默认模式网络
纤维肌痛
剧痛
神经影像学
随机对照试验
心理学
慢性疼痛
扣带回前部
脑岛
认知
认知行为疗法
物理医学与康复
临床心理学
物理疗法
医学
神经科学
精神科
内科学
作者
Jeungchan Lee,Asimina Lazaridou,Myrella Paschali,Marco L. Loggia,Michael P. Berry,Dan‐Mikael Ellingsen,Kylie Isenburg,Alessandra Anzolin,Arvina Grahl,Ajay D. Wasan,Vitaly Napadow,Robert R. Edwards
摘要
Objective Fibromyalgia (FM) is characterized by pervasive pain‐related symptomatology and high levels of negative affect. Mind–body treatments such as cognitive behavioral therapy (CBT) appear to foster improvement in FM via reductions in pain‐related catastrophizing, a set of negative, pain‐amplifying cognitive and emotional processes. However, the neural underpinnings of CBT's catastrophizing‐reducing effects remain uncertain. This randomized controlled mechanistic trial was designed to assess CBT's effects on pain catastrophizing and its underlying brain circuitry. Methods Of 114 enrolled participants, 98 underwent a baseline neuroimaging assessment and were randomized to 8 weeks of individual CBT or a matched FM education control (EDU) condition. Results Compared with EDU, CBT produced larger decreases in pain catastrophizing post treatment ( P < 0.05) and larger reductions in pain interference and symptom impact. Decreases in pain catastrophizing played a significant role in mediating those functional improvements in the CBT group. At baseline, brain functional connectivity between the ventral posterior cingulate cortex (vPCC), a key node of the default mode network (DMN), and somatomotor and salience network regions was increased during catastrophizing thoughts. Following CBT, vPCC connectivity to somatomotor and salience network areas was reduced. Conclusion Our results suggest clinically important and CBT‐specific associations between somatosensory/motor‐ and salience‐processing brain regions and the DMN in chronic pain. These patterns of connectivity may contribute to individual differences (and treatment‐related changes) in somatic self‐awareness. CBT appears to provide clinical benefits at least partially by reducing pain‐related catastrophizing and producing adaptive alterations in DMN functional connectivity.
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