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Pathophysiology

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

The pathophysiology of nerve compression syndromes can be attributable to several key processes:

  • ischaemia:
    • pressure on a nerve leads to reduction of its blood flow
    • clinical examples include classical external mechanical pressure eg the application of a tourniquet, 'Saturday night palsy'
    • paraesthesia or transient motor weakness result
    • there is reduced epineurial blood flow at 20-30mmHg of pressure
    • axonal transport is slowed; can occur at as little as 30 mmHg of pressure
  • fibrosis:
    • ischaemia ultimately results in fibrosis if pressure is very elevated or prolonged in duration
    • prior to this, there is a period of epineurial oedema with pressures of 50mmHg for two hours or more
  • focal demyelination:
    • attributable more to mechanical pressure than oedema
    • tends to affect motor rather than sensory fibres
    • occurs chronically over weeks to months
  • traction:
    • entrapment from localised fibrosis or a reduction in the space for a nerve to transit can result in a traction injury
    • with limb motion, the nerve gets repeatedly traumatised
  • double-crush phenomenon:
    • compression at one level along a nerve lowers the threshold for a second injury at another point along the nerve
    • probably related to endoneural oedema inhibiting axonal transport of cytoskeletal proteins, nutrients and neurotransmitters
    • clinically examples include a thoracic outlet syndrome increasing the threshold for carpal tunnel symptoms and vice versa
  • systemic conditions: a range of conditions can lower the threshold for a nerve to be compressed and dysfunction:
    • pregnancy
    • diabetes mellitus
    • infection
    • rheumatoid arthritis
    • gout
    • hypothyroidism
    • alcoholism
    • obesity
    • mucopolysaccharidoses
    • mucolipidoses
    • environmental exposures eg industrial solvents

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