Topography and severity of axonal injury in human spinal cord trauma using amyloid precursor protein as a marker of axonal injury.
METHODS
Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI.


OBJECTIVE
To topographically map and semiquantitate axonal injury in spinal cord compression of sufficient severity to produce para- or quadriplegia.


BACKGROUND
Amyloid precursor protein is carried along the axon by fast axoplasmic transport and has been extensively used as a marker of traumatic axonal injury.


METHODS
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).


RESULTS
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.


CONCLUSIONS
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.
Cornish
R
R
Neuropathology Laboratory, Institute of Medical and Veterinary Science, Department of Neurosurgery, Royal Adelaide Hospital, and University of Adelaide, South Australia.
Blumbergs
P C
PC
Manavis
J
J
Scott
G
G
Jones
N R
NR
Reilly
P L
PL
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016564:Amyloid beta-Protein Precursor / Q000032:analysis* / Q000276:immunology; D000911:Antibodies, Monoclonal; D001369:Axons / Q000737:chemistry* / Q000473:pathology*; D015415:Biomarkers; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D010264:Paraplegia / Q000473:pathology; D011782:Quadriplegia / Q000473:pathology; D013117:Spinal Cord Compression / Q000473:pathology*
D016564:Amyloid beta-Protein Precursor; D000911:Antibodies, Monoclonal; D015415:Biomarkers