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Pain. 2019 Mar 4. doi: 10.1097/j.pain.0000000000001541. [Epub ahead of print]

Somatotopically-specific primary somatosensory connectivity to salience and default mode networks encodes clinical pain.

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Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Division of Clinical Research, Korea Institute of Oriental Medicine, Daejeon, 34054, Korea.
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02215, USA.
Department of Anesthesiology, Center for Pain Research, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.


While several studies have found that chronic pain is characterized by increased cross-network connectivity between salience, sensorimotor, and default mode (DMN) networks, a large sample-size investigation allowing a more reliable evaluation of somatotopic specificity and subgroup analyses with linkage to clinical pain intensity has been lacking. We enrolled healthy adults and a large cohort of patients (N=181) suffering from chronic low back pain (cLBP). To specifically link brain connectivity with clinical pain intensity, patients were scanned at baseline and after performing physical maneuvers that exacerbated pain. Compared to healthy adults, cLBP patients demonstrated increased connectivity between the functionally-localized back representation in primary somatosensory cortex (S1back) and both salience and DMN networks. Pain exacerbation maneuvers increased S1back connectivity to salience network regions, but decreased connectivity to DMN, with greater pain intensity increase associated with greater shifts in these connectivity patterns. Furthermore, only in cLBP patients reporting high pain catastrophizing, DMN connectivity was increased to a cardinal node of the salience network, anterior insula cortex, which was correlated with increased post-maneuver pain in this cLBP subgroup. Hence, increased information transfer between salience processing regions, particularly anterior insula, and DMN may be strongly influenced by pain catastrophizing. Increased information transfer between salience network and S1 likely plays an important role in shifting nociceptive afference away from self-referential processing, re-allocating attentional focus and affective coding of nociceptive afference from specific body areas. These results demonstrate S1 somatotopic specificity for cross-network connectivity in encoding clinical back pain, and moderating influence of catastrophizing for DMN/insula connectivity.

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