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Chronic Nerve Compression Injury Alters Neurovascular Blood Flow
James Jung; Peter Hahn, BS; Bernard Choi, PhD; Ranjan Gupta
University of California, Irvine, Irvine, CA, USA
Hypothesis: It is generally believed that chronic nerve compression (CNC) injuries, such as carpal tunnel syndrome, decrease blood flow at the site of compression, which may be reversed after surgical intervention. Previous studies have demonstrated the effects of a crush injury on the microvascular supply of peripheral nerves; however, the effects of CNC injury on blood flow have not been well established. The current study hypothesizes that CNC injury likely alters neural blood flow and induces ischemia differently than other neural injuries.
Materials and Methods: An inert tube was atraumatically placed around the sciatic nerve (SN) of six-week old, male mice through a gluteal splitting approach. SNs were harvested for western blot analysis after 2, 4, and 6 weeks and analyzed for cellular hypoxic markers such as HIF-1, catalase, and SOD. Laser speckle imaging (LSI) was used to measure blood perfusion through the SNs before and after compression at these same time points. Mice with 2-week (early) and 6-week (late) CNC injury were decompressed via surgical removal of the tubing, after which neural blood flow was again analyzed via the LSI system. One-way ANOVA with Bonferroni correction was performed with p-value<0.05 constituting significance.
Results: In contrast to the immediate decrease of blood flow from baseline seen in neural crush injuries, CNC injury, instead, initially creates a period of hyperemia (1.37 ± 0.50). This initial hyperemia is then followed by a decline in neural blood flow to achieve a new baseline flow by 4 weeks (0.66 ± 0.14). Furthermore, neurovascular flow dynamics assessed with early decompression shows a stepwise return to a hyperemic state superseding the original baseline value within 3 weeks (1.35 ± 0.16). Moreover, western blot analysis of the CNC injury showed increased protein levels of cellular hypoxic markers such as SOD, HIF, and catalase relative to the uninjured contralateral nerve at all time points of compression.
Summary:
- Chronic nerve compression injuries induce ischemia with an initial hyperemia that is followed by a substantial decrease in neural blood flow.
- The ischemia induced by CNC injury appears to increase cellular hypoxic markers such as HIF, SOD, and catalase.
- These data present a clinical correlate to the variable functional outcomes seen following surgical release of compressive nerve injuries.
   | Figure 1: Neural blood flow for CNC injury in the sciatic nerve (A) and after early decompression in animals (B) and late decompression in animals. *p-value<0.05; **p-value<0.01. |
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