Analysis of clinicaland electrophysiologicalfeaturesin patients withnitrous oxide-induced neuropathy

doi:10.19854/j.cnki.1008-2425.2022.06.0007

Abstract

Abstract: Objective To analyse the features of clinicalandnerve conduction in patientswithnitrous oxide-induced neuropathy.Methods The clinicaIandelectrophysiological data of 7 patients with nitrous oxide-induced neuropathy in the First Affiliated Hospitalof Scienceand Technologyof Chinawere analyzed.Results All patients in this group had sensory or motor dysfunction symptoms,including 3 cases (3/7) with numbness and weakness of limbs and 4 cases (4/7) with numbness and weakness of lower limbs.Motor nerve conduction in lower limbs was more likely to be involved and the degree was more severe than that in upper limbs:the abnormal rate of motor nerve conduction in lower limbs was higherthan that in upper limbs [100% (28/28) vs 17.9% (5/28),P＜0.001],and the proportion of CAMP not elicited in lower limbs was higher than that in upper limbs [42.9%(12/28) vs0.0% (0/28),P＜0.05].Motor nerve conduction was more seriously damaged than sensory nerve conduction:the proportion of motor wave amplitude not elicited was greater than that of sensory [21.4% (12/56) vs 4.0% (2/50),P＜0.05].The slowing down of sensory nerve conduction velocity was more common than the decrease of amplitude:the proportion of the slowing down of sensory conduction velocity was greater than the decrease of amplitude [48.0% (24/50) vs 20.0% (10/50),P＜0.05].Conclusion In patients with nitrous oxide toxic peripheral neuropathy,motor and sensory nerves are involved.Lower limbs are heavier than upper limbs,and movement is heavier than sensation.

Key words: Nitrous oxide, Peripheral neuropathy, Nerve conduction, Vitamin B12, Homocysteine

摘要： 目的分析一氧化二氮所致周围神经损害患者的临床及神经传导特点。方法对2019年9月至2022年6月中国科学技术大学附属第一医院诊治的7例N2O相关周围神经损害患者的临床特点进行总结,结合患者运动和感觉神经传导检查结果进行分析。结果本组患者均以感觉或运动功能障碍症状起病,四肢麻木无力3例(3/7),双下肢麻木无力4例(4/7)。下肢的运动神经传导较上肢更容易受累且程度更重:下肢运动神经传导异常率大于上肢[100.0%(28/28)与17.9%(5/28),P＜0.001],下肢CAMP未引出的比例大于上肢[42.9%(12/28)与0.0%(0/28),P＜0.001];运动神经传导较感觉神经传导损害更严重:运动波幅未引出比例大于感觉[21.4%(12/56)与4.0%(2/50),P＜0.05];感觉神经传导速度减慢较波幅降低更普遍:感觉传导速度减慢比例大于波幅减低[48.0%(24/50)与20.0%(10/50),P＜0.05]。结论一氧化二氮中毒性周围神经病患者运动和感觉神经均受累。下肢重于上肢,运动较感觉更重。

关键词: 一氧化二氮, 周围神经病, 神经传导检查, 维生素B12, 同型半胱氨酸

CLC Number:

R741

Meng Qingyun, Shen Ping, Li Jing, et al. Analysis of clinicaland electrophysiologicalfeaturesin patients withnitrous oxide-induced neuropathy[J]. Chinese Journal of Stereotactic and Functional Neurosurgery, 2022, 35(6): 354-358.

孟庆云, 沈萍, 李静, 梅加明. N2O相关周围神经损害的临床与电生理特点分析[J]. 立体定向和功能性神经外科杂志, 2022, 35(6): 354-358.

References

[1] GarakaniA,JaffeRJ,SavlaD,et al.Neurologic,psychiatric,and other medical manifestations of nitrous oxide abuse:A systematic review of the case literature[J].Am J Addict,2016,25(5):358~369.
[2] Dongming Zheng,Fang Ba,Guorong Bi,et al.The sharp rise of neurological disorders associated with recreational nitrous oxide use in China:a single center experience and a brief review of Chinese literature[J].Journal of Neurology,2020,267(2):422~429.
[3] Choi C,Kim T,Park KD,Lim OK,Lee JK.Subacute combined degeneration caused by nitrous oxide intoxication:a report of two cases[J].Ann Rehabil Med.2019,43(4):530~534.
[4] Li HT,ChuCC,ChangKH,et al.Clinical and electrodiagnostic characteristics of nitrous oxide-induced neuropathy in Taiwan[J].Clin Neurophysiol,2016,127(10):3288~3293.
[5] Franques J,Chiche L,De Paula AM et al.Characteristics of patients with vitamin B12-responsive neuropathy:a case series with systematic repeated electrophysiological assessment[J].Neurol Res.2019,41(6):569~576.
[6] Osmani K,Vignes S,Aissi M,Wade F,Milani P,Levy BI,et al.Taxane-induced peripheral neuropathy has good long-term prognosis:a 1- to 13-year evaluation[J].J Neurol.2012,259(9):1936~1943.
[7] Park SB,Lin CS,Krishnan AV,Goldstein D,Friedlander ML,Kiernan MC.Long-term neuropathy after oxaliplatin treatment:challenging the dictum of reversibility[J].Oncologist.2011,16(5):708~716.
[8] 宋文静,鲍磊,李庆节,等,笑气滥用导致神经功能缺损的临床特点[J].临床神经病学杂志,2021,34(1):58~61.
[9] Savage S,Ma D.The neurotoxicity of nitrous oxide:the facts and “putative” mechanisms[J].Brain Sci,2014,4(1):73~90.
[10] Reynolds E.Vitamin B12,folic acid,and the nervous system[J].The LancetNeurology,2006,5(11):949~960.
[11] Morris N,Lynch K,Greenberg SA.Severe motor neuropathy or neuronopathy due to nitrous oxide toxicity after correction of vitamin B12 deficiency[J].Muscle Nerve.2015,51(4):614~616.
[12] Lei Bao,Qing Li,Qingjie Li,et al.Clinical,Electrophysiological and Radiological Features of Nitrous Oxide-Induced Neurological Disorders[J].Neuropsychiatr Dis Treat,2020,16:977~984.
[13] Haout L,El-saden s.Nittrous oxide-induced B12 denciency myelopathy:perspectives on the clinical biochemistry 0f vitamin B12[J].J Neurol sci,2011,301(1-2):1~8.
[14] Waters MF,Kang GA,Mazziotta JC,Degiorgio CM.Nitrous oxide inhalation as a cause of cervical myelopathy[J].Acta Neurol Scand.2010,112(4):270~272.
[15] Thompson AG,Leite MI,Lunn MP,Bennett DLH.Whippits,nitrous oxide and the dangers of legal highs[J].Pract Neurol,2015,15(3):207~209.
[16] TaniJ.Weng,H.Chen,et al.Elucidating unique axonal dysfunction between nitrous oxide abuse and vitamin B12 deficiency[J].Front Neurol,2019,10:704.
[17] Zoccolella S,Bendotti C,Beghi E,Logroscino G.Homocysteine levels and amyotrophic lateral sclerosis:a possible link[J].Amyotroph Lateral Scler,2010,11(1-2):140~147.
[18] Tjiattas L,Ortiz DO,DhivantS et al.Folatedefciency and homocysteine induce toxicity in cultured dorsal root ganglion neurons via cytosolic calcium accumulation[J].Aging Cell,2004,3:71~76.