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
Related pages
Create an account to add page annotations
Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.