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Quantitative Histological Analysis of Nerve Compression and Recovery at Different Regions Along a Compressed Nerve
Kory M Ford, BS; Joseph A Buckwalter V, MD, PhD; Ignacio Garcia Fleury, MD
University of Iowa, Iowa City, IA

Introduction: Chronic compressive nerve injuries are common and result in both microscopic and macroscopic changes in nerve structure and function. This study seeks to quantitatively analyze the progression of nerve damage and healing at various regions along a compressed nerve and at different timepoints after compression and recovery, in both healthy controls and diabetic populations.
Methods: 20 healthy rats and 20 ZDF diabetic rats were divided into four groups of n=10 each: Group 1 - non-diabetic rats; Group 2 - ZDF diabetic rats; Group 3 - non-diabetic rats with sciatic nerve compression; and Group 4 - ZDF diabetic rats with sciatic nerve compression. Groups 1 and 2 went through sham surgery. Groups 3 and 4 underwent surgery to place a compression device around the sciatic nerve to induce peripheral compressive neuropathy. After 6 weeks, n=5 rats from each group were euthanized. Remaining animals from each group received a second sham (Groups 1 and 2) or decompression surgery (Groups 3 and 4) to remove the compression device. 6 weeks later, all remaining animals were euthanized. Histology analysis of four unique nerve segments was used to compare the harvested nerves after euthanasia: (1) proximal to compression and bulge, (2) proximal bulge, (3) compression, and (4) distal to compression.
Results: After slice quality screening, quantitative analysis of nerve segments from 20 healthy and 17 diabetic rats demonstrated trends in both axon number and myelin thickness calculations. Slices on non-operative nerves and sham nerves consistently showed no difference in axon number or myelin thickness at different locations along the nerve. Among compressed nerves, axon number increased and myelin thickness decreased at slices 2 and 3, the site of compression and just proximal to it. After compression was released, these findings were sustained and expanded to the most distal segment, slice 4. Non-diabetic rats demonstrated a more robust response to compression and recovery compared to diabetic rats.
Conclusions: These data quantitatively demonstrate a mechanism of demyelination and remyelination with concurrent axonal sprouting starting just proximal to an area of compression. This pathophysiology of compressive nerve injury may be driven by a combination of ischemia distal to the site of compression, disruption of axoplasmic flow, and baseline pathology, as seen in diabetes. This study provides a more complete picture of the pathologic changes of nerves during compression and after decompression surgery along different areas of a compressed nerve, upon which novel therapeutics may be developed.


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