Endocrinology · USMLE Step 1 and Step 2

Diabetic Neuropathy song

Diabetic Neuropathy - Mechanism & Pathways, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

Diabetic Neuropathy

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Key points in this song10

Diabetic neuropathy is the most common cause of peripheral neuropathy in the United States, primarily caused by chronic hyperglycemia leading to polyol pathway activation, oxidative stress, and advanced glycation end-product accumulation.
The most common presentation is a length-dependent, distal symmetric polyneuropathy with "stocking-and-glove" distribution of burning pain, tingling, and numbness beginning in the toes.
Autonomic neuropathy manifestations include orthostatic hypotension, gastroparesis (early satiety, nausea, erratic blood glucose), erectile dysfunction, neurogenic bladder, and gustatory sweating.
Charcot arthropathy (neuropathic joint) occurs due to loss of protective sensation, leading to painless joint destruction, most commonly affecting the midfoot, with a classic "rocker-bottom" deformity on imaging.
Diabetic amyotrophy (lumbosacral radiculoplexus neuropathy) presents with severe, asymmetric proximal leg pain and weakness, typically in older Type 2 diabetics, and is distinct from distal symmetric polyneuropathy.
First-line pharmacologic treatments for painful diabetic neuropathy are duloxetine (SNRI) or pregabalin/gabapentin; tricyclic antidepressants (e.g., amitriptyline) are effective but limited by side effects.
The single most important intervention to slow progression of diabetic neuropathy is strict glycemic control, as demonstrated by the DCCT trial in Type 1 diabetes.
Screening for distal symmetric polyneuropathy should begin at Type 2 diabetes diagnosis and 5 years after Type 1 diabetes diagnosis, using the 10-gram Semmes-Weinstein monofilament test to assess protective sensation.
Loss of the Achilles tendon reflex is often the earliest objective sign of distal symmetric polyneuropathy on physical examination.
Mononeuropathy multiplex in diabetics can involve cranial nerves, classically CN III palsy with pupillary sparing (ischemic etiology), distinguishing it from a compressive CN III lesion which affects the pupil.