Peripheral nerve dysfunction seen in diabetes; several patterns described:
- Symmetric polyneuropathy
- Distal sensory or sensorimotor
- Mononeuropathy, radiculopathy, and polyradiculopathy
- Cranial neuropathy
- Focal limb or truncal neuropathy
- Radiculoplexus neuropathy (diabetic amyotrophy)
- Acute painful small fiber neuropathy
- Autonomic neuropathies
- Chronic inflammatory demyelinating polyneuropathy (CIDP)
- Generalized polyneuropathy
- 10–30% at diabetes diagnosis
- 50% at 10 years
- Cross-sectional prevalence: 15% by symptoms; 50% by nerve conduction
- Autonomic neuropathy: 16.7% in a United Kingdom study
Etiology and Pathophysiology
- Metabolic derangement due to hyperglycemia and dyslipidemia
- Aldose reductase converts excess glucose to sorbitol, which causes nerve damage.
- Nonenzymatic glycation of neural proteins and lipids forms damaging advanced glycosylation end products.
- Protein kinase C activation causes vascular endothelial changes.
- Oxidative stress from excessive production of reactive oxygen species
- Mitochondrial dysfunction and impaired mitochondrial trafficking within the neurons
- Vasculopathy causing nerve ischemia: predominant factor in mononeuropathies
- Poor glycemic control
- Duration of diabetes
- Tobacco and alcohol consumption
- Maintenance of normal blood sugar
- Exercise and appropriate diet
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