Diabetic Polyneuropathy

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Basics

Description

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)

Epidemiology

Prevalence

  • Generalized polyneuropathy
    • 10% 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
    • 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
    • Cyclooxygenase-2 and poly (ADP-ribose) polymerase activation
  • Vasculopathy causing nerve ischemia: predominant factor in mononeuropathies

Risk Factors

  • Poor glycemic control
  • Duration of diabetes
  • Hypertension
  • Hyperlipidemia
  • Tobacco and alcohol consumption

General Prevention

  • Maintenance of normal blood sugar
  • Exercise and appropriate diet

-- To view the remaining sections of this topic, please or --

Basics

Description

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)

Epidemiology

Prevalence

  • Generalized polyneuropathy
    • 10% 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
    • 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
    • Cyclooxygenase-2 and poly (ADP-ribose) polymerase activation
  • Vasculopathy causing nerve ischemia: predominant factor in mononeuropathies

Risk Factors

  • Poor glycemic control
  • Duration of diabetes
  • Hypertension
  • Hyperlipidemia
  • Tobacco and alcohol consumption

General Prevention

  • Maintenance of normal blood sugar
  • Exercise and appropriate diet

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