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Autologous nerve grafts inregeneration of motoaxons after C7 ventral root avulsion
SI42
Basic Sciences - Trauma
and blooddegradationproducts,can bepreventedor eliminatedbynimodipine to someextent. In thisstudy, nimodipineshowed its effectson the disruptionof neuronalCa2 - channeldecreasethe permeabilityof BBBandcerebraledema. Therefore, it may be apromissingagent in thetreatmentof traumaticcerebral edema and fortreatmentof severecraniocerebralinjuries.
I P-3-3071 Neuroprotectivepropertiesof emoxypin anddiavitol
in brain trauma: Experimental and clinical aspects
F.Oleshkevich,A. Fedulov,N. Mezen, L. Plenina, S. Hljustov,L. Marchenko. Departmentof NeurologyandNeurosurgery,MedicalInstitute,Minsk, Belarus Introduction:Hypoxiaandfree-radicaloxidationof lipidsare the main mechanismsofsecondarynervoustissue damagefollowingbraintrauma. Therefore, the use ofneuroprotectors(antihypoxantsandantioxidants)createspreconditionsfor more successfultreatmentresultsfor brain injuries. Purpose of Research: To study the action of the antihypoxicmedication DIAVITOL (D) and the antioxidant EMOXYPIN (E) on: 1. glial cellsmetabolism; 2. dynamicsof neurologicaldisordersandevolutionof CT data. Objects of Research: 1.Astrocytesculture, culture of C6 rat'sglioma; 2. Laboratoryanimals(rats); 3. 357 patientswith brain contusions(BG). Research Methods: 1.Assessmentof mitoticactivity,swollencells quantities and level of water and osmogenicelectrolytesin brain tissue,biophysical criteriacharacterizingthe degree of hypoxic astrocytesdamage; 2. CT; 3. Dyneurologicalobservations;3. Nonparametricanalysisofvariance namicclinical was used. Results: The use of0 and E has shownpreventionofdamage to or death ofastrocytesin the culture inhypoxia.Thus, undertheinfluenceof Dthe mitotic activity has beenrestored to nearnormalcy,the quantity ofhypoxia-affected cells hasdramaticallydropped. The curative effect ofE has beensomewhat Jess manifest.Incubatedastrocytesand C6 rat's glioma in hypoxia conditions while addingE and especially0 to the culturemedium, results inreducing damage to cell proteins and disruptionof pyridoxalphosphates metabolism, which isascertainedthroughcorrespondingshifts ofspectrumparametersof the cells culturefluorescence.The use of 0 in hypoxiaalso brought about normalizationof the cultured cells membraneslipid bilayerparameters,which wasestimatedbythe degreeofeximerizationof themembranotropicfluorescent pyreneprobe. In an experimentalbrain injuryE alsoprovidesa non-specific antiedemicaction,apparently.via membrane-stabilizingeffect. 0 and E have shownpositiveinfluenceon pathomorphological alterationsin the brainrevealed byCT. The use of0 and E in the complexpharmacotherapyof BCresultedin a fasterreversalof neurologicaldisorders.
Ip-3-30al from Postinjurytreatmentwith rhlL·2 improves outcome experimentaltraumaticbrain injuryin rats S.K. Qian1, C. Zhu2 , J.Y.Jian2 . 1 DepartmentofNeurosurgery,94 Hospitalof PLA,Nanchang. (330002), JiangXinProvince, China, 2 Departmentof Neurosurgery,ChangzhengHospitalof the SecondMillitary University, Shanghai(200003), China Other studiesshowed that interleukin2-like immunoreactivityat the lesioned sites exists inabundancein themammal brain(Lapchak, 1991). IL-2supports the survivalof neurons(Awatsuji,1993), and stimulatesoligodendroglialproliferationand maturationin vitro(Benvensite,1986). The roleof IL-2 in brain recombinedhuis unknown.This study was designedto evaluatethe effectof maninterleukin-2(rhIL-2) onneurologicaldeficitsandhistopathologicchanges followingmoderatelateral fluidpercussionin SO rat brain. Therh1L-2 was administratedbyintraventricular(i.c.v.)injection3 days after injury,with 30U, 60 control.The resultsshowedthat rh1L-2 had U, 300 U, with injectionNS as the marlkedprotectionon neurologicalfunctionaftertraumaticbraininjury,improvingweightloss,promotingbeam-walkingandbeam-balance,especiallyat 60 U treatment.The cortical cavity with 60 U rh1L-2 injectionwas smaller than NS injection,0.07 mm x 0.10 mm vs 0.51 mm x 1.00 mm (P< 0.D1). We observed that rhlL-2supportedthe survival of neuronsin the hippocampalCA2, CA3 regions.These data suggest thatlL-2 might be one of importantendogenous the neurotrophicfactors in CNS, acting on repair in responseto traumaticbrain injury.We suggest that postinjury IL-2 applicationsmay havepotentialclinical value fortreatinghumanbraininjury.
