Plasticity of lower limb motor axons after cervical cord injury.
OBJECTIVE
To assess changes in peripheral motor excitability after traumatic spinal cord injury (SCI).


METHODS
Conventional nerve conduction and nerve excitability studies were longitudinally investigated in a patient diagnosed as C6 American Spinal Injury Association (ASIA) C incomplete. Recordings were undertaken from the peroneal nerve to tibialis anterior, and the median nerve to abductor pollicus brevis throughout the period of hospital admission.


RESULTS
Recordings were acutely abnormal in common peroneal axons 6 days after injury. Threshold electrotonus was "fanned in"; during the recovery cycle superexcitability was abolished, and refractoriness at 2.5ms was increased (patient 152.84%; controls 37.13+/-3.83%). All parameters recovered briefly after surgical stabilization on day 9, before regressing by day 13. Excitability values recovered by day 68 when the patient was discharged ambulant as ASIA D. Recordings remained relatively unaffected in median axons throughout the admission period.


CONCLUSIONS
Decentralisation after SCI had significant effects on lower limb axons, not attributable to direct trauma. Conversely, median axons remained spared. Modeling of the lower limb excitability changes suggested that interruption of energy-dependent processes contributed to the peripheral abnormalities, perhaps through involvement of upstream transynaptic processes.


CONCLUSIONS
These findings may suggest the potential for plasticity of peripheral axonal excitability in response to acute SCI.
Boland
Robert A
RA
Spinal Injuries Research Centre, Prince of Wales Medical Research Institute, Randwick, NSW, Australia.
Bostock
Hugh
H
Kiernan
Matthew C
MC
D000200:Action Potentials / Q000502:physiology; D000328:Adult; D001369:Axons / Q000502:physiology*; D004558:Electric Stimulation / Q000379:methods; D004576:Electromyography; D007839:Functional Laterality; D006801:Humans; D035002:Lower Extremity / Q000503:physiopathology*; D008297:Male; D008954:Models, Biological; D008962:Models, Theoretical; D009046:Motor Neurons / Q000473:pathology*; D018482:Muscle, Skeletal / Q000473:pathology*; D009431:Neural Conduction / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D010525:Peripheral Nerves / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000601:surgery; D013997:Time Factors