Risk factors for internalizing symptoms: The influence of empathy, theory of mind, and negative thinking processes.

Internalizing symptoms such as elevated stress and sustained negative affect can be important warning signs for developing mental disorders. A recent theoretical framework suggests a complex interplay of empathy, theory of mind (ToM), and negative thinking processes as a crucial risk combination for internalizing symptoms. To disentangle these relationships, this study utilizes neural, behavioral, and self-report data to examine how the interplay between empathy, ToM, and negative thinking processes relates to stress and negative affect. We reanalyzed the baseline data of N = 302 healthy participants (57% female, Mage = 40.52, SDage = 9.30) who participated in a large-scale mental training study, the ReSource project. Empathy and ToM were assessed using a validated fMRI paradigm featuring naturalistic video stimuli and via self-report. Additional self-report scales were employed to measure internalizing symptoms (perceived stress, negative affect) and negative thinking processes (rumination and self-blame). Our results revealed linear associations of self-reported ToM and empathic distress with stress and negative affect. Also, both lower and higher, compared to average, activation in the anterior insula during empathic processing and in the middle temporal gyrus during ToM performance was significantly associated with internalizing symptoms. These associations were dependent on rumination and self-blame. Our findings indicate specific risk constellations for internalizing symptoms. Especially people with lower self-reported ToM and higher empathic distress may be at risk for more internalizing symptoms. Quadratic associations of empathy- and ToM-related brain activation with internalizing symptoms depended on negative thinking processes, suggesting differential effects of cognitive and affective functioning on internalizing symptoms. Using a multi-method approach, these findings advance current research by shedding light on which complex risk combinations of cognitive and affective functioning are relevant for internalizing symptoms.

Age-Related Enhancements in Positive Emotionality across The Life Span: Structural Equation Modeling of Brain and Behavior.

Aging is associated with a bias in attention and memories toward positive and away from negative emotional content. In addition, emotion regulation appears to improve with age, despite concomitant widespread cognitive decline coupled with gray matter volume loss in cortical and subcortical regions thought to subserve emotion regulation. Here, we address this emotion-aging paradox using the behavioral data of an emotion regulation task from a population-derived, male and female, human sample (CamCAN) and use structural equation modeling together with multivariate analysis of structural MRI images of the same sample to investigate brain-behavior relationships. In a series of measurement models, we show the relationship between age and emotionality is best explained by a four-factor model, compared with single and hierarchical factor models. These four latent factors are interpreted as Basal Negative Affect, Positive Reactivity, Negative Reactivity and Positive Regulation (upregulating positive emotion to negative content). Increasing age uniquely contributes to increased Basal Negative Affect, Positive Reactivity, and Positive Regulation, but not Negative Reactivity. Furthermore, we show gray matter volumes, namely in the bilateral frontal operculum, medial frontal gyrus, bilateral hippocampal complex, bilateral middle temporal gyri, and bilateral angular gyrus, are distinctly related to these four latent factors. Finally, we show that a subset of these brain-behavior relationships remain significant when accounting for age and demographic data. Our results support the notion of an age-related increase in positivity and are interpreted in the context of the socioemotional selectivity theory of improved emotion regulation in older age.SIGNIFICANCE STATEMENT Aging is associated with a paradoxical increase in well-being and improved emotion regulation despite widespread cognitive decline and gray matter volume loss in neural regions that underlie emotion regulation. Using a population-derived sample, we test the theories behind this emotion/aging paradox with an emotion regulation task and structural MRI data. We report robust age-related increases in positivity across the life span and show structural neural integrity influences this relationship with increasing age. Several brain-behavior relationships remained unaffected by age and may represent empirically derived neural markers to explore the paradox of increased well-being in old age. The results support the predictions of socioemotional selectivity theory of improved emotion regulation in older age and challenge the amygdala-focused neural predictions of the aging brain model.

Memory bias for social hierarchical information is modulated by perceived social rank.

