Attention retraining in social anxiety disorder: an fMRI study

Research suggests that patients with social anxiety disorder (SAD) have an attentional bias toward socially threatening stimuli, and recent studies have shown that computerized interventions designed to train attention away from such stimuli decrease attentional bias and SAD symptomatology. The current study sought to replicate findings from previous attention retraining studies and to examine neural mechanisms underlying attentional biases in SAD using functional magnetic resonance imaging (fMRI). Thirty-two SAD patients were randomized to complete either eight 15-minute sessions of a probe detection task designed to train attention away from disgust faces (n=16), or a placebo control task (n=16). Before and after these sessions, patients completed an fMRI probe detection task. Sixteen matched healthy controls also completed this fMRI task on one occasion. Study hypotheses were as follows: (a) post-intervention, SAD patients in the retraining condition would show greater reductions in attentional bias and SAD symptomatology compared to patients in the placebo condition; (b) SAD patients would show greater amygdala activation, and less prefrontal cortex (PFC) activation, when viewing negative faces than healthy controls; and (c) post-intervention, SAD patients in the retraining condition would show less amygdala activation, and greater PFC activation, when viewing negative faces than patients in the placebo condition. Results showed no between-group differences in attentional bias or SAD symptomatology post-intervention, with both groups showing significant symptom reduction. However, attentional bias change was significantly correlated with symptom change across the entire SAD sample (N=32) and was predictive of Liebowitz Social Anxiety Scale scores at post-intervention. Neuroimaging results showed hypo-activation in the orbitofrontal cortex and anterior cingulate cortex at pre-treatment for the SAD group compared to healthy controls. At post-treatment, this difference was no longer significant across the entire SAD group (N=32). Finally, results indicated that activation at pre-treatment in the posterior cingulate cortex/precuneus was significantly correlated with symptom change across the entire SAD sample. These results suggest that SAD patients may not be engaging higher-level cortical regions as readily as healthy controls and add to the recent growing body of research suggesting that attention retraining may not be an effective treatment for patients with SAD

Single-Session Attention Bias Modification Training in Victims of Work-Related Accidents

Individuals who experienced traumatic work-related accidents frequently show cognitive deficits and biased processing of trauma-relevant information, which, in turn, could increase the risk of further accidents. The attention bias modification training (ABMT) is designed to reduce hypervigilance toward and enhance attentional disengagement from threat stimuli. The aim of the present study was to assess whether it is possible to implicitly reduce the attentional bias toward trauma-related stimuli through a single session of ABMT in individuals who experienced a traumatic occupational accident. Nineteen individuals who had experienced a traumatic work-related accident and 11 workers who never experienced a work accident (control group) underwent a preliminary assessment of cognitive performance (executive functions and sustained attention) and an evaluation of the attentional bias toward accident-related pictures by means of a dot-probe task. The results showed that injured workers performed more poorly than controls in tasks of executive functions and concentration abilities. Also, injured workers showed an attentional bias toward trauma reminders (i.e., faster reaction times to probes replacing trauma-related pictures). Injured workers were then randomly allocated to a single-session of ABMT (N = 10) or to an Attention Control Condition (ACC; N = 9). After the training, the dot-probe task was administered again to assess changes in the attentional bias toward trauma-relevant pictures. Injured workers who underwent the ABMT, but not those who underwent the ACC, showed a significant reduction of the attentional bias from pre- to post-training. Overall, these results support previous findings reporting an association between traumatic occupational accidents and cognitive dysfunctions. More importantly, these preliminary findings add to a growing body of evidence suggesting the effectiveness of a short ABMT in reducing the attentional bias after a traumatic workplace accident

Understanding vulnerability for depression from a cognitive neuroscience perspective: a reappraisal of attentional factors and a new conceptual framework

