Nerve repair by end-to-side nerve coaptation: histologic and morphometric evaluation of axonal origin in a rat sciatic nerve model.
OBJECTIVE
We compared the origin and quality of regenerating myelinated axons after end-to-side neurorrhaphy or end-to-end neurorrhaphy.


METHODS
Transected adult rat tibial nerves were either end-to-end coapted or the distal stump was sutured to a perineurial window of the fibular nerve. Electromyographic recordings from the gastrocnemius muscle 8 weeks later revealed reinnervation by tibial nerve axons. Retrograde tracing of neurons projecting across the coaptation sites was performed with Dil for the tibial nerve and FluoroGold for the fibular nerve to reveal the origin of regenerating axons. Orientation of regenerating axons was demonstrated by immunohistochemical staining of the coaptation sites. Nerve cross-sections proximal and distal to the coaptation sites were evaluated regarding quality and quantity of myelinated axons inside the donor and acceptor nerves in comparison to nonoperated nerve samples.


RESULTS
Compound muscle action potential responses were not different 8 weeks after end-to-side as compared with end-to-end coaptation. Double fluorescence of spinal motoneurons (L4-L6) and dorsal root ganglion neurons (L4-L6) elucidated events of collateral sprouting of sensory and motor donor axons. Morphometric analysis demonstrated significantly higher numbers of regenerated myelinated axons distal to end-to-end as distal to end-to-side repair. Furthermore, events of axonal sprouting in the donor nerve proximal to the end-to-side coaptation site were discovered. However, with quantitative parameters such as fiber density and g-ratio, no impairment of the donor nerve was evident.


CONCLUSIONS
The current study supports the hypothesis that end-to-side neurorrhaphy represents an opportunity for peripheral nerve repair when a proximal nerve stump is not available.
Haastert
Kirsten
K
Hannover Medical School, Institute of Neuroanatomy and Center for Systems Neuroscience, Hannover, Germany. haastert.kirsten@mh-hannover.de
Joswig
Holger
H
Jäschke
Katharina-Anne
KA
Samii
Madjid
M
Grothe
Claudia
C
D000596:Amino Acids / Q000187:drug effects; D000818:Animals; D001369:Axons / Q000473:pathology*; D004195:Disease Models, Animal; D004576:Electromyography / Q000379:methods; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D019922:GAP-43 Protein / Q000378:metabolism; D005727:Ganglia, Spinal / Q000378:metabolism / Q000473:pathology; D046529:Microscopy, Electron, Transmission / Q000379:methods; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology; D009413:Nerve Fibers, Myelinated / Q000473:pathology / Q000502:physiology* / Q000648:ultrastructure; D009416:Nerve Regeneration / Q000502:physiology*; D009431:Neural Conduction / Q000502:physiology; D016900:Neurofilament Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D019651:Plastic Surgery Procedures / Q000379:methods*; D020429:Tibial Neuropathy / Q000473:pathology / Q000503:physiopathology / Q000601:surgery
D000596:Amino Acids; D019922:GAP-43 Protein; D016900:Neurofilament Proteins; C098463:dolaisoleucine