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Pain is one of the most pervasive symptoms in clinical medicine and always presents a challenge, both in terms of diagnosis and management. Abnormal voltage gated sodium channels (VGSCs) are emerging as key determinants in painful neuropathies. Genetic, metabolic or immunological factors have independently been demonstrated to alter ion channel properties, providing insight into complex pathophysiological mechanisms in pain. Specifically, modification of the Nav 1.7 isoform, encoded by the SCN9A gene, can profoundly impact pain sensitivity.1 Nav 1.7 is expressed in the peripheral nervous system in sensory and sympathetic neurons. Activating mutations in SCN9A produce severe pain due to gain-of-function in …
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