli. This suggests that SCNP alters MSI. This study presents novel EEG findings that demonstrate MSI differences in a group of individuals with SCNP.

Identifying electrophysiological markers of autism spectrum disorder and schizophrenia against a backdrop of normal brain development.

An examination of electroencephalographic and magnetoencephalographic studies demonstrates how age-related changes in brain neural function temporally constrain their use as diagnostic markers. A first example shows that, given maturational changes in the resting-state peak alpha frequency in typically developing children but not in children who have autism spectrum disorder (ASD), group differences in alpha-band activity characterize only a subset of children who have ASD. A second example, auditory encoding processes in schizophrenia, shows that the complication of normal age-related brain changes on detecting and interpreting group differences in neural activity is not specific to children. MRI studies reporting group differences in the rate of brain maturation demonstrate that a group difference in brain maturation may be a concern for all diagnostic brain markers. Attention to brain maturation is needed whether one takes a DSM-5 or a Research Domain Criteria approach to research. For example, although there is interest in cross-diagnostic studies comparing brain measures in ASD and schizophrenia, such studies are difficult given that measures are obtained in one group well after and in the other much closer to the onset of symptoms. In addition, given differences in brain activity among infants, toddlers, children, adolescents, and younger and older adults, creating tasks and research designs that produce interpretable findings across the life span and yet allow for development is difficult at best. To conclude, brain imaging findings show an effect of brain maturation on diagnostic markers separate from (and potentially difficult to distinguish from) effects of disease processes. Available research with large samples already provides direction about the age range(s) when diagnostic markers are most robust and informative.

Cathodal tDCS impacts the fear network activity and connectivity patterns during a therapy-like extinction session

Background Transcranial direct current stimulation (tDCS) has been studied as an add-on enhancer of extinction-based treatments for anxiety disorders. Previous studies have showed that although anodal tDCS enhances fear extinction it also leads to decreased stimuli discrimination and consequent generalization of the fear response. Here we aim to understand the impact of cathodal tDCS in the neural activity and connectivity patterns between the tDCS target site (the right dorsolateral prefrontal cortex; rDLPFC) and the extant fear network (the bilateral amygdala, bilateral hippocampus, bilateral insula and the ventro medial prefrontal cortex [vmPFC]). Additionally we aim to see if cathodal tDCS leads to adverse effects similar to the ones observed with anodal stimulation. Methods We used a three-day fear conditioning procedure (day 1–fear acquisition; day 2–20-min 1 mA cathodal tDCS (only tDCS group)+ fear extinction; day 3–fear re-instatement and fear re-extinction). Thirty-four female participants where randomly assigned to either the tDCS group (n = 16) or the control group (n = 18). In day 1 fear acquisition was confirmed by self-reported contingency ratings. In day 2 we observed the between group differences in neural activity and connectivity patterns during extinction. In day 3 we observed the self-reported measures of stimuli contingency and reaction times during an approach-avoidance task to tackle the unconscious, automatic and involuntary avoidance responses. Results Functional magnetic resonance imagining (fMRI) group-level maps showed that cathodal tDCS over rDLPFC effectively reduces the right hippocampus activity during the processing of the conditioned stimuli during extinction. Furthermore, group-level psychophysiological interaction analysis (PPI) showed that cathodal tDCS effectively interferes with the fear response neural network. In particular, during the processing of the conditioned stimuli in late extinction phase, tDCS inverts the positive coupling between the vmPFC and a broad range of prefrontal structures, in particular the right and left DLPFC that participate in the regulation of negative emotions. Finally, day 3 measures showed decreased contingency ratings for the neutral cue and increased stimuli discrimination in the tDCS group, suggesting that cathodal tDCS does not lead to increased generalization. Conclusion Our promising results show that 1 mA cathodal tDCS effectively interferes with a large-scale cortico-subcortical fear network during extinction, and confirms that tDCS is a potential add-on strategy to enhance extinction-based treatments. Future studies should observe the adequate parameters of stimulation for the simultaneous enhancement of extinction learning and increased stimuli discrimination.

Face perception enhances insula and motor network reactivity in Tourette syndrome.

