Neural circuitry of abdominal pain-related fear learning and reinstatement in irritable bowel syndrome
Neural circuitry of abdominal pain-related fear learning and reinstatement in irritable bowel syndrome
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DOI：
10.1111/nmo.12489
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发表时间：
2015-01-01
影响因子：
3.5
通讯作者：
Elsenbruch, S.
中科院分区：
文献类型：
--
作者：
Icenhour, A.;Langhorst, J.;Elsenbruch, S.
背景改变的疼痛预期可能会导致肠易激综合征（IBS）等慢性疼痛疾病的中枢疼痛处理紊乱，但对形成疼痛预期的学习过程仍知之甚少。我们评估了神经回路介导的形成，灭绝，并在IBS患者的腹痛相关的记忆和再激活相比，健康对照组（HC）在差分恐惧conditioningparadigm.MethodsDuring恐惧收购，预测视觉线索（CS+）与直肠扩张（US）配对，而控制线索（CS-）提出不配对。在消退期间，仅列出CS。随后，通过涉及意外US的恢复程序评估记忆再激活。使用功能性磁共振成像，分析CS（+）与CS-的神经激活的组间差异，沿着皮肤电导反应（SCR）、CS效价、CS-US应急、状态焦虑、唾液皮质醇和α-淀粉酶活性。焦虑症状的贡献是在协方差analysis.Key ResultsFear收购IBS的改变，更准确的应急意识，更大的CS相关的效价变化，增强CS+诱导的差异激活的前额叶皮层和杏仁核。IBS患者进一步揭示了增强的差异扣带回激活过程中灭绝和更大的差异海马激活过程中恢复。焦虑影响记忆形成和reinstation.Conclusions和InferencesAbdominal疼痛相关的恐惧学习和记忆过程中改变IBS，杏仁核，扣带皮层，前额区，海马介导。增强的恢复可能有助于过度警觉和中枢疼痛放大，特别是在焦虑患者中。利用预防性干预措施预防习得性恐惧的复发可能是IBS的一个有希望的治疗目标。
BackgroundAltered 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.MethodsDuring fear acquisition, predictive visual cues (CS+) were paired with rectal distensions (US), while control cues (CS-) were presented unpaired. During extinction, only CSs were presented. Subsequently, memory reactivation was assessed with a reinstatement procedure involving unexpected USs. 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 ResultsFear 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 & InferencesAbdominal 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.