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Brain Advance Access originally published online on January 30, 2007
Brain 2007 130(4):985-994; doi:10.1093/brain/awl339
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© The Author (2007). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Axonal changes in spinal cord injured patients distal to the site of injury

Cindy Shin-Yi Lin1, Vaughan G. Macefield1, Mikael Elam3, B. Gunnar Wallin3, Stella Engel2 and Matthew C. Kiernan1

1Prince of Wales Medical Research Institute and Prince of Wales Clinical School, University of New South Wales, 2Spinal Unit, Prince of Wales Hospital, Sydney, Australia and 3Department of Clinical Neurophysiology, Sahlgren University Hospital, Gothenburg, Sweden

Correspondence to: Associate Professor Matthew C. Kiernan, Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, NSW 2031, Australia E-mail: m.kiernan{at}unsw.edu.au

It is generally assumed that the peripheral nervous system remains intact following a spinal injury. Accordingly, the electrical thresholds of motor axons in a peripheral nerve below the lesion should be similar to those in intact subjects. Yet in attempts to enter the common peroneal nerve with microelectrodes in 24 quadriplegic or paraplegic individuals it was often found that electrical stimulation over or within the nerve failed to elicit contractions in the pre-tibial flexors. To investigate whether consistent changes in axonal physiology occurred distal to the site of injury in patients with spinal cord injury (SCI), motor nerve excitability was formally tested in 15 of these patients. Threshold tracking techniques were used to measure axonal excitability parameters (stimulus–response curves, strength–duration properties, threshold electrotonus, a current–threshold relationship and the recovery cycle) of motor axons in the median and common peroneal nerves. In these patients motor axons were uniformly of high threshold and consequently, stimulus–response curves were shifted to the right. In some SCI patients, axons were completely inexcitable. Amplitudes of compound motor action potentials were reduced, consistent with axonal loss and strength–duration time constant was significantly reduced in SCI patients (SCI 0.13 ± 0.02 ms, controls 0.43 ± 0.02 ms, mean ± SE, P < 0.0001). Excitability changes were more prominent the more clinically severe the injury, with progressive deterioration over time since the original injury. While compression and traction sustained during the original injury or subsequent hospital rehabilitation may contribute in part to some of these changes, it is difficult to attribute these findings solely to such processes. Changes in axonal structure and ion channel function, but perhaps more critically decentralization and consequent inactivity, are likely to underlie the complex changes observed in axonal excitability in SCI patients.

Key Words: peripheral nerve; spinal cord injury

Abbreviations: APB, abductor pollicis brevis; CMAP, compound muscle action potential; RRP, relative refactory period; SCI, spinal cord injury; SDTC, strength–duration time constant; TA, tibialis anterior

Received January 23, 2006. Revised October 30, 2006. Accepted November 7, 2006.


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