Tourette syndrome is a neurodevelopmental disorder, characterized by motor and phonic tics. Tics are typically experienced as avolitional, compulsive, and associated with premonitory urges. They are exacerbated by stress and can be triggered by external stimuli, including social cues like the actions and facial expressions of others. Importantly, emotional social stimuli, with angry facial stimuli potentially the most potent social threat cue, also trigger behavioural reactions in healthy individuals, suggesting that such mechanisms may be particularly sensitive in people with Tourette syndrome. Twenty-one participants with Tourette syndrome and 21 healthy controls underwent functional MRI while viewing faces wearing either neutral or angry expressions to quantify group differences in neural activity associated with processing social information. Simultaneous video recordings of participants during neuroimaging enabled us to model confounding effects of tics on task-related responses to the processing of faces. In both Tourette syndrome and control participants, face stimuli evoked enhanced activation within canonical face perception regions, including the occipital face area and fusiform face area. However, the Tourette syndrome group showed additional responses within the anterior insula to both neutral and angry faces. Functional connectivity during face viewing was then examined in a series of psychophysiological interactions. In participants with Tourette syndrome, the insula showed functional connectivity with a set of cortical regions previously implicated in tic generation: the presupplementary motor area, premotor cortex, primary motor cortex, and the putamen. Furthermore, insula functional connectivity with the globus pallidus and thalamus varied in proportion to tic severity, while supplementary motor area connectivity varied in proportion to premonitory sensations, with insula connectivity to these regions increasing to a greater extent in patients with worse symptom severity. In addition, the occipital face area showed increased functional connectivity in Tourette syndrome participants with posterior cortical regions, including primary somatosensory cortex, and occipital face area connectivity with primary somatosensory and primary motor cortices varied in proportion to tic severity. There were no significant psychophysiological interactions in controls. These findings highlight a potential mechanism in Tourette syndrome through which heightened representation within insular cortex of embodied affective social information may impact the reactivity of subcortical motor pathways, supporting programmed motor actions that are causally implicated in tic generation. Medicinal and psychological therapies that focus on reducing insular hyper-reactivity to social stimuli may have potential benefit for tic reduction in people with Tourette syndrome.

A Pilot Study of Neural Correlates of Loss of Control Eating in Children With Overweight/Obesity: Probing Intermittent Access to Food as a Means of Eliciting Disinhibited Eating.

Neural substrates of loss of control (LOC) eating are undercharacterized. We aimed to model intermittent access to food to elicit disinhibited eating in youth undergoing neuroimaging, given evidence that restricted food access may increase subsequent food intake via enhancing reward value of food and diminishing eating-related self-control. Participants were 18 preadolescents (aged 9-12 years) who were overweight/obese with recent LOC eating (OW-LOC; n = 6); overweight/obese with no history of LOC eating (OW-CON; n = 5); or non-overweight with no history of LOC eating (NW-CON; n = 7). Participants underwent functional magnetic resonance imaging during a simulated food restriction paradigm in which they were alternately given restricted or unrestricted access to milkshake solutions. There were no significant main effects of restricted versus unrestricted access to milkshake flavors. Group main effects revealed increased activation for OW-LOC relative to OW-CON in areas related to attentional processes (right middle frontal gyrus), inhibitory control/attentional shifts (right and left cuneus), and emotion regulation (left cingulate gyrus); and for OW-LOC relative to NW-CON in areas related to response inhibition (right inferior frontal gyrus). Significant block type × group interaction effects were found for the right middle frontal gyrus, left cingulate gyrus, and left cuneus, but these appeared to be accounted for primarily by group. There were clear group differences in neural activity in brain regions related to self-regulation during a food restriction paradigm. Elevations in these regions among OW-LOC relative to OW-CON and NW-CON, respectively, may suggest that youth with LOC eating expended more cognitive effort to regulate ingestive behavior.

The real-life costs of emotion regulation in anorexia nervosa: a combined ecological momentary assessment and fMRI study

