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Pain that serves as a survival mechanism is a warning signal to the organism from tissue damage that has occurred or is about to occur. When this damage occurs in the nerve system, it causes neuropathic pain, which affects 7% to 8% of the general population and accounts for 20% to 25% of chronic pain sufferers. The pathogenesis of neuropathic pain is mainly related to the generation of ectopic electrical activity following nerve injury, also accompanied by the involvement of a range of inflammatory factors. Although neuropathic pain is often treated with a mix of pharmaceutical and non-pharmacological treatments (often including physical therapy and psychotherapy), a radical cure is not achievable due to the pathogenesis’s complexity and uncertainty. In this research, the processes of quantitative and morphological changes that occur in microglia in neuropathic pain and how such changes evoke the pain hypersensitivity response are discussed from a non-neural perspective. Simultaneously, glutamate communication routes between neurons and glial cells under normal settings and disruption of the glutamatergic system in various forms of neuropathic pain are explored. On the basis of the preceding, it is recommended to investigate the pathophysiology and treatment methods of neuropathic pain from a non-neurological perspective.
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