Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3061586 | Journal of Clinical Neuroscience | 2010 | 5 Pages |
Entrapment neuropathy is a frequent clinical problem that can be caused by, among other factors, mechanical compression; however, exactly how a compressive force affects the peripheral nerves remains poorly understood. In this study, using a rabbit model of sciatic nerve injury (n = 12), we evaluated the time-course of changes in intraneural blood flow, compound nerve action potentials, and functioning of the blood–nerve barrier during graded mechanical compression. Nerve injury was applied using a compressor equipped with a custom-made pressure transducer. Cessation of intraneural blood flow was noted at a mean compressive force of 0.457 ± 0.022 N (±SEM), and the compound action potential became zero at 0.486 ± 0.031 N. Marked extravasation of Evans blue albumin was noted after 20 min of intraneural ischemia. The functional changes induced by compression are likely due to intraneural edema, which could subsequently result in impairment of nerve function. These changes may be critical factors in the development of symptoms associated with nerve compression.