Diabetic neuropathy – bilateral and symmetric – think stocking and gloves – should have bilateral slowing and lower amplitudes on NCS and spontaneous potentials including positive sharp waves (notes PSWs are inverted than what you would expect) on EMG/NCS

Pathophysiology of diabetic neuropathy

• Advanced glycosylation end products – plasma proteins, amino acids, and lipids can undergo glycation reactions spontaneously when exposed to high glucose environments. These reactions give rise to AGEs which result in neuronal damage via pro-inflammatory pathways. Specifically, AGEs agonise receptor-AGEs → inflammation cascade→ ischemia and oxidative stress
• Polyol pathway – excessive glucose enters nerve cell and converts to sorbitol via aldose reductase. Aldose reductase reaction consumes NADPH that could be used to prevent damage from free radicals thus allowing for increased oxidative stress to intensify.
• Protein Kinase C – excessive glucose in the serum is converted to diacylglycerol. Diacylglycerol activates protein kinase C causing vasoconstriction → ischemia
• Poly (ADP-ribose) polymerase (PARP) – activated at high glucose levels. Associated with high levels of oxidative stress and protein kinase C activity

Treatment for diabetic neuropathy

• FDA approved TCAs, Lyrica, cymbalta 
• Gabapentin is not technically approved
• TCAs are 5ht, ach, and norepi
• Lyrica is alpha delta 2 sub unit of voltage gated ca channels
• Cymbalta is a SNRI
• May consider opioids for refractory cases
• May consider SCS trial as well – High frequency is now FDA approved for diabetic neuropathy
• Don’t forget to get blood sugar under control with medications and diet.