IP-3-3091 An ultrastructuralstudy ofmicrovascularchanges after rootavulsion
C.A.J. Holtzer1.2, E. Marani1 , W. de Priester3, R.TW.M.Thomeer1,2. 1 NeuroregulationGroup, Dept.ofPhysiology,LeidenUniversityMedical Centre, theNetherlands,2 Dept. ofNeurosurgery,LeidenUniversityMedical Centre, theNetherlands,3 Dept. ofBiology,LeidenUniversity;theNetherlands An electron microscopicalstudy was carried out on the cat spinal cord gray
Tuesday, 8 July 1997 matter in order toinvestigatethe microvascularevents after a C7 ventral root avulsion. Edema andglialreactions:From2 days up to 30 daysafteravulsionperivascular edema was present around blood vessels and neutrophilicgranulocytes mainly in theperiendothelialspace. Eight days afteravulsionan increase in astrocyteprocessesaround the blood vessels was noted, the phagocyticactivity ofpericytes notablyincreased and myelinsheath-like structureswere encounteredin phagosomesof pericytes.After 14 days anuniformdistribution present. The phagoof astrocyticalprocessesaround the blood vessels was cytic activitydecreased and the myelinsheath-likematerial in thepericytical phagosomesgraduallydisappeared.The amount of microgliaaround the blood vesselsshowedan increaseafter 30 days survivaland then stabilized. Endothelialcells:At 2 daysafteravulsionthe endothelialcellscontainedvacfibrous-likesubstances.After 14daystheendothelialcytoplasm uolesfilledwith alsocontainedmyelinsheath-likeand"soap-bubble"structures.Tight junctions betweentheendothelialcellswere presentwithout exception.After 14days and up to 90 dayssurvivalintraluminaldebris wasnoted. The morphologicalchangesin theneuropil,pericytes.and endothelialcells describedin thisstudyindicatetransportof debrisfrom the neuropiltowardsthe avulsion. bloodvessel lumenafter ventralroot
IP-3-310 I A study of the~erikaryal reaction ofmotoneurons after rootavulslons
C.A.J.Holtzer1 2, E. Marani " C. Hoffmann,R.T.W.M. Thomeer1,2. 1 NeuroregulationGroup, Dept. ofPhysiology,LeidenUniversityMedical Centre, theNetherlands,2 Dept. ofNeurosurgery,Leiden UniversityMedical Centre, theNetherlands After C7 ventral rootavulsion the populationof motoneuronsdecreases as compared to a sharptranssectionof the rootlets at the pial surface. At light microscopicalJevel ceil death of thesemotoneuronswas not obviouslycharacterizedby darkdegeneration. Toinvestigatethisphenomenonan electromicroscopical study was carried out on 15 cats afteravulsionof the C7ventrafrootlets,with survivaltime of 2,8, 14,30, 60 and 90 days. Thecytoplasmof thesomataofinvolvedmotoneuronsshowedswollenmitochondriaand a dispersedrough endoplasmaticreticulum(RER). In the vicinity of the nuclearenvelopedarklysosomalprofiles wereencountered.Sometimes a streamof small, darlkvesicle-likestructuresconnectedtheIysosomeswith the motoneuronnuclearenvelope.Exocytosisofendoplasmaticdropletsand of mitochondriawaspresent.The numberofsynapsesattachedto themotoneuronal somata notablydecreased. Those synapses still present contained swollen lamellae. Sporadicallydarkdegenerationprofiles were present in the axonal pathways.The motoneuronsomatashoweddegenerationof both the light and the darktype.Aroundthesedegeneratingsomataan increaseofastrocytesand microglialcells wasobserved. Thisdegenerationof the light type explains how the disappearanceof motoneuronsafteravulsionmayescapelightmicroscopicalobservation.
