Neuropathic pain is a chronic pain condition caused by lesion or inflammation affecting the nervous system. It is relatively common, can be severely debilitating and clinically significant relief is often difficult to achieve in part because conventional opioid therapy is typically less effective for neuropathic pain. The common symptoms of neuropathic pain include allodynia (pain resulting from normally innocuous stimulus), hyperalgesia (increased sensitivity to painful stimuli) and spontaneous pain. It has been widely known that a number of mechanisms are involved such as ectopic excitability of sensory neurons, altered gene expression of sensory neurons, and sensitization of neurons in the dorsal horn of the spinal cord. However, increasing evidence and research points to the interaction between the immune system and the nervous system playing a crucial role in the the underlying mechanisms of neuropathic pain (1). Following nerve damage, an inflammatory response is initiated: complement system is activated, a variety of inflammatory cells are recruited to the site of nerve injury, dorsal root ganglia (DRG) and to the spinal dorsal horn. Activation of immune-like glial cells and an upregulation of inflammatory mediators all contribute to neuropathic pain (1-10).