Laser injury ofperipheral nerve:a modelforfocal endoneurial damage

SUMMARY A modelofendoneurial oedemaispresented whichproduces localised nervefibre injury including Wallerian degeneration, endoneurial oedemaandincreased endoneurial fluid pressure.A carbon dioxide laser was usedtoirradiate ratsciatic nerveandquantitative results were collected 2daysand6daysafter irradiation. Theincrease inendoneurial fluid pressureis compared withother models ofWallerian degeneration inwhichtheentire fascicle was involved toaidina comparative study oftherole ofoedemainneuropathy. A lesion produced bythelaser isoneofseveral models ofendoneurial damageassociated withWallerian degeneration (table). Theseverity ofthe lesion isinfluenced bythefrequency, energy density andduration ofirradiation aswell astheabsorption coefficients ofthetissue. Carbondioxide laser irradiation ofnervous system tissue produces localised lesions characterised histologically byaconcentric zoneofcoagulation necrosis surrounded bypersistent nerveoedema.' 2Inthis paperwereport the useofacarbon dioxide laser asamodelofnerve injury whichproduces focal nervefibre damage including Wallerian degeneration andaxonal dystrophy, endoneurial oedema,and increased endoneurial fluid pressure. Peripheral nerve fibres aremaintained inaunique microenvironment3 created bytheselective permeability characteristics ofthevasanervorum and theperineurial membrane whichencloses fibres in discrete fascicles. Since theperineurium alsohas semi-elastic biomechanical properties,4 endoneurial TableEndoneurial oedema andincreased EFPassociated withWallerian degeneration andlesions oftheaxon