PRRT2 and Hyperglycemia: The mechanism is that a large number of advanced glycation end products (ages) through protein kinase C (PKC) and transcription nuclear factor signaling pathway and other oxidative stress mechanisms in nerve tissue in hyperglycemia environment, causing excessive accumulation of sorbitol, increasing intracellular osmotic pressure, leading to edema of nerve tissue, demyelination or axonal degeneration [27, 28].