Boland Robert A, Bostock Hugh, Kiernan Matthew C
Spinal Injuries Research Centre, Prince of Wales Medical Research Institute, Randwick, NSW, Australia.
Clin Neurophysiol. 2009 Jan;120(1):204-9. doi: 10.1016/j.clinph.2008.10.009. Epub 2008 Nov 25.
To assess changes in peripheral motor excitability after traumatic spinal cord injury (SCI).
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.
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.
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.
These findings may suggest the potential for plasticity of peripheral axonal excitability in response to acute SCI.
评估创伤性脊髓损伤(SCI)后外周运动兴奋性的变化。
对一名被诊断为美国脊髓损伤协会(ASIA)C级不完全损伤的C6患者进行常规神经传导和神经兴奋性的纵向研究。在整个住院期间,从腓总神经记录到胫前肌,从中神经记录到拇短展肌。
损伤后6天,腓总神经轴突的记录急性异常。阈下电紧张呈“扇形展开”;在恢复周期中,超兴奋性消失,2.5毫秒时的不应期增加(患者为152.84%;对照组为37.13±3.83%)。在第9天手术稳定后,所有参数短暂恢复,然后在第13天再次下降。当患者以ASIA D级出院时,兴奋性值在第68天恢复。在整个住院期间,正中神经轴突的记录相对未受影响。
SCI后的去神经支配对下肢轴突有显著影响,并非直接创伤所致。相反,正中神经轴突未受影响。下肢兴奋性变化的模型表明,能量依赖过程的中断导致了外周异常,可能是通过上游跨突触过程的参与。
这些发现可能提示外周轴突兴奋性在急性SCI后具有可塑性的潜力。