We propose a framework to understand increases in vulnerability for depression after recurrent episodes that links attention processes and schema activation to negative mood states, by integrating cognitive and neurobiological findings. Depression is characterized by a mood-congruent attentional bias at later stages of information processing. The basic idea of our framework is that decreased activity in prefrontal areas, mediated by the serotonin metabolism which the HPA axis controls, is associated with an impaired attenuation of subcortical regions, resulting in prolonged activation of the amygdala in response to stressors in the environment. Reduced prefrontal control in interaction with depressogenic schemas leads to impaired ability to exert attentional inhibitory control over negative elaborative processes such as rumination, leading in turn to sustained negative affect. These elaborative processes are triggered by the activation of negative schemas after confrontation with stressors. In our framework, attentional impairments are postulated as a crucial process in explaining the increasing vulnerability after depressive episodes, linking cognitive and biological vulnerability factors. We review the empirical data on the biological factors associated with the attentional impairments and detail how they are associated with rumination and mood regulation. The aim of our framework is to stimulate translational research

Recalibrating valence weighting biases to promote changes in rejection sensitivity and risk-taking

Past research has found that modifying individuals' valence weighting tendencies by recalibrating them to weight positive and negative valence in a more balanced manner influenced a variety of judgments. The current research examines the utility of the recalibration procedure as a targeted intervention. In Experiment 1, we recruited participants high in rejection sensitivity (who are known to exhibit a negative weighting bias) and in Experiment 2, we recruited participants with high risk tendencies (who are known to exhibit a positive weighting bias). In both experiments, participants first played BeanFest, in which they were presented with beans varying in shape and speckles and learned which increased or decreased points. They later classified the game beans, as well as novel ones varying in their resemblance to the known positives or known negatives, as good or bad. In the recalibration condition, participants were told if they classified each bean correctly, thus receiving feedback regarding the appropriate weighting of resemblance to a known positive versus a negative. The controls, who received no feedback, were less accurate at classifying the novel the beans than the recalibration participants. Furthermore, in Experiment 1, the recalibration condition subsequently exhibited lower sensitivity to rejection than the control condition, with this reduction being stronger for individuals initially higher in rejection sensitivity. This effect was still present a week later. In Experiment 2, the recalibration condition reported diminished risk-tendencies, again with this effect being stronger for individuals with initially higher riskiness, and persisting for a week. Even more importantly, recalibration participants also engaged in less risky behavior on a laboratory task

Loneliness Across the Life Span

Most people have experienced loneliness and have been able to overcome it to reconnect with other people. In the current review, we provide a life-span perspective on one component of the evolutionary theory of loneliness—a component we refer to as the reaffiliation motive (RAM). The RAM represents the motivation to reconnect with others that is triggered by perceived social isolation. Loneliness is often a transient experience because the RAM leads to reconnection, but sometimes this motivation can fail, leading to prolonged loneliness. We review evidence of how aspects of the RAM change across development and how these aspects can fail for different reasons across the life span. We conclude with a discussion of age-appropriate interventions that may help to alleviate prolonged lonelines

Investigating hyper-vigilance for social threat of lonely children

The hypothesis that lonely children show hypervigilance for social threat was examined in a series of three studies that employed different methods including advanced eye-tracking technology. Hypervigilance for social threat was operationalized as hostility to ambiguously motivated social exclusion in a variation of the hostile attribution paradigm (Study 1), scores on the Children’s Rejection-Sensitivity Questionnaire (Study 2), and visual attention to socially rejecting stimuli (Study 3). The participants were 185 children (11 years-7 months to 12 years-6 months), 248 children (9 years-4 months to 11 years-8 months) and 140 children (8 years-10 months to 12 years-10 months) in the three studies, respectively. Regression analyses showed that, with depressive symptoms covaried, there were quadratic relations between loneliness and these different measures of hypervigilance to social threat. As hypothesized, only children in the upper range of loneliness demonstrated elevated hostility to ambiguously motivated social exclusion, higher scores on the rejection sensitivity questionnaire, and disengagement difficulties when viewing socially rejecting stimuli. We found that very lonely children are hypersensitive to social threat