Hierarchies pervade human society, characterising its members along diverse dimensions ranging from their abilities or skills in a particular domain to their economic status or physical stature. One intriguing aspect of the centrality of hierarchies, relative to egalitarian constructs, is that hierarchically-organised social information appears to be remembered more easily than non-hierarchically-organised information. However, it is not yet clear how one's social rank within a hierarchy influences processing. In a pre-registered study with 66 healthy participants, we examined memory recall for hierarchical information when participants themselves were positioned higher in the hierarchy versus lower in the hierarchy, both relative to an egalitarian control condition. The results replicate previous work showing that hierarchical information is memorised faster relative to the egalitarian control. Importantly, this effect was modulated by the participant's position within the hierarchy, with higher positioned participants memorising information faster than lower-positioned participants. This study provides new evidence showing biases in memory will favour hierarchical information if modulated by perceptions of one's own social rank.

Mood and neural responses to social rejection do not seem to be altered in resilient adolescents with a history of adversity.

Childhood adversity (CA) increases the risk of subsequent mental health problems. Adolescent social support (from family and/or friends) reduces the risk of mental health problems after CA. However, the mechanisms of this effect remain unclear, and we speculate that they are manifested on neurodevelopmental levels. Therefore, we investigated whether family and/or friendship support at ages 14 and 17 function as intermediate variables for the relationship between CA before age 11 and affective or neural responses to social rejection feedback at age 18. We studied 55 adolescents with normative mental health at age 18 (26 with CA and therefore considered "resilient"), from a longitudinal cohort. Participants underwent a Social Feedback Task in the magnetic resonance imaging scanner. Social rejection feedback activated the dorsal anterior cingulate cortex and the left anterior insula. CA did not predict affective or neural responses to social rejection at age 18. Yet, CA predicted better friendships at age 14 and age 18, when adolescents with and without CA had comparable mood levels. Thus, adolescents with CA and normative mood levels have more adolescent friendship support and seem to have normal mood and neural responses to social rejection.

Memory network plasticity after temporal lobe resection: a longitudinal functional imaging study.

Anterior temporal lobe resection can control seizures in up to 80% of patients with temporal lobe epilepsy. Memory decrements are the main neurocognitive complication. Preoperative functional reorganization has been described in memory networks, but less is known of postoperative reorganization. We investigated reorganization of memory-encoding networks preoperatively and 3 and 12 months after surgery. We studied 36 patients with unilateral medial temporal lobe epilepsy (19 right) before and 3 and 12 months after anterior temporal lobe resection. Fifteen healthy control subjects were studied at three equivalent time points. All subjects had neuropsychological testing at each of the three time points. A functional magnetic resonance imaging memory-encoding paradigm of words and faces was performed with subsequent out-of-scanner recognition assessments. Changes in activations across the time points in each patient group were compared to changes in the control group in a single flexible factorial analysis. Postoperative change in memory across the time points was correlated with postoperative activations to investigate the efficiency of reorganized networks. Left temporal lobe epilepsy patients showed increased right anterior hippocampal and frontal activation at both 3 and 12 months after surgery relative to preoperatively, for word and face encoding, with a concomitant reduction in left frontal activation 12 months postoperatively. Right anterior hippocampal activation 12 months postoperatively correlated significantly with improved verbal learning in patients with left temporal lobe epilepsy from preoperatively to 12 months postoperatively. Preoperatively, there was significant left posterior hippocampal activation that was sustained 3 months postoperatively at word encoding, and increased at face encoding. For both word and face encoding this was significantly reduced from 3 to 12 months postoperatively. Patients with right temporal lobe epilepsy showed increased left anterior hippocampal activation on word encoding from 3 to 12 months postoperatively compared to preoperatively. On face encoding, left anterior hippocampal activations were present preoperatively and 12 months postoperatively. Left anterior hippocampal and orbitofrontal cortex activations correlated with improvements in both design and verbal learning 12 months postoperatively. On face encoding, there were significantly increased left posterior hippocampal activations that reduced significantly from 3 to 12 months postoperatively. Postoperative changes occur in the memory-encoding network in both left and right temporal lobe epilepsy patients across both verbal and visual domains. Three months after surgery, compensatory posterior hippocampal reorganization that occurs is transient and inefficient. Engagement of the contralateral hippocampus 12 months after surgery represented efficient reorganization in both patient groups, suggesting that the contralateral hippocampus contributes to memory outcome 12 months after surgery.

Working memory network plasticity after anterior temporal lobe resection: a longitudinal functional magnetic resonance imaging study.