I P-3-311 I Autologousnerve grafts inregenerationof motoaxonsafter C7 ventral rootavulsion
C.A.J.Holtzer1.2, E. Marani 1, R.TW.M.Thomeer1.2. 1 NeuroregulationGroup, Dept. ofPhysiology,LeidenUniversityMedicalCentre, theNetherlands,2 Dept. ofNeurosurgery,LeidenUniversityMedicalCentre, theNetherlands Thisstudyinvestigatesthepossibilityofregenerationof themotoneuronalaxons fromthe cord in relationwithtime. Eightmaleadult cats were used.Via a ventral approachtheC7ventralrootletswereselectivelyavulsedfromthecord,resected andSUbsequentlyreplaced by saphenousnerveautografts.After survival pereoperated upon. The C7 riodsrangingfrom 7 up to 120 days, the cats were spinalnervewastransecteddistallyand HRP wasadministeredto theproximal stump.Twodays later the animalswere perfusedand the C6 throughC8 spinal cordsegmentsweresectionedandstained. HRP andacetylcholinesteraseenzyme histochemistry,neurofilamentimmunocytochemistryand Nissl staining werecarried out. From 30 dayssurvivalonwards, HRP labelled axons andretrogradelylabelledmotoneuronsweredetectedin the spinal motorarea. The neurofilament stainingdemonstratedregeneratingaxonsat thetransitionzonebetweenspinal cordandgraft.Withinthe nervegraftbothHRPand neurofilamentwerepresent. It isconcludedthatmoto-axonscan bridgeboth the proximal,intramedullary and the distalcoaptationsites of a graft andelongateinto the spinal nerve.
Basic Sciences - Trauma
and blooddegradationproducts,can bepreventedor eliminatedbynimodipine to someextent. In thisstudy, nimodipineshowed its effectson the disruptionof neuronalCa2 - channeldecreasethe permeabilityof BBBandcerebraledema. Therefore, it may be apromissingagent in thetreatmentof traumaticcerebral edema and fortreatmentof severecraniocerebralinjuries.
I P-3-3071 Neuroprotectivepropertiesof emoxypin anddiavitol
in brain trauma: Experimental and clinical aspects
F.Oleshkevich,A. Fedulov,N. Mezen, L. Plenina, S. Hljustov,L. Marchenko. Departmentof NeurologyandNeurosurgery,MedicalInstitute,Minsk, Belarus Introduction:Hypoxiaandfree-radicaloxidationof lipidsare the main mechanismsofsecondarynervoustissue damagefollowingbraintrauma. Therefore, the use ofneuroprotectors(antihypoxantsandantioxidants)createspreconditionsfor more successfultreatmentresultsfor brain injuries. Purpose of Research: To study the action of the antihypoxicmedication DIAVITOL (D) and the antioxidant EMOXYPIN (E) on: 1. glial cellsmetabolism; 2. dynamicsof neurologicaldisordersandevolutionof CT data. Objects of Research: 1.Astrocytesculture, culture of C6 rat'sglioma; 2. Laboratoryanimals(rats); 3. 357 patientswith brain contusions(BG). Research Methods: 1.Assessmentof mitoticactivity,swollencells quantities and level of water and osmogenicelectrolytesin brain tissue,biophysical criteriacharacterizingthe degree of hypoxic astrocytesdamage; 2. CT; 3. Dyneurologicalobservations;3. Nonparametricanalysisofvariance namicclinical was used. Results: The use of0 and E has shownpreventionofdamage to or death ofastrocytesin the culture inhypoxia.Thus, undertheinfluenceof Dthe mitotic activity has beenrestored to nearnormalcy,the quantity ofhypoxia-affected cells hasdramaticallydropped. The curative effect ofE has beensomewhat Jess manifest.Incubatedastrocytesand C6 rat's glioma in hypoxia conditions while addingE and especially0 to the culturemedium, results inreducing damage to cell proteins and disruptionof pyridoxalphosphates metabolism, which isascertainedthroughcorrespondingshifts ofspectrumparametersof the cells culturefluorescence.The use of 0 in hypoxiaalso brought about normalizationof the cultured cells membraneslipid bilayerparameters,which wasestimatedbythe degreeofeximerizationof themembranotropicfluorescent pyreneprobe. In an experimentalbrain injuryE alsoprovidesa non-specific antiedemicaction,apparently.via membrane-stabilizingeffect. 0 and E have shownpositiveinfluenceon pathomorphological alterationsin the brainrevealed byCT. The use of0 and E in the complexpharmacotherapyof BCresultedin a fasterreversalof neurologicaldisorders.
