Diabetic neuropathy

Hyperglycemia contributes to the pathogenesis of neuropathy in both type 1 and type 2 diabetes. Other metabolic and vascular factors, particularly hypertriglyceridemia, are important.

The clinical presentation comprises a broad constellation of symptoms and deficits, involving sensory, motor, and autonomic nerve fibers, and multiple organ systems.

Diabetic peripheral neuropathy is the most common chronic complication of diabetes, characterized by the presence of peripheral nerve dysfunction, diagnosed after the exclusion of other causes. Pain is the outstanding complaint in most patients, but many patients are completely asymptomatic.

Treatment has traditionally focused on control of hyperglycemia as a means of slowing progression or delaying onset, on targeting potential pathogenetic mechanisms, and on pain reduction.

Although pain is generated principally by peripheral nerve injury, there is recent evidence that the central nervous system may play a significant role in the disinhibition and amplification of pain. Indeed, the most effective drugs in treating painful diabetic neuropathy are centrally acting. Pregabalin (a voltage-gated calcium channel modulator), duloxetine (a selective dual serotonin-norepinephrine reuptake inhibitor), and tapentadol (an agonist of the mu-opioid receptor and norepinephrine reuptake inhibitor) are the only prescription drugs currently approved for treating painful diabetic neuropathy in some countries.

Diabetic neuropathy (DN) is a highly prevalent complication of diabetes (type 1 or type 2) and is characterized by the presence of symptoms and/or signs of peripheral nerve dysfunction and/or autonomic nerve dysfunction. It is diagnosed after the exclusion of other causes. Frequently, however, people with DN are asymptomatic.