[Neuronal plasticity and neuropathic pain]

The authors have analysis the physiopathology of neuropathic pain, focusing in particular on the plastic phenomena at the level of the central nervous system. Plastic phenomena take the form of anatomic and neurochemical alterations. In relation to the former, excitatory amino acids play a fundamental role, causing a state of hypersensitivity of N-menthyl-D aspartate (NMDA) receptors (excitation toxicity) which in turn cause the degeneration of inhibitory interneurons localised in the I-III laminae of the dorsal cornu. This hyperactivation is responsible for the presence of a discharge input that lasts for minutes after a nociceptive stimulus, a phenomenon known as long-term potentiation (LTP) on long term depression (LTD). The authors also analysed the role of other neurotransmitters and their possible interactions. Neurochemical alterations are coupled with anatomic modifications, like sprouting, at the level of the dorsal cornu laminae and dorsal root ganglia. These neuroplastic phenomena lead to an alteration in the central mechanisms of pain, for A-fibre mediated mechano-allodynia, a clinical phenomenon that differs from thermal hyperalgesia in both physiopathology and clinical prognosis. The role played by the sympathetic system in neuropathic pain is also discussed. The authors also raise a number of clinical considerations regarding the different nature of spontaneous pain, allodynia and hyperalgesia. New physiopathological knowledge is a useful tool for pharmacological and clinical research, as well as for treatment of syndromes secondary to neuropathic pain.