Ip-3-30al from Postinjurytreatmentwith rhlL·2 improves outcome experimentaltraumaticbrain injuryin rats S.K. Qian1, C. Zhu2 , J.Y.Jian2 . 1 DepartmentofNeurosurgery,94 Hospitalof PLA,Nanchang. (330002), JiangXinProvince, China, 2 Departmentof Neurosurgery,ChangzhengHospitalof the SecondMillitary University, Shanghai(200003), China Other studiesshowed that interleukin2-like immunoreactivityat the lesioned sites exists inabundancein themammal brain(Lapchak, 1991). IL-2supports the survivalof neurons(Awatsuji,1993), and stimulatesoligodendroglialproliferationand maturationin vitro(Benvensite,1986). The roleof IL-2 in brain recombinedhuis unknown.This study was designedto evaluatethe effectof maninterleukin-2(rhIL-2) onneurologicaldeficitsandhistopathologicchanges followingmoderatelateral fluidpercussionin SO rat brain. Therh1L-2 was administratedbyintraventricular(i.c.v.)injection3 days after injury,with 30U, 60 control.The resultsshowedthat rh1L-2 had U, 300 U, with injectionNS as the marlkedprotectionon neurologicalfunctionaftertraumaticbraininjury,improvingweightloss,promotingbeam-walkingandbeam-balance,especiallyat 60 U treatment.The cortical cavity with 60 U rh1L-2 injectionwas smaller than NS injection,0.07 mm x 0.10 mm vs 0.51 mm x 1.00 mm (P< 0.D1). We observed that rhlL-2supportedthe survival of neuronsin the hippocampalCA2, CA3 regions.These data suggest thatlL-2 might be one of importantendogenous the neurotrophicfactors in CNS, acting on repair in responseto traumaticbrain injury.We suggest that postinjury IL-2 applicationsmay havepotentialclinical value fortreatinghumanbraininjury.
IP-3-3091 An ultrastructuralstudy ofmicrovascularchanges after rootavulsion
C.A.J. Holtzer1.2, E. Marani1 , W. de Priester3, R.TW.M.Thomeer1,2. 1 NeuroregulationGroup, Dept.ofPhysiology,LeidenUniversityMedical Centre, theNetherlands,2 Dept. ofNeurosurgery,LeidenUniversityMedical Centre, theNetherlands,3 Dept. ofBiology,LeidenUniversity;theNetherlands An electron microscopicalstudy was carried out on the cat spinal cord gray
Tuesday, 8 July 1997 matter in order toinvestigatethe microvascularevents after a C7 ventral root avulsion. Edema andglialreactions:From2 days up to 30 daysafteravulsionperivascular edema was present around blood vessels and neutrophilicgranulocytes mainly in theperiendothelialspace. Eight days afteravulsionan increase in astrocyteprocessesaround the blood vessels was noted, the phagocyticactivity ofpericytes notablyincreased and myelinsheath-like structureswere encounteredin phagosomesof pericytes.After 14 days anuniformdistribution present. The phagoof astrocyticalprocessesaround the blood vessels was cytic activitydecreased and the myelinsheath-likematerial in thepericytical phagosomesgraduallydisappeared.The amount of microgliaaround the blood vesselsshowedan increaseafter 30 days survivaland then stabilized. Endothelialcells:At 2 daysafteravulsionthe endothelialcellscontainedvacfibrous-likesubstances.After 14daystheendothelialcytoplasm uolesfilledwith alsocontainedmyelinsheath-likeand"soap-bubble"structures.Tight junctions betweentheendothelialcellswere presentwithout exception.After 14days and up to 90 dayssurvivalintraluminaldebris wasnoted. The morphologicalchangesin theneuropil,pericytes.and endothelialcells describedin thisstudyindicatetransportof debrisfrom the neuropiltowardsthe avulsion. bloodvessel lumenafter ventralroot
