Neuropathy, Peripheral

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  • Peripheral neuropathy (PN) is a functional or structural disorder of the peripheral nervous system (PNS).
  • PN affects any combination of motor, sensory, or autonomic nerves.
  • The motor PNS comprises spinal cord motor neurons, their nerve roots that combine to form plexus, and branches that form individual nerves innervating skeletal muscles. Peripheral motor involvement causes muscle atrophy, weakness, cramps, and fasciculations.
  • The sensory PNS consists of sensory organs, which transmit touch, vibration, and position sensation in large-diameter myelinated fibers; pain and temperature in small-diameter, lightly myelinated and unmyelinated C fibers to the dorsal root ganglia. Sensory signals are relayed to the central nervous system (CNS) for integration. Disorders of sensory nerves produce negative phenomena (loss of sensibility, lack of balance) or heightened phenomena (tingling or pain). Large sensory fiber dysfunction impairs touch and vibration sensation, whereas small fiber sensory neuropathy (SFSN) affects pin and thermal sensation and causes neuropathic pain.
  • The autonomic nervous system (ANS) includes the sympathetic and parasympathetic systems. ANS dysfunction causes cardiovascular, gastrointestinal, and sudomotor symptoms.
  • The PNS can be affected from the cell body (sensory ganglionopathy or motor neuronopathy), root (radiculopathy), or plexus (plexopathy) to the nerve (demyelinating or axonal neuropathy).


Approximately 2.4% of general population, to an estimated 8% of people >55 years old, are affected by distal symmetric PN, the most common form of PN.

Etiology and Pathophysiology

  • PN can be acquired or hereditary.
  • The most common cause of acquired PN is diabetes mellitus.
  • Other categories of acquired PN with illustrative examples are the following:
    • Vascular: ischemia, vasculitis
    • Infectious: HIV, hepatitis C, cryoglobulinemia, Lyme disease
    • Traumatic: compression, crush, or transection
    • Autoimmune: rheumatoid arthritis, Sjögren, postinfectious Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), sarcoidosis
    • Metabolic: diabetes, renal failure, hypothyroidism, vitamin B12 deficiency, celiac disease
    • Iatrogenic/toxic: chemotherapy, platinum, taxanes, metronidazole, colchicine, infliximab, alcoholism
    • Idiopathic: 30% of PN
    • Neoplastic/paraneoplastic: paraproteinemia, Waldenström macroglobulinemia, multiple myeloma, amyloidosis, neurofibromatosis
  • PN occurs due to demyelination or axonal degeneration.
  • Demyelination results from Schwann cell dysfunction, mutations in myelin protein genes, or direct damage to myelin sheaths.
  • Axonal degeneration occurs when injury/dysfunction occurs at the cell body or axon.

  • Approximately 50% of undiagnosed PN is hereditary.
  • Currently, there are >70 known genetic causes of hereditary PN.
  • Charcot-Marie-Tooth (CMT) neuropathies: the most common hereditary PN
    • CMT1A (duplication of the PMP22 gene) is the most common CMT.
    • A PMP22 deletion causes hereditary neuropathy with liability to pressure palsy (HNPP).

Risk Factors

Systemic disorders predispose to PN.

General Prevention

  • Healthy nutrition and avoidance of alcoholism and of pressure at nerve entrapment sites
  • Surveillance for glucose dysmetabolism and tight glycemic control may prevent diabetic PN.

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