Neural correlates of individual performance differences in resolving perceptual conflict

Attentional mechanisms are a crucial prerequisite to organize behavior. Most situations may be characterized by a 'competition' between salient, but irrelevant stimuli and less salient, relevant stimuli. In such situations top-down and bottom-up mechanisms interact with each other. In the present fMRI study, we examined how interindividual differences in resolving situations of perceptual conflict are reflected in brain networks mediating attentional selection. Doing so, we employed a change detection task in which subjects had to detect luminance changes in the presence and absence of competing distractors. The results show that good performers presented increased activation in the orbitofrontal cortex (BA 11), anterior cingulate (BA 25), inferior parietal lobule (BA 40) and visual areas V2 and V3 but decreased activation in BA 39. This suggests that areas mediating top-down attentional control are stronger activated in this group. Increased activity in visual areas reflects distinct neuronal enhancement relating to selective attentional mechanisms in order to solve the perceptual conflict. Opposed to good performers, brain areas activated by poor performers comprised the left inferior parietal lobule (BA 39) and fronto-parietal and visual regions were continuously deactivated, suggesting that poor performers perceive stronger conflict than good performers. Moreover, the suppression of neural activation in visual areas might indicate a strategy of poor performers to inhibit the processing of the irrelevant non-target feature. These results indicate that high sensitivity in perceptual areas and increased attentional control led to less conflict in stimulus processing and consequently to higher performance in competitive attentional selection

The good, the bad, and the ugly

Avoidance behaviors are shaped by associative learning processes in response to fear of impending threats, particularly physical harm. As part of a defensive repertoire, avoidance is highly adaptive in case of acute danger, serving a potent protective function. However, persistent or excessive fear and maladaptive avoidance are considered key factors in the etiology and pathophysiology of anxiety- and stress-related psychosomatic disorders. In these overlapping conditions, avoidance can increase the risk of mental comorbidities and interfere with the efficacy of cognitive behavioral treatment approaches built on fear extinction. Despite resurging interest in avoidance research also in the context of psychosomatic medicine, especially in conditions associated with pain, disturbed interoception, and disorders of the gut-brain axis, current study designs and their translation into the clinical context face significant challenges limiting both, the investigation of mechanisms involved in avoidance and the development of novel targeted treatment options. We herein selectively review the conceptual framework of learning and memory processes, emphasizing how classical and operant conditioning, fear extinction, and return of fear shape avoidance behaviors. We further discuss pathological avoidance and safety behaviors as hallmark features in psychosomatic diseases, with a focus on anxiety- and stress-related disorders. Aiming to emphasize chances of improved translational knowledge across clinical conditions, we further point out limitations in current experimental avoidance research. Based on these considerations, we propose means to improve existing avoidance paradigms to broaden our understanding of underlying mechanisms, moderators and mediators of avoidance, and to inspire tailored treatments for patients suffering from psychosomatic disorders

Altered brain structure in chronic visceral pain

Structural brain alterations in chronic pain conditions remain incompletely understood, especially in chronic visceral pain. Patients with chronic-inflammatory or functional bowel disorders experience recurring abdominal pain in concert with other gastrointestinal symptoms, such as altered bowel habits, which are often exacerbated by stress. Despite growing interest in the gut-brain axis and its underlying neural mechanisms in health and disease, abnormal brain morphology and possible associations with visceral symptom severity and chronic stress remain unclear. We accomplished parallelized whole-brain voxel-based morphometry analyses in two patient cohorts with chronic visceral pain, i.e., ulcerative colitis in remission and irritable bowel syndrome, and healthy individuals. In addition to analyzing changes in gray matter volume (GMV) in each patient cohort vs. age-matched healthy controls using analysis of covariance (ANCOVA), multiple regression analyses were conducted to assess correlations between GMV and symptom severity and chronic stress, respectively. ANCOVA revealed reduced GMV in frontal cortex and anterior insula in ulcerative colitis compared to healthy controls, suggesting alterations in the central autonomic and salience networks, which could however not be confirmed in supplemental analyses which rigorously accounted for group differences in the distribution of sex. In irritable bowel syndrome, more widespread differences from healthy controls were observed, comprising both decreased and increased GMV within the sensorimotor, central executive and default mode networks. Associations between visceral symptoms and GMV within frontal regions were altered in both patient groups, supporting a role of the central executive network across visceral pain conditions. Correlations with chronic stress, on the other hand, were only found for irritable bowel syndrome, encompassing numerous brain regions and networks. Together, these findings complement and expand existing brain imaging evidence in chronic visceral pain, supporting partly distinct alterations in brain morphology in patients with chronic-inflammatory and functional bowel disorders despite considerable overlap in symptoms and comorbidities. First evidence pointing to correlations with chronic stress in irritable bowel syndrome inspires future translational studies to elucidate the mechanisms underlying the interconnections of stress, visceral pain and neural mechanisms of the gut-brain axis