2014
DOI: 10.1111/nmo.12489
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Neural circuitry of abdominal pain‐related fear learning and reinstatement in irritable bowel syndrome

Abstract: 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.

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Cited by 101 publications
(117 citation statements)
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“…This mechanism may also perpetuate food avoidance in atypical cases of AN that lack fear of fatness and is consistent with a recent fMRI study demonstrating impaired abdominal pain-related fear conditioning and fear extinction in individuals with irritable bowel syndrome [88].…”
Section: Accepted Manuscriptsupporting
confidence: 57%
“…This mechanism may also perpetuate food avoidance in atypical cases of AN that lack fear of fatness and is consistent with a recent fMRI study demonstrating impaired abdominal pain-related fear conditioning and fear extinction in individuals with irritable bowel syndrome [88].…”
Section: Accepted Manuscriptsupporting
confidence: 57%
“…Analogous to classicallyconditioned taste aversion in rotation-chair induced motion sickness, pairing neutral stimuli (such as, visual cues) with visceral pain results in a learned emotional response to formerly neutral cues. [162][163][164] Intriguingly, this effect of emotional learning through association with aversive visceral cues seems to be disturbed in patients with IBS, in part owing to changes in the corticotropin-releasing factor system. 165 Whether and how classical conditioning contributes to hyperalgesia and pain chronicity is a subject of ongoing work, and this might involve perceptual discrimination.…”
Section: Visceral Painmentioning
confidence: 96%
“…Despite the absence of perceptual hypersensitivity to rectal distension, these patients exhibit chronic gastrointestinal (GI) symptoms and demonstrate alterations in brain responses to experimental pain stimuli (Elsenbruch et al, 2010a, Elsenbruch et al, 2010b, Icenhour et al, 2015). Even though there is evidence suggesting differences between hypersensitive and normosensitive patients in response to painful stimuli (Larsson et al, 2012, Van Oudenhove et al, 2010), the relation between altered FC of brain networks and visceral sensitivity remains unknown.…”
Section: Introductionmentioning
confidence: 99%