Regulation of emotions is necessary for successful attainment of short-term and long-term goals. However, over-regulation may also have its costs. In anorexia nervosa (AN), forgoing food intake despite emaciation and endocrine signals that promote eating is an example of “too much” self-control. Here we investigated whether voluntary emotion regulation in AN patients comes with associated disorder-relevant costs. Thirty-five patients with acute AN and thirty-five age-matched healthy controls (HCs) performed an established emotion regulation paradigm during functional magnetic resonance imaging after an overnight fast. The task required reducing emotions induced by positively valenced pictures via distancing. We calculated a neural regulation score from responses recorded in a reward-related brain region of interest (ventral striatum; VS) by subtracting activation measured on “positive distance” trials from that elicited under the “positive watch” (baseline) condition. Complementing the imaging data, we used ecological momentary assessment (EMA) to probe disorder-related rumination and affect six times/day for 2 weeks following the scanning session. The neural regulation score indicating reduced VS activation during emotion regulation was used as a predictor in hierarchical linear models with EMA measures as outcomes. No group differences in neural activity were found for the main contrasts of the task. However, regulation of VS activity was associated with increased body-related rumination and increased negative affect in AN, but not in HC. In line with this finding, correlational analysis with longitudinal BMI measurements revealed a link between greater VS regulation and poorer treatment outcome after 60 and 90 days. Together, these results identify a neural correlate of altered emotion regulation in AN, which seems to be detrimental to psychological well-being and may interfere with recovery.

Hypersensitivity to low intensity fearful faces in autism when fixation is constrained to the eyes.

Previous studies that showed decreased brain activation in people with autism spectrum disorder (ASD) viewing expressive faces did not control that participants looked in the eyes. This is problematic because ASD is characterized by abnormal attention to the eyes. Here, we collected fMRI data from 48 participants (27 ASD) viewing pictures of neutral faces and faces expressing anger, happiness, and fear at low and high intensity, with a fixation cross between the eyes. Group differences in whole brain activity were examined for expressive faces at high and low intensity versus neutral faces. Group differences in neural activity were also investigated in regions of interest within the social brain, including the amygdala and the ventromedial prefrontal cortex (vmPFC). In response to low intensity fearful faces, ASD participants showed increased activation in the social brain regions, and decreased functional coupling between the amygdala and the vmPFC. This oversensitivity to low intensity fear coupled with a lack of emotional regulation capacity could indicate an excitatory/inhibitory imbalance in their socio-affective processing system. This may result in social disengagement and avoidance of eye-contact to handle feelings of strong emotional reaction. Our results also demonstrate the importance of careful control of gaze when investigating emotional processing in ASD. Hum Brain Mapp 38:5943-5957, 2017. © 2017 Wiley Periodicals, Inc.

Hypersensitivity to low intensity fearful faces in autism when fixation is constrained to the eyes

Previous studies that showed decreased brain activation in people with autism spectrum disorder (ASD) viewing expressive faces did not control that participants looked in the eyes. This is problematic because ASD is characterized by abnormal attention to the eyes. Here, we collected fMRI data from 48 participants (27 ASD) viewing pictures of neutral faces and faces expressing anger, happiness, and fear at low and high intensity, with a fixation cross between the eyes. Group differences in whole brain activity were examined for expressive faces at high and low intensity versus neutral faces. Group differences in neural activity were also investigated in regions of interest within the social brain, including the amygdala and the ventromedial prefrontal cortex (vmPFC). In response to low intensity fearful faces, ASD participants showed increased activation in the social brain regions, and decreased functional coupling between the amygdala and the vmPFC. This oversensitivity to low intensity fear coupled with a lack of emotional regulation capacity could indicate an excitatory/inhibitory imbalance in their socio-affective processing system. This may result in social disengagement and avoidance of eye-contact to handle feelings of strong emotional reaction. Our results also demonstrate the importance of careful control of gaze when investigating emotional processing in ASD. Hum Brain Mapp 38:5943-5957, 2017. © 2017 Wiley Periodicals, Inc.

Blunted Neural Responses to Reward in Remitted Major Depression: A High-Density Event-Related Potential Study

BackgroundMajor depressive disorder (MDD) is a highly recurrent condition, and improving our understanding of the abnormalities that persist in remitted MDD (rMDD) may provide insight into mechanisms that contribute to relapse. Reward learning deficits linked to dysfunction in frontostriatal regions are characteristic of MDD. Although initial behavioral evidence of reward learning deficits in rMDD has emerged, it is unclear whether these deficits reflect impairments in neural reward processing that persist into remission. MethodsWe examined behavioral reward learning and 128-channel event-related potentials (ERPs) during a well-validated probabilistic reward task in 26 individuals with rMDD and 34 control subjects with no history of depression. Temporospatial principal components analysis was used to separate overlapping ERP components, and group differences in neural activity in a priori regions were examined using low-resolution electromagnetic tomography. ResultsIndividuals with rMDD displayed reduced behavioral reward learning and blunted ERP amplitude to reward feedback. The reduction in ERP amplitude occurred at a principal components analysis factor that peaked during the time at which phasic reward feedback-related signaling—hypothesized to originate in the striatum and project to the anterior cingulate cortex—is thought to modulate scalp-recorded activity. Consistent with this finding, low-resolution electromagnetic tomography analyses revealed reduced activity in the anterior cingulate cortex in the rMDD group, and this blunting correlated with poorer reward learning. ConclusionsThese findings suggest that the reward learning impairment observed in acute MDD persists into full remission and that these impairments may be attributable to abnormalities in the neural processes that support reward feedback monitoring, particularly within the anterior cingulate cortex.