IP-3-310 I A study of the~erikaryal reaction ofmotoneurons after rootavulslons
C.A.J.Holtzer1 2, E. Marani " C. Hoffmann,R.T.W.M. Thomeer1,2. 1 NeuroregulationGroup, Dept. ofPhysiology,LeidenUniversityMedical Centre, theNetherlands,2 Dept. ofNeurosurgery,Leiden UniversityMedical Centre, theNetherlands After C7 ventral rootavulsion the populationof motoneuronsdecreases as compared to a sharptranssectionof the rootlets at the pial surface. At light microscopicalJevel ceil death of thesemotoneuronswas not obviouslycharacterizedby darkdegeneration. Toinvestigatethisphenomenonan electromicroscopical study was carried out on 15 cats afteravulsionof the C7ventrafrootlets,with survivaltime of 2,8, 14,30, 60 and 90 days. Thecytoplasmof thesomataofinvolvedmotoneuronsshowedswollenmitochondriaand a dispersedrough endoplasmaticreticulum(RER). In the vicinity of the nuclearenvelopedarklysosomalprofiles wereencountered.Sometimes a streamof small, darlkvesicle-likestructuresconnectedtheIysosomeswith the motoneuronnuclearenvelope.Exocytosisofendoplasmaticdropletsand of mitochondriawaspresent.The numberofsynapsesattachedto themotoneuronal somata notablydecreased. Those synapses still present contained swollen lamellae. Sporadicallydarkdegenerationprofiles were present in the axonal pathways.The motoneuronsomatashoweddegenerationof both the light and the darktype.Aroundthesedegeneratingsomataan increaseofastrocytesand microglialcells wasobserved. Thisdegenerationof the light type explains how the disappearanceof motoneuronsafteravulsionmayescapelightmicroscopicalobservation.
I P-3-311 I Autologousnerve grafts inregenerationof motoaxonsafter C7 ventral rootavulsion
C.A.J.Holtzer1.2, E. Marani 1, R.TW.M.Thomeer1.2. 1 NeuroregulationGroup, Dept. ofPhysiology,LeidenUniversityMedicalCentre, theNetherlands,2 Dept. ofNeurosurgery,LeidenUniversityMedicalCentre, theNetherlands Thisstudyinvestigatesthepossibilityofregenerationof themotoneuronalaxons fromthe cord in relationwithtime. Eightmaleadult cats were used.Via a ventral approachtheC7ventralrootletswereselectivelyavulsedfromthecord,resected andSUbsequentlyreplaced by saphenousnerveautografts.After survival pereoperated upon. The C7 riodsrangingfrom 7 up to 120 days, the cats were spinalnervewastransecteddistallyand HRP wasadministeredto theproximal stump.Twodays later the animalswere perfusedand the C6 throughC8 spinal cordsegmentsweresectionedandstained. HRP andacetylcholinesteraseenzyme histochemistry,neurofilamentimmunocytochemistryand Nissl staining werecarried out. From 30 dayssurvivalonwards, HRP labelled axons andretrogradelylabelledmotoneuronsweredetectedin the spinal motorarea. The neurofilament stainingdemonstratedregeneratingaxonsat thetransitionzonebetweenspinal cordandgraft.Withinthe nervegraftbothHRPand neurofilamentwerepresent. It isconcludedthatmoto-axonscan bridgeboth the proximal,intramedullary and the distalcoaptationsites of a graft andelongateinto the spinal nerve.