Albrecht DS, et al. - Considering the numerous preclinical studies supporting the role of spinal neuroimmune activation in the pathogenesis of chronic pain, and targeting glia (eg, microglia/astrocyte)- or macrophage-mediated neuroinflammatory responses effectively prevents or reverses the establishment of persistent nocifensive behaviors in laboratory experimental models, researchers demonstrate that patients suffering from a common chronic pain disorder (lumbar radiculopathy) display elevated levels of the neuroinflammation marker 18 kDa translocator protein, in both the neuroforamina (containing dorsal root ganglion and nerve roots) and spinal cord in comparison to healthy volunteers. In human radicular pain, immunoactivation at multiple levels of the nervous system was implicated to be a potentially important and clinically relevant mechanism. Thereby suggesting therapies targeting immune cell activation to be beneficial for chronic pain patients.