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Topography and severity of axonal injury in human spinal cord trauma using amyloid precursor protein as a marker of axonal injury

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dc.contributor.authorCornish, R.
dc.contributor.authorBlumbergs, P.
dc.contributor.authorManavis, J.
dc.contributor.authorScott, G.
dc.contributor.authorJones, N.
dc.contributor.authorReilly, P.
dc.date.issued2000
dc.description.abstract<h4>Study design</h4>Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI.<h4>Objectives</h4>To topographically map and semiquantitate axonal injury in spinal cord compression of sufficient severity to produce para- or quadriplegia.<h4>Summary of background data</h4>Amyloid precursor protein is carried along the axon by fast axoplasmic transport and has been extensively used as a marker of traumatic axonal injury.<h4>Methods</h4>The study group comprised 18 cases of spinal cord compression (17 due to fracture dislocation of the vertebral column and 1 iatrogenic compression from Harrington rods) and two normal control. All the cords were examined according to a standard protocol, and at least 10 segmental levels were immunostained using a monoclonal antibody to amyloid precursor protein and immunopositive AI was semiquantitated using a grading system to provide the axonal injury severity score (AISS). The focal injury at the site of cord compression (haemorrhage, haemorrhagic necrosis, ischaemic necrosis) was also semiquantitated to provide the focal injury area score (FIAS). AI occurring around the site of focal compression (focal axonal injury severity score or FAISS) was distinguished from AI distant to the focal injury (nonfocal axonal injury severity score or NFAISS).<h4>Results</h4>All 18 cases showed widespread amyloid precursor protein immunoreactive axonal injury and the AISS ranged from 28 to 60%. In all cases, the FAISS was greater than the NFAISS and there was a statistically significant relationship between the AISS and the FIAS.<h4>Conclusion</h4>Acute spinal cord compression of sufficient severity to produce permanent paralysis causes widespread axonal damage that is maximal at the site of compression but also present throughout the length of the cord in segments far distant from the site of the focal injury.
dc.identifier.citationSpine, 2000; 25(10):1227-1233
dc.identifier.doi10.1097/00007632-200005150-00005
dc.identifier.issn0362-2436
dc.identifier.issn1528-1159
dc.identifier.orcidManavis, J. [0000-0001-7381-7781] [0000-0003-1268-561X]
dc.identifier.urihttp://hdl.handle.net/2440/10667
dc.language.isoen
dc.publisherLippincott Williams & Wilkins
dc.source.urihttps://doi.org/10.1097/00007632-200005150-00005
dc.subjectAxons
dc.subjectHumans
dc.subjectSpinal Cord Compression
dc.subjectParaplegia
dc.subjectQuadriplegia
dc.subjectNecrosis
dc.subjectAmyloid beta-Protein Precursor
dc.subjectAntibodies, Monoclonal
dc.subjectAdolescent
dc.subjectAdult
dc.subjectAged
dc.subjectAged, 80 and over
dc.subjectMiddle Aged
dc.subjectFemale
dc.subjectMale
dc.subjectBiomarkers
dc.titleTopography and severity of axonal injury in human spinal cord trauma using amyloid precursor protein as a marker of axonal injury
dc.typeJournal article
pubs.publication-statusPublished

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