简介:一氧化二氮(N2O)的滥用在发达国家的终生患病率异常高,在全世界范围内引起严重关注。吸入剂滥用后的髓神经病通常归因于维生素B12代谢紊乱,经常注意到严重的运动障碍。本研究旨在阐明其潜在的病理生理学。方法:收集18例N2O滥用或维生素B12缺乏的患者。进行了全面的中枢和外周神经诊断检查,包括整个脊柱MRI,和热定量感官测试(QST)。具体来说,进行了配对的运动和感觉神经兴奋性测试,以获得感觉运动轴突损伤的完整图片。结果:N2O滥用患者N2O暴露的平均持续时间为17.13±7.23个月。MRI显示,有87.5%的N2O滥用患者和50%的维生素B12缺乏患者的T2高强度。在N2O滥用患者中,运动神经兴奋性试验显示峰值反应降低(7.08±0.87mV,P=0.05),延迟增加(7.09±0.28ms,P<0.01),超适性增加(-32.95±1.74%,P<0.05),和减少适应去极化电流[TEd(40-60ms)56.53±0.70%,P<0.05];感官测试显示仅降低峰响应(30.54±5.98μV,P<0.05)。同时,维生素B12缺乏症患者的运动测试显示,去极化电流[TEd(40-60ms)55.72±1.60%,P<0.01];感官测试显示峰响应降低(25.86±3.44μV,P<0.05)超兴奋度增加(-28.58±3.71%,P<0.001),亚兴奋性增加(8.31±1.64%,P<0.05),和减少适应去极化电流[TEd(峰值)67.31±3.35%,P<0.001]。结论:与维生素B12缺乏相比,N2O滥用患者表现出突出的运动超兴奋变化和较不突出的感觉超兴奋变化,提示与维生素B12缺乏不同的独特病理过程。N2O滥用可能不仅通过阻断蛋氨酸代谢,而且通过影响节旁区域的毒性而导致轴突功能障碍。
Introduction: Abuse of nitrous oxide (N2O) has an unusually high lifetime prevalence in developed countries and represents a serious concern worldwide. Myeloneuropathy following the inhalant abuse is commonly attributed to the disturbance of vitamin B12 metabolism, with severe motor deficits are often noted. The present study aims to elucidate its underlying pathophysiology. Methods: Eighteen patients with N2O abuse or vitamin B12 deficiency were recruited. Comprehensive central and peripheral neuro-diagnostic tests were performed, including whole spine MRI, and thermal quantitative sensory testing (QST). Specifically, paired motor and sensory nerve excitability tests were performed in order to obtain a complete picture of the sensorimotor axonal damage. Results: The mean duration of N2O exposure for the N2O abuse patients was 17.13 ± 7.23 months. MRI revealed T2 hyperintensity in 87.5% of the N2O abuse patients and 50% of the vitamin B12 deficiency patients. In N2O abuse patients, the motor nerve excitability test showed decreased in peak response (7.08 ± 0.87 mV, P = 0.05), increased latency (7.09 ± 0.28 ms, P < 0.01), increased superexcitability (-32.95 ± 1.74%, P < 0.05), and decreased accommodation to depolarizing current [TEd (40-60 ms) 56.53 ± 0.70%, P < 0.05]; the sensory test showed only decreased peak response (30.54 ± 5.98 μV, P < 0.05). Meanwhile, motor test in vitamin B12 deficiency patients showed only decreased accommodation to depolarizing current [TEd (40-60 ms) 55.72 ± 1.60%, P < 0.01]; the sensory test showed decreased peak response (25.86 ± 3.44 μV, P < 0.05) increased superexcitability (-28.58 ± 3.71%, P < 0.001), increased subexcitability (8.31 ± 1.64%, P < 0.05), and decreased accommodation to depolarizing current [TEd (peak) 67.31 ± 3.35%, P < 0.001]. Conclusion: Compared to vitamin B12 deficiency, N2O abuse patients showed prominent motor superexcitability changes and less prominent sensory superexcitability changes, hinting a unique pathological process different from that of vitamin B12 deficiency. N2O abuse might cause axonal dysfunction not only by blocking methionine metabolism but also by toxicity affecting the paranodal region.