Working memory is a crucial cognitive function that is disrupted in temporal lobe epilepsy. It is unclear whether this impairment is a consequence of temporal lobe involvement in working memory processes or due to seizure spread to extratemporal eloquent cortex. Anterior temporal lobe resection controls seizures in 50-80% of patients with drug-resistant temporal lobe epilepsy and the effect of surgery on working memory are poorly understood both at a behavioural and neural level. We investigated the impact of temporal lobe resection on the efficiency and functional anatomy of working memory networks. We studied 33 patients with unilateral medial temporal lobe epilepsy (16 left) before, 3 and 12 months after anterior temporal lobe resection. Fifteen healthy control subjects were also assessed in parallel. All subjects had neuropsychological testing and performed a visuospatial working memory functional magnetic resonance imaging paradigm on these three separate occasions. Changes in activation and deactivation patterns were modelled individually and compared between groups. Changes in task performance were included as regressors of interest to assess the efficiency of changes in the networks. Left and right temporal lobe epilepsy patients were impaired on preoperative measures of working memory compared to controls. Working memory performance did not decline following left or right temporal lobe resection, but improved at 3 and 12 months following left and, to a lesser extent, following right anterior temporal lobe resection. After left anterior temporal lobe resection, improved performance correlated with greater deactivation of the left hippocampal remnant and the contralateral right hippocampus. There was a failure of increased deactivation of the left hippocampal remnant at 3 months after left temporal lobe resection compared to control subjects, which had normalized 12 months after surgery. Following right anterior temporal lobe resection there was a progressive increase of activation in the right superior parietal lobe at 3 and 12 months after surgery. There was greater deactivation of the right hippocampal remnant compared to controls between 3 and 12 months after right anterior temporal lobe resection that was associated with lesser improvement in task performance. Working memory improved after anterior temporal lobe resection, particularly following left-sided resections. Postoperative working memory was reliant on the functional capacity of the hippocampal remnant and, following left resections, the functional reserve of the right hippocampus. These data suggest that working memory following temporal lobe resection is dependent on the engagement of the posterior medial temporal lobes and eloquent cortex.

Language dominance assessment in a bilingual population: validity of fMRI in the second language.

OBJECTIVE: Assessment of language dominance using functional magnetic resonance imaging (fMRI) is a standard tool to estimate the risk of language function decline after epilepsy surgery. Although there has been considerable research in the characterization of language networks in bilingual individuals; little is known about the clinical usefulness of language mapping in a secondary language in patients with epilepsy, and how language lateralization assessed by fMRI may differ by the use of native or a secondary language paradigms. In this study we investigate language representation in a population of nonnative English speakers to assess differences in fMRI language lateralization between the first (native) and second language (English). METHODS: Sixteen nonnative English-speaking patients with focal drug-resistant epilepsy underwent language fMRI in their first (native) language (L1) and in English (L2). Differences between language maps using L1 and L2 paradigms were examined at the single subject level by comparing within-subject lateralization indexes obtained for each language. Differences at the group level were examined for each of the tasks and languages. RESULTS: Group maps for the second language (English) showed overlapping areas of activation with the native language, but with larger clusters, and more bilaterally distributed than for the first language. However, at the individual level, lateralization indexes were concordant between the two languages, except for one patient with bilateral hippocampal sclerosis who was left dominant in English and showed bilateral dominance for verb generation and right dominance for verbal fluency in his native tongue. SIGNIFICANCE: Language lateralization can generally be reliably derived from fMRI tasks in a second language provided that the subject can follow the task. Subjects with greater likelihood of atypical language representation should be evaluated more carefully, using more than one language paradigm.

A functional magnetic resonance imaging study mapping the episodic memory encoding network in temporal lobe epilepsy.

