• Pain · Sep 2016

    Perturbed connectivity of the amygdala and its subregions with the central executive and default mode networks in chronic pain.

    • Ying Jiang, Desmond Oathes, Julia Hush, Beth Darnall, Mylea Charvat, Sean Mackey, and Amit Etkin.
    • aDepartment of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA bSierra-Pacific Mental Illness Research, Education, and Clinical Center (MIRECC), Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA cDepartment of Health Professions, Macquarie University, Sydney, Australia dDepartment of Anesthesiology, Perioperative and Pain Medicine, Division of Pain Medicine, Stanford University, Stanford, CA, USA.
    • Pain. 2016 Sep 1; 157 (9): 1970-8.

    AbstractMaladaptive responses to pain-related distress, such as pain catastrophizing, amplify the impairments associated with chronic pain. Many of these aspects of chronic pain are similar to affective distress in clinical anxiety disorders. In light of the role of the amygdala in pain and affective distress, disruption of amygdalar functional connectivity in anxiety states, and its implication in the response to noxious stimuli, we investigated amygdala functional connectivity in 17 patients with chronic low back pain and 17 healthy comparison subjects, with respect to normal targets of amygdala subregions (basolateral vs centromedial nuclei), and connectivity to large-scale cognitive-emotional networks, including the default mode network, central executive network, and salience network. We found that patients with chronic pain had exaggerated and abnormal amygdala connectivity with central executive network, which was most exaggerated in patients with the greatest pain catastrophizing. We also found that the normally basolateral-predominant amygdala connectivity to the default mode network was blunted in patients with chronic pain. Our results therefore highlight the importance of the amygdala and its network-level interaction with large-scale cognitive/affective cortical networks in chronic pain, and help link the neurobiological mechanisms of cognitive theories for pain with other clinical states of affective distress.

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