Neuropathic pain; what we know and what we should do about it

Neuropathic pain results from nervous system injury or disease and is difficult to treat. The review discusses how peripheral nerve injury activates Schwann cells, leading to immune cell invasion at injury sites and sensory structures. This process involves signaling between neurons, glia, and immune cells, promoting hyperexcitability and spontaneous activity crucial for pain onset. Classical animal models have revealed features of pain aetiology, they do not adequately model the multiplicity of disease states or injuries that may bring forth neuropathic pain in the clinic. This review integrates information from multiple disciplines and underlines ongoing refinements in basic science and clinical practice for improved pain management. The review highlights the urgent need for new neuropathic pain treatments, emphasizing that current animal models don't fully represent the variety of clinical pain conditions. It seeks to combine knowledge from immunology, cell biology, and other fields to improve pain management approaches.

• 1
  Peripheral nerve injury leads to the release of primary inflammatory mediators, activating immunocompetent cells and causing neuroinflammation.
• 2
  Primary afferent hyperexcitability and spontaneous activity are crucial for neuropathic pain, highlighting ion channels as potential therapeutic targets.
• 3
  Neurogenic neuroinflammation, resulting from neuronal activity, alters glial and immune cell function, contributing to the persistence of neuropathic pain.