Painful neuropathies: the emerging role of sodium channelopathies.

摘要: Pain is a frequent debilitating feature reported in peripheral neuropathies with involvement of small nerve (Aδ and C) fibers. Voltage-gated sodium channels are responsible for the generation conduction action potentials nociceptive neuronal pathway where NaV 1.7, 1.8, 1.9 (encoded by SCN9A, SCN10A, SCN11A) preferentially expressed. The human genetic pain conditions inherited erythromelalgia paroxysmal extreme disorder were first to be linked gain-of-function SCN9A mutations. Recent studies have expanded this spectrum mutations patients fiber neuropathy new syndrome pain, dysautonomia, hands feet (acromesomelia). In addition, painful been recently SCN10A Patch-clamp shown that effect dependent upon cell-type background. functional effects mutation dorsal root ganglion (DRG) neurons sympathetic neuron cells may differ per mutation, reflecting pattern expression autonomic symptoms who carry question. Peripheral not always length-dependent, as demonstrated initial facial scalp showing hyperexcitability both trigeminal DRG neurons. There some evidence suggesting can lead degeneration axons. This review will focus on emerging role channelopathies neuropathies, which could serve basis novel therapeutic strategies.