pathophysiology
Last reviewed 01/2018
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