Neurorehabilitation for Multiple Sclerosis Patients with Emotional Dysfunctions

Depression frequently develops in multiple sclerosis (MS) patients, exacerbating the manifestations of the disease and making its management challenging. To date, no consensus has been reached regarding effective treatments for these sufferers due to limited understanding regarding the underlying mechanisms responsible for emotional disorders that are highly comorbid with this disease. There is an urgent need to rethink current treatment options for these patients. This article aims to optimize the treatment outcomes and improve the quality of life for MS patients. Based on an in-depth and critical review of the current literature, we provide a neurorehabilitative framework that explains possible regulatory mechanisms underlying the emotional symptoms highly developed in MS. This article offers practical knowledge and therapeutic strategies to optimize the treatment options in the current care system for MS, as well as for other disabling diseases. Approximately half of all patients with multiple sclerosis (MS) experience clinically significant depression at least once in their lifetimes and even more exhibit emotional symptoms. The depressive disorders observed in MS exacerbate the manifestations of the disease and make its management challenging (1). Yet, the majority of MS patients with depressive symptoms receive neither antidepressant medication nor psychotherapy. The side effect profile of conventional antidepressant treatments can complicate MS management, compromising treatment efficacy and compliance (2). No consensus to date has been reached regarding effective treatment options for these sufferers, due to limited understanding regarding the underlying mechanisms that may be responsible for the emotional disorders that are highly comorbid with MS. There is therefore an urgent need for clinicians and neuroscientists to rethink current treatment options for these patients and improve the quality of their care. Here, we provide a neurorehabilitative framework that explains possible regulatory mechanisms underlying the emotional symptoms frequently developed in MS and suggest practical strategies to optimize its treatment outcomes. Patients with MS, a heterogeneous central nervous system disease causing focal brain lesions and diffuse demyelination, suffer from pronounced physical and cognitive disabilities (3). Though retaining their intellectual abilities, MS patients exhibit various cognitive deficits involving both verbal and non-verbal memory, attention and speed of processing, as well as executive functioning. The progression of MS introduces a chronic stress in patients, associated with impaired neurocognitive functions and diminished brain resources (cognitive reserve), which involve pathology of not only the cortex but also deep brain structures, including the limbic system. In particular, impaired brain connectivity in MS patients has been observed between the prefrontal lobe and the amygdale (4) – brain circuits important for the regulation of emotions (Figures 1A,B) (5). Deficits in executive functions also contribute to problems of impulsivity and lack of emotional control. Abnormal emotional processing takes place in the dysregulated brain with limited neurocognitive resources, and the MS patients experience negative attentional bias and use maladaptive cognitive appraisal toward daily life events. These cognitive deficiencies create a susceptibility to the development of emotional symptoms and disorders such as depression (Figures 1B,C). Neuroimaging evidence suggests that the depressive symptoms in MS are related to the total extent of brain lesions and the degree of impaired cortical-subcortical connections.Canadian Institutes of Health ResearchAthinoula A. Martinos Center for Biomedical ImagingSt. Michael's Hospital. Department of the Neurosurgery-Neuroscience Research

The Impact of Worry on Attention to Threat

Prior research has often linked anxiety to attentional vigilance for threat using the dot probe task, which presents probes in spatial locations that were or were not preceded by a putative threat stimulus. The present study investigated the impact of worry on threat vigilance by administering this task during a worry condition and during a mental arithmetic control condition to 56 undergraduate students scoring in the low normal range on a measure of chronic worry. The worry induction was associated with faster responses than arithmetic to probes in the attended location following threat words, indicating the combined influence of worry and threat in facilitating attention. Within the worry condition, responses to probes in the attended location were faster for trials containing threat words than for trials with only neutral words, whereas the converse pattern was observed for responses to probes in the unattended location. This connection between worry states and attentional capture by threat may be central to understanding the impact of hypervigilance on information processing in anxiety and its disorders