Denne sier mye om nervenes blodgjennomstrømmning. Spesielt interessant er avnittet om hvor lite trykk som skal til før blodgjennomstrømningen stopper. Om trykket opprettholdes i 8 timer vil det skje en skade i nerven. Så lite som 20 mm Hg er nok til at blodsirkluasjonen blir dårligere.

http://ptjournal.apta.org/content/86/1/92.full

Simply placing the hand on a computer mouse was shown to increase the tunnel pressure from the resting 5 mm Hg to 16 to 21 mm Hg,⁷⁹ and actively using the mouse to point and click increased the tunnel pressure to 28 to 33 mm Hg, a pressure high enough to reduce nerve blood flow.

In subjects with carpal tunnel syndrome, pressure in the carpal tunnel was 32 mm Hg with the wrist in a neutral position and rose to a mean of 110 mm Hg with full wrist extension in subjects with carpal tunnel syndrome.⁷⁶ These tunnel pressures exceed the threshold of 20 to 30 mm Hg for vascular perfusion even at rest. Taken together, these findings suggest that even functional positions, such as the use of a computer keyboard and mouse, place the wrist in a position of increased carpal tunnel pressure, compromising nerve blood flow and placing people at risk for median nerve injury.

Arterial and endoneurial capillary blood flows were stopped at pressures of 50 to 70 mm Hg⁶⁷ and 80 mm Hg,⁷⁵ respectively. Interestingly, in humans, intraneural blood flow and sensory responses are blocked at extraneural tissue pressures 45 mm Hg below the mean arterial pressure.⁸² A compressive stress of only 30 mm Hg, if maintained for 2 hours, results in endoneurial edema,⁸³ and, if maintained for 8 hours, results in endoneurial pressure high enough to subsequently impair blood flow.⁸⁴ The endoneurial edema is thought to result from ischemic damage to endoneurial capillary endothelial cells and an alteration in the blood-nerve barrier. The same compressive stress of 30 mm Hg applied for 8 hours is sufficient to impair both anterograde axonal transport and retrograde axonal transport.^85,86Increasing pressure results in greater tissue damage, as a compressive force of 150 mm Hg maintained for 30 minutes was shown to induce a degeneration of 30% of the distal fibers,⁴⁸ and compressive forces of 200 and 400 mm Hg maintained for 2 hours were shown to block axonal transport for 1 and 3 days, respectively.⁸⁷

The pathological consequences of prolonged compression include subperineurial edema; inflammation; deposition of fibrin; activation of endoneurial fibroblasts, mast cells, and macrophages; demyelination; axon degeneration; and fibrosis.⁸³ Compression of a very long duration has been modeled in animals with loose ligatures,⁸⁸ Silastic* tubes,^89,90and pressure balloons placed within an anatomical tunnel.⁹¹ The pathological findings are thought to result from both inflammatory and cellular phenomena and include changes in the blood-nerve barrier, thickening of the perineurium and epineurium, thinning of myelin, demyelination and degeneration of axons in the fascicle periphery, and slowed nerve conduction velocity.