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Neural circuitry of abdominal pain‐related fear learning and reinstatement in irritable bowel syndrome
Author(s) -
Icenhour A.,
Langhorst J.,
Benson S.,
Schlamann M.,
Hampel S.,
Engler H.,
Forsting M.,
Elsenbruch S.
Publication year - 2015
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12489
Subject(s) - hypervigilance , psychology , neuroscience , irritable bowel syndrome , prefrontal cortex , amygdala , anterior cingulate cortex , anxiety , functional magnetic resonance imaging , posterior cingulate , cingulate cortex , medicine , cognition , psychiatry , central nervous system
Background 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. Methods During fear acquisition, predictive visual cues ( CS + ) were paired with rectal distensions ( US ), while control cues ( CS − ) were presented unpaired. During extinction, only CS s were presented. Subsequently, memory reactivation was assessed with a reinstatement procedure involving unexpected US s. 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. Key Results 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. Conclusions & Inferences 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 .