Neural circuitry of abdominal pain‐related fear learning and reinstatement in irritable bowel syndrome

Altered pain anticipation likely contributes to disturbed central pain processing in chronic pain conditions like irritable bowel syndrome (IBS), but the learning processes shaping the expectation of pain remain poorly understood. We assessed the neural circuitry mediating the formation, extinction, and reactivation of abdominal pain-related memories in IBS patients compared to healthy controls (HC) in a differential fear conditioning paradigm. During fear acquisition, predictive visual cues (CS(+)) were paired with rectal distensions (US), while control cues (CS(-)) were presented unpaired. During extinction, only CSs were presented. Subsequently, memory reactivation was assessed with a reinstatement procedure involving unexpected USs. Using functional magnetic resonance imaging, group differences in neural activation to CS(+) vs CS(-) were analyzed, along with skin conductance responses (SCR), CS valence, CS-US contingency, state anxiety, salivary cortisol, and alpha-amylase activity. The contribution of anxiety symptoms was addressed in covariance analyses. Fear acquisition was altered in IBS, as indicated by more accurate contingency awareness, greater CS-related valence change, and enhanced CS(+)-induced differential activation of prefrontal cortex and amygdala. IBS patients further revealed enhanced differential cingulate activation during extinction and greater differential hippocampal activation during reinstatement. Anxiety affected neural responses during memory formation and reinstatement. Abdominal pain-related fear learning and memory processes are altered in IBS, mediated by amygdala, cingulate cortex, prefrontal areas, and hippocampus. Enhanced reinstatement may contribute to hypervigilance and central pain amplification, especially in anxious patients. Preventing a 'relapse' of learned fear utilizing extinction-based interventions may be a promising treatment goal in IBS.

Neural and cortisol responses during play with human and computer partners in children with autism.

Children with autism spectrum disorder (ASD) exhibit impairment in reciprocal social interactions, including play, which can manifest as failure to show social preference or discrimination between social and nonsocial stimuli. To explore mechanisms underlying these deficits, we collected salivary cortisol from 42 children 8-12 years with ASD or typical development during a playground interaction with a confederate child. Participants underwent functional MRI during a prisoner's dilemma game requiring cooperation or defection with a human (confederate) or computer partner. Search region of interest analyses were based on previous research (e.g. insula, amygdala, temporal parietal junction-TPJ). There were significant group differences in neural activation based on partner and response pattern. When playing with a human partner, children with ASD showed limited engagement of a social salience brain circuit during defection. Reduced insula activation during defection in the ASD children relative to TD children, regardless of partner type, was also a prominent finding. Insula and TPJ BOLD during defection was also associated with stress responsivity and behavior in the ASD group under playground conditions. Children with ASD engage social salience networks less than TD children during conditions of social salience, supporting a fundamental disturbance of social engagement.

Reward-based spatial learning in unmedicated adults with obsessive-compulsive disorder.

