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. SIGNIFICANCE: These findings may suggest the potential for plasticity of peripheral axonal excitability in response to acute SCI.
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. SIGNIFICANCE: These findings may suggest the potential for plasticity of peripheral axonal excitability in response to acute SCI.
Authors: Dirk Czesnik; James Howells; Michael Bartl; Elisabeth Veiz; Rebecca Ketzler; Olga Kemmet; Arthur S Walters; Claudia Trenkwalder; David Burke; Walter Paulus Journal: J Physiol Date: 2018-11-24 Impact factor: 5.182
Authors: Michelle A Farrar; Steve Vucic; Cindy S-Y Lin; Susanna B Park; Heather M Johnston; Desirée du Sart; Hugh Bostock; Matthew C Kiernan Journal: Brain Date: 2011-09-16 Impact factor: 13.501
Authors: Susan E Tomlinson; S Veronica Tan; David Burke; Robyn W Labrum; Andrea Haworth; Vaneesha S Gibbons; Mary G Sweeney; Robert C Griggs; Dimitri M Kullmann; Hugh Bostock; Michael G Hanna Journal: Brain Date: 2016-02 Impact factor: 13.501