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Neuro-immune signatures in chronic low back pain subtypes
Brain  (IF13.501),  Pub Date : 2021-09-16, DOI: 10.1093/brain/awab336
Zeynab Alshelh, Ludovica Brusaferri, Atreyi Saha, Erin Morrissey, Paulina Knight, Minhae Kim, Yi Zhang, Jacob M Hooker, Daniel Albrecht, Angel Torrado-Carvajal, Michael S Placzek, Oluwaseun Akeju, Julie Price, Robert R Edwards, Jeungchan Lee, Roberta Sclocco, Ciprian Catana, Vitaly Napadow, Marco L Loggia

We recently showed that patients with different chronic pain conditions (such as chronic low back pain, fibromyalgia, migraine, and Gulf War Illness) demonstrated elevated brain and/or spinal cord levels of the glial marker 18 kDa translocator protein, which suggests that neuroinflammation might be a pervasive phenomenon observable across multiple etiologically heterogeneous pain disorders. Interestingly, the spatial distribution of this neuroinflammatory signal appears to exhibit a degree of disease specificity (e.g. with respect to the involvement of the primary somatosensory cortex), suggesting that different pain conditions may exhibit distinct “neuroinflammatory signatures”. To further explore this hypothesis, we tested whether neuroinflammatory signal can characterize putative etiological subtypes of chronic low back pain patients based on clinical presentation. Specifically, we explored neuroinflammation in patients whose chronic low back pain either did or did not radiate to the leg (i.e. “radicular” vs. “axial” back pain).