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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

Cornish, Ryan B Health Sc (Hons)*; Blumbergs, Peter C. FRCPA, FRACP*; Manavis, Jim BSc (Hons)*; Scott, Grace FRCPath*; Jones, Nigel R. DPHIL, FRACS; Reilly, Peter L. MD, FRACS

Basic Science

Study Design. Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI.

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

Summary of Background Data. 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 semiquantited 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.

Conclusion. 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.

From the *Neuropathology Laboratory, Institute of Medical and Veterinary Science, †Department of Neurosurgery, Royal Adelaide Hospital, and University of Adelaide, Adelaide, South Australia.

Supported by grants from the Motor Accident Commission and the Neurosurgical Research Foundation.

Acknowledgment date: February 11, 1999.

First revision date: May 24, 1999.

Acceptance date: August 16, 1999.

Address reprint requests to

Dr. Peter Blumbergs

Neuropathology Laboratory

Institute of Medical & Veterinary Science

PO Box 14, Rundle Mall

Adelaide, South Australia, 5000

E-mail: peter.blumbergs@imvs.sa.gov.au

Device status category: 1.

Conflict of interest category: 12.

© 2000 Lippincott Williams & Wilkins, Inc.