Functional magnetic resonance imaging has demonstrated reorganization of memory encoding networks within the temporal lobe in temporal lobe epilepsy, but little is known of the extra-temporal networks in these patients. We investigated the temporal and extra-temporal reorganization of memory encoding networks in refractory temporal lobe epilepsy and the neural correlates of successful subsequent memory formation. We studied 44 patients with unilateral temporal lobe epilepsy and hippocampal sclerosis (24 left) and 26 healthy control subjects. All participants performed a functional magnetic resonance imaging memory encoding paradigm of faces and words with subsequent out-of-scanner recognition assessments. A blocked analysis was used to investigate activations during encoding and neural correlates of subsequent memory were investigated using an event-related analysis. Event-related activations were then correlated with out-of-scanner verbal and visual memory scores. During word encoding, control subjects activated the left prefrontal cortex and left hippocampus whereas patients with left hippocampal sclerosis showed significant additional right temporal and extra-temporal activations. Control subjects displayed subsequent verbal memory effects within left parahippocampal gyrus, left orbitofrontal cortex and fusiform gyrus whereas patients with left hippocampal sclerosis activated only right posterior hippocampus, parahippocampus and fusiform gyrus. Correlational analysis showed that patients with left hippocampal sclerosis with better verbal memory additionally activated left orbitofrontal cortex, anterior cingulate cortex and left posterior hippocampus. During face encoding, control subjects showed right lateralized prefrontal cortex and bilateral hippocampal activations. Patients with right hippocampal sclerosis showed increased temporal activations within the superior temporal gyri bilaterally and no increased extra-temporal areas of activation compared with control subjects. Control subjects showed subsequent visual memory effects within right amygdala, hippocampus, fusiform gyrus and orbitofrontal cortex. Patients with right hippocampal sclerosis showed subsequent visual memory effects within right posterior hippocampus, parahippocampal and fusiform gyri, and predominantly left hemisphere extra-temporal activations within the insula and orbitofrontal cortex. Correlational analysis showed that patients with right hippocampal sclerosis with better visual memory activated the amygdala bilaterally, right anterior parahippocampal gyrus and left insula. Right sided extra-temporal areas of reorganization observed in patients with left hippocampal sclerosis during word encoding and bilateral lateral temporal reorganization in patients with right hippocampal sclerosis during face encoding were not associated with subsequent memory formation. Reorganization within the medial temporal lobe, however, is an efficient process. The orbitofrontal cortex is critical to subsequent memory formation in control subjects and patients. Activations within anterior cingulum and insula correlated with better verbal and visual subsequent memory in patients with left and right hippocampal sclerosis, respectively, representing effective extra-temporal recruitment.

Imaging the interaction: epileptic discharges, working memory, and behavior.

Interictal generalized epileptiform discharges may impair cognition. We used simultaneous video-electroencephalography and functional imaging to quantify changes, induced by epileptiform discharges, in the task-related activations during a spatial working-memory paradigm. The number of epileptiform discharges increased during the task with its level of complexity, but were not significantly associated with wrong responses during the task. We observed hemodynamic responses in working-memory related frontal-lobe-network, motor-cortex, precuneus, and parietal lobes in the absence of epileptiform discharges. In the presence of epileptiform discharges during the task, task-related hemodynamic changes were seen only in motor-cortex, precuneus, and parietal lobes. These findings suggest that generalized epileptiform discharges during a high demanding working memory task may change the working memory-related hemodynamic responses in frontal-lobe-network.

Optic radiation tractography and vision in anterior temporal lobe resection.

OBJECTIVE: Anterior temporal lobe resection (ATLR) is an effective treatment for refractory temporal lobe epilepsy but may result in a contralateral superior visual field deficit (VFD) that precludes driving in the seizure-free patient. Diffusion tensor imaging (DTI) tractography can delineate the optic radiation preoperatively and stratify risk. It would be advantageous to incorporate display of tracts into interventional magnetic resonance imaging (MRI) to guide surgery. METHODS: We studied 20 patients undergoing ATLR. Structural MRI scans, DTI, and visual fields were acquired before and 3 to 12 months following surgery. Tractography of the optic radiation was performed on preoperative images and propagated onto postoperative images. The anteroposterior extent of the damage to Meyer's loop was determined, and visual loss was quantified using Goldmann perimetry. RESULTS: Twelve patients (60%) suffered a VFD (10-92% of upper quadrant; median, 39%). Image registration took <3 minutes and predicted that Meyer's loop was 4.4 to 18.7mm anterior to the resection margin in these patients, but 0.0 to 17.6mm behind the resection margin in the 8 patients without VFD. The extent of damage to Meyer's loop significantly correlated with the degree of VFD and explained 65% of the variance in this measure. INTERPRETATION: The optic radiation can be accurately delineated by tractography and propagated onto postoperative images. The technique is fast enough to propagate accurate preoperative tractography onto intraoperative scans acquired during neurosurgery, with the potential to reduce the risk of VFD.

