Inflammation has been linked to chronic pain, including peripheral neuropathic pain. CCP is often associated with root injury, i.e., PNP: this triggers local inflammation and supraspinal changes in cytokine or chemokine expression (neuroinflammation) [1]. Since inflammation has been associated, among many others, with depression, aggressively targeting supraspinal pro-inflammatory mediators at critical time points in appropriate clinical populations is likely to be a novel avenue to treat debilitating affective disturbances in neuropathic conditions [2].