Pathophysiology

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