Structural correlates of impaired working memory in hippocampal sclerosis.

PURPOSE: Temporal lobe epilepsy (TLE) has been considered to impair long-term memory, whilst not affecting working memory, but recent evidence suggests that working memory is compromised. Functional MRI (fMRI) studies demonstrate that working memory involves a bilateral frontoparietal network the activation of which is disrupted in hippocampal sclerosis (HS). A specific role of the hippocampus to deactivate during working memory has been proposed with this mechanism faulty in patients with HS. Structural correlates of disrupted working memory in HS have not been explored. METHODS: We studied 54 individuals with medically refractory TLE and unilateral HS (29 left) and 28 healthy controls. Subjects underwent 3T structural MRI, a visuospatial n-back fMRI paradigm and diffusion tensor imaging (DTI). Working memory capacity assessed by three span tasks (digit span backwards, gesture span, motor sequences) was combined with performance in the visuospatial paradigm to give a global working memory measure. Gray and white matter changes were investigated using voxel-based morphometry and voxel-based analysis of DTI, respectively. KEY FINDINGS: Individuals with left or right HS performed less well than healthy controls on all measures of working memory. fMRI demonstrated a bilateral frontoparietal network during the working memory task with reduced activation of the right parietal lobe in both patient groups. In left HS, gray matter loss was seen in the ipsilateral hippocampus and parietal lobe, with maintenance of the gray matter volume of the contralateral parietal lobe associated with better performance. White matter integrity within the frontoparietal network, in particular the superior longitudinal fasciculus and cingulum, and the contralateral temporal lobe, was associated with working memory performance. In right HS, gray matter loss was also seen in the ipsilateral hippocampus and parietal lobe. Working memory performance correlated with the gray matter volume of both frontal lobes and white matter integrity within the frontoparietal network and contralateral temporal lobe. SIGNIFICANCE: Our data provide further evidence that working memory is disrupted in HS and impaired integrity of both gray and white matter is seen in functionally relevant areas. We suggest this forms the structural basis of the impairment of working memory, indicating widespread and functionally significant structural changes in patients with apparently isolated HS.

Risk-taking behavior in juvenile myoclonic epilepsy.

OBJECTIVE: Patients with juvenile myoclonic epilepsy (JME) often present with risk-taking behavior, suggestive of frontal lobe dysfunction. Recent studies confirm functional and microstructural changes within the frontal lobes in JME. This study aimed at characterizing decision-making behavior in JME and its neuronal correlates using functional magnetic resonance imaging (fMRI). METHODS: We investigated impulsivity in 21 JME patients and 11 controls using the Iowa Gambling Task (IGT), which measures decision making under ambiguity. Performance on the IGT was correlated with activation patterns during an fMRI working memory task. RESULTS: Both patients and controls learned throughout the task. Post hoc analysis revealed a greater proportion of patients with seizures than seizure-free patients having difficulties in advantageous decision making, but no difference in performance between seizure-free patients and controls. Functional imaging of working memory networks showed that overall poor IGT performance was associated with an increased activation in the dorsolateral prefrontal cortex (DLPFC) in JME patients. Impaired learning during the task and ongoing seizures were associated with bilateral medial prefrontal cortex (PFC) and presupplementary motor area, right superior frontal gyrus, and left DLPFC activation. SIGNIFICANCE: Our study provides evidence that patients with JME and ongoing seizures learn significantly less from previous experience. Interictal dysfunction within "normal" working memory networks, specifically, within the DLPFC and medial PFC structures, may affect their ability to learn.

Reduced social risk-taking in depression.

Evolutionary models of depression posit that depressed mood represents an adaptive response to unacceptably low social status, motivating the inhibition of social risk-taking in favor of submissive behaviors which reduce the likelihood of social exclusion. We tested the hypothesis of reduced social risk taking using a novel adaptation of the Balloon Analogue Risk Task (BART) in participants with major depressive disorder (MDD; n = 27) and never-depressed comparison participants (n = 35). The BART requires participants to pump up virtual balloons. The more the balloon is pumped up, the more money a participant gains on that trial. However, more pumps also increase the risk the balloon will burst such that all money is lost. Prior to performing the BART, participants took part in a team induction in small groups in order to prime social-group membership. Participants then completed two conditions of the BART: an Individual condition where they risked only their own money, and a Social condition, where they risked the money of their social group. The groups did not differ in their performance in the individual condition (Cohen's d = 0.07). However, the MDD group risked fewer pumps in the Social condition than the never-depressed group (d = 0.57). The study supports the notion of an aversion to social risk-taking in depression. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Reappraisal capacity is unrelated to depressive and anxiety symptoms.