The authors assessed the functioning of mesolimbic and striatal areas involved in reward-based spatial learning in unmedicated adults with obsessive-compulsive disorder (OCD). Functional MRI blood-oxygen-level-dependent response was compared in 33 unmedicated adults with OCD and 33 healthy, age-matched comparison subjects during a reward-based learning task that required learning to use extramaze cues to navigate a virtual eight-arm radial maze to find hidden rewards. The groups were compared in their patterns of brain activation associated with reward-based spatial learning versus a control condition in which rewards were unexpected because they were allotted pseudorandomly to experimentally prevent learning. Both groups learned to navigate the maze to find hidden rewards, but group differences in neural activity during navigation and reward processing were detected in mesolimbic and striatal areas. During navigation, the OCD group, unlike the healthy comparison group, exhibited activation in the left posterior hippocampus. Unlike healthy subjects, participants in the OCD group did not show activation in the left ventral putamen and amygdala when anticipating rewards or in the left hippocampus, amygdala, and ventral putamen when receiving unexpected rewards (control condition). Signal in these regions decreased relative to baseline during unexpected reward receipt among those in the OCD group, and the degree of activation was inversely associated with doubt/checking symptoms. Participants in the OCD group displayed abnormal recruitment of mesolimbic and ventral striatal circuitry during reward-based spatial learning. Whereas healthy comparison subjects exhibited activation in this circuitry in response to the violation of reward expectations, unmedicated OCD participants did not and instead over-relied on the posterior hippocampus during learning. Thus, dopaminergic innervation of reward circuitry may be altered, and future study of anterior/posterior hippocampal dysfunction in OCD is warranted.

Neural changes with attention bias modification for anxiety: a randomized trial.

Attention bias modification (ABM) procedures typically reduce anxiety symptoms, yet little is known about the neural changes associated with this behavioral treatment. Healthy adults with high social anxiety symptoms (n = 53) were randomized to receive either active or placebo ABM. Unlike placebo ABM, active ABM aimed to train individuals' attention away from threat. Using the dot-probe task, threat-related attention bias was measured during magnetic resonance imaging before and after acute and extended training over 4 weeks. A subset of participants completed all procedures (n = 30, 15 per group). Group differences in neural activation were identified using standard analyses. Linear regression tested predictive factors of symptom reduction (i.e., training group, baseline indices of threat bias). The active and placebo groups exhibited different patterns of right and left amygdala activation with training. Across all participants irrespective of group, individuals with greater left amygdala activation in the threat-bias contrast prior to training exhibited greater symptom reduction. After accounting for baseline amygdala activation, greater symptom reduction was associated with assignment to the active training group. Greater left amygdala activation at baseline predicted reductions in social anxiety symptoms following ABM. Further research is needed to clarify brain-behavior mechanisms associated with ABM training.

A comparison of neural correlates underlying social cognition in Klinefelter syndrome and autism

Klinefelter syndrome (KS) is a genetic syndrome characterized by the presence of an extra X chromosome that appears to increase the risk of psychopathology, such as autism symptoms. This study used functional magnetic resonance imaging to determine underlying mechanisms related to this risk, with the aim of gaining insight into neural mechanisms behind social-cognitive dysfunction in KS and autism, and understanding similarities and differences in social information processing deficits. Fourteen boys with KS, seventeen boys with autism spectrum disorders (ASD) and nineteen non-clinical male controls aged 10-18 years were scanned while matching and labeling facial expressions (i.e. face processing and affect labeling, respectively). No group differences in neural activation were found during face processing. However, during affect labeling, the ASD group showed increased activation in the amygdala compared with controls, while the KS group showed increased activation in frontal areas compared with both controls and the ASD group. No group differences in task performance were found. Although behavioral symptoms of social dysfunction appear similar both in boys with KS and ASD, this is the first study to demonstrate different underlying etiologies. These results may aid in identifying different pathways to autism symptoms, which may help understanding variability within the ASD spectrum.

Lack of long-term fMRI differences after multiple sports-related concussions

Introduction: Mild traumatic brain injury (mTBI) or concussion has been acutely associated with several cognitive symptoms, including deficits in response inhibition, working memory and motor performance. The pervasiveness of these cognitive symptoms has been more controversial. The effects of multiple concussions on neuropsychological functioning and brain activation following at least 6-months post-mTBI were examined.Methods: Twenty right-handed male athletes with a history of at least two concussions and 20 age/pre-morbid IQ/athletic-experience matched controls underwent neuropsychological assessment and fMRI scanning where they performed versions of a colour-word Stroop interference task, an operation-span working memory task and a finger-tapping task.Results: The Attention index score on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) was lower for the concussion group, but only at liberal statistical threshold. Total RBANS score approached statistical significance. Reaction time during neurobehavioural tasks was similar across groups, but accuracy was reduced in the concussed group on the working memory task. Despite expected activation patterns within each group, there were no group differences in neural activation on any functional tasks using either whole-brain or ROI-specific analyses at liberal statistical thresholds.Conclusion: There were minimal differences between the two closely matched groups. Results point to the relative plasticity of younger adults’ cognitive abilities following concussion.