Research suggests affective symptoms are associated with reduced habitual use of reappraisal as an emotion regulation strategy in individuals with mental health problems. Less is known, however, about whether mental health problems are related to reduced reappraisal capacity per se. The current study investigates this question using a film-based emotion regulation task that required participants to use reappraisal to downregulate their emotional response to highly evocative real-life film footage. We pooled data (N = 512, age: 18-89 years, 54% female) from 6 independent studies using this task. In contrast to our predictions, symptoms of depression and anxiety were unrelated to self-reported negative affect after reappraisal or to emotional reactivity to negative films. Implications for the measurement of reappraisal as well as future directions for research in the field of emotion regulation are discussed.

Script-driven imagery of socially salient autobiographical memories in major depressive disorder.

Cues of social rejection and affiliation represent proximal risk and protective factors in the onset and maintenance of depression. Such cues are thought to activate an evolutionarily primed neuro-cognitive alarm system, alerting the agent to the benefits of inclusion or the risk of social exclusion within social hierarchies focused on ensuring continued access to resources. In tandem, autobiographical memory is thought to be over-general and negatively biased in Major Depressive Disorder (MDD) which can contribute to maintenance and relapse. How memories of social rejection and affiliation are experienced and processed in MDD remains unexplored. Eighteen participants with recurrent and chronic MDD and 18 never-depressed controls listened to and vividly revisited autobiographical social experiences in an ecologically valid script-driven imagery paradigm using naturalistic memory narratives in an fMRI paradigm. Memories of Social Inclusion and Social Rejection broadly activated a common network of regions including the bilateral insula, thalamus and pre/postcentral gyrus across both groups. However, having a diagnosis of MDD was associated with an increased activation of the right middle frontal gyrus irrespective of memory type. Changes in positive affect were associated with activity in the dorsal ACC in the MDD group and in the insular cortex of the Control group. Our findings add to the evidence for complex representations for both positive and negative social signals in MDD and suggest neural sensitivity in MDD towards any socially salient information as opposed to selective sensitivity towards negative social experiences.

Memory in frontal lobe epilepsy: an fMRI study.

PURPOSE: Focal epilepsies are often associated with structural and functional changes that may extend beyond the area of seizure onset. In this study we investigated the functional anatomy of memory in patients with frontal lobe epilepsy (FLE), focusing on the local and remote effects of FLE on the networks supporting memory encoding. METHODS: We studied 32 patients with drug-resistant FLE and 18 controls using a functional magnetic resonance imaging (fMRI) memory encoding paradigm. KEY FINDINGS: During encoding of stimuli, patients with FLE recruited more widely distributed areas than healthy controls, in particular within the frontal lobe contralateral to the seizure onset. Normal memory performance was associated with increased recruitment of frontal areas, and conversely a poor performance was associated with an absence of this increased recruitment and decreased activation in mesial temporal lobe areas. SIGNIFICANCE: In patients with FLE, recruitment of wider areas, particularly in the contralateral frontal lobe, appears to be an effective compensatory mechanism to maintain memory function. Impaired hippocampal activation is relatively rare and, in turn, associated with poor recognition memory.

Connectivity of the supplementary motor area in juvenile myoclonic epilepsy and frontal lobe epilepsy.

PURPOSE: Subtle structural abnormalities of frontal lobe gray and white matter have been described in cryptogenic frontal lobe and idiopathic generalized epilepsies. The supplementary motor area (SMA) has a role in motor control, and its involvement during frontal lobe epileptic seizures is characterized by a typical asymmetric tonic posturing. Moreover, motor networks are dysfunctional in juvenile myoclonic epilepsy (JME). We tested the hypothesis that SMA structural connectivity is altered in focal frontal lobe epilepsy (FLE) and JME compared to healthy controls. METHODS: Diffusion tensor imaging (DTI) and probabilistic tractography were used to map the structural connectivity of the SMA, defined by motor functional magnetic resonance imaging (MRI), in 15 patients with JME, 36 patients with FLE, and 18 healthy controls. KEY FINDINGS: Structural connectivity of the SMA was significantly reduced in JME compared to controls (reduced fractional anisotropy and increased mean diffusivity). In FLE there was no significant difference compared to controls, and in all groups there was stronger connectivity in the left hemisphere (higher fractional anisotropy) compared to the right. There was no difference in SMA connectivity between patients with medial or lateral frontal lobe epileptic foci. SIGNIFICANCE: Reduced white matter connectivity is the structural correlate of functional frontal lobe abnormalities in JME. In FLE, the structural connectivity of the SMA was preserved, suggesting a robust motor network that is not compromised by longstanding epilepsy involving the medial frontal lobes.

Converging evidence for enduring perceptions of low social status in individuals in remission from depression.

BACKGROUND: The risk of depressive relapse and recurrence is associated with social risk factors that may be amplified by a submissive socio-cognitive profile. METHODS: In Study 1 we aimed to identify perceptions of low social status in a community sample (N = 613) with a self-reported history of mental health difficulties (n = 232) and, more specifically in Study 2 (N = 122), in individuals in clinical remission from depression (n = 18), relative to a never-depressed control group (n = 64), and relative to a group experiencing a current depressive episode (n = 40). RESULTS: In Study 1, a total of 225 of the 232 participants in the self-reported mental health difficulties group opted to provide further information regarding their mental health history, of whom 153 (68%) reported a history of anxiety, 168 (74.7%) reported a history of depression, and 13 (5.8%) reported an unspecified mental health history. Elevated depressive symptoms were associated with perceptions of low social status which significantly differed between individuals with and without a self-reported history of mental health difficulties. In Study 2 we found enduring perceptions of low social status in remitted depressed individuals. LIMITATIONS: We were unable to discern between historical or current clinical diagnosis in the community sample of Study 1, as we were reliant on self-report. We were unable to explore the effects of medication or causal relationships between depressive symptoms and social status as the studies were cross-sectional in nature. CONCLUSIONS: These findings suggest that evolutionarily rooted socio-cognitive profiles could impact affiliative processes and may confer increased vulnerability to future depressive episodes.

How biopsychosocial depressive risk shapes behavioral and neural responses to social evaluation in adolescence.

INTRODUCTION: Understanding the emotional responsivity style and neurocognitive profiles of depression-related processes in at-risk youth may be helpful in revealing those most likely to develop affective disorders. However, the multiplicity of biopsychosocial risk factors makes it difficult to disentangle unique and combined effects at a neurobiological level. METHODS: In a population-derived sample of 56 older adolescents (aged 17-20), we adopted partial least squares regression and correlation models to explore the relationships between multivariate biopsychosocial risks for later depression, emotional response style, and fMRI activity, to rejecting and inclusive social feedback. RESULTS: Behaviorally, higher depressive risk was associated with both reduced negative affect following negative social feedback and reduced positive affect following positive social feedback. In response to both cues of rejection and inclusion, we observed a general neural pattern of increased cingulate, temporal, and striatal activity in the brain. Secondly, in response to rejection only, we observed a pattern of activity in ostensibly executive control- and emotion regulation-related brain regions encompassing fronto-parietal brain networks including the angular gyrus. CONCLUSION: The results suggest that risk for depression is associated with a pervasive emotional insensitivity in the face of positive and negative social feedback.

Age-related decline in positive emotional reactivity and emotion regulation in a population-derived cohort.

Human older age ushers in functional decline across the majority of cognitive domains. A notable exception seems to be affective processing, with older people reporting higher levels of emotional well-being. Here we evaluated age-related changes in emotional reactivity and regulation in a representative subsample (N = 104; age range: 23-88 years) of the population-derived Cambridge Centre for Ageing and Neuroscience cohort. Performance on a film-based emotion reactivity and regulation task in the magnetic resonance imaging scanner showed an age-related decline in positive reactivity, alongside a similar decline in the capacity to down-regulate negative affect. Decreased positivity with age was associated with reduced activation in the middle frontal gyrus. These findings, from the largest neuroimaging investigation to-date, provide no support for age-related increases in positive emotional reactivity.