Clinical and radiological analysis of subacute combined degeneration caused by different etiologies
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摘要:
目的 分析一氧化二氮(nitrous oxide, N2O)滥用致脊髓亚急性联合变性(subacute combined degeneration, SCD)和非N2O相关性SCD临床、影像学及预后间的差异。 方法 回顾性分析2017年1月—2021年4月在杭州师范大学附属医院、浙江大学附属邵逸夫医院及浙江大学附属第二医院确诊的43例SCD患者的临床资料。根据病因分为N2O滥用组(23例)及非N2O滥用组(20例)。比较2组在临床表现、影像学检查、实验室检查及预后间的差异。 结果 N2O滥用组的发病年龄[21(19,25)岁]显著低于非N2O滥用组[69(62,74)岁, P < 0.001]。N2O滥用组出现尿便功能障碍的概率(34.78%,8/23)较非N2O滥用组低(65.00%,13/20, P=0.048)。N2O滥用组出现脊髓肿胀的概率(56.52%, 13/23)较非N2O滥用组高(20.00%,4/20, P=0.015)。N2O滥用组入院时的改良Rankin评分量表(mRS)评分[3.0(2.5,4.0)分]较非N2O滥用组低[4.0(3.5,4.0)分, P=0.033];治疗3个月后的mRS评分[2.0(1.0,2.0)分]也较非N2O滥用组低[3.0(3.0,4.0)分,P < 0.001]。 结论 与非N2O滥用组相比,N2O滥用致SCD的神经功能损伤程度低,发生脊髓肿胀概率高,预后较好。 Abstract:Objective This study aims to compare the clinical, radiological features and outcomes between patients with subacute combined degeneration (SCD) induced by recreational nitrous oxide (N2O) abuse and patients with N2O-unrelated SCD. Methods From January 2017 to April 2021, the clinical data of 43 patients with SCD diagnosed at Affiliated Hospital of Hangzhou Normal University, Sir Run Run Shaw Hospital Zhejiang University and Zhejiang Second Hospital were retrospectively analysed. According to the etiology, case data were divided into 23 patients with recreational N2O-induced SCD and 20 patients with N2O-unrelated SCD. The clinical and MRI features, laboratory tests and prognosis were compared between the two groups. Results Of the 23 patients with recreational N2O-induced SCD, the mean age of onset was lower than those with N2O-unrelated SCD [21 (19, 25) vs. 69 (62, 74) years, P < 0.001]]. The incidence of urinary and stool dysfunction was lower in the N2O-induced SCD group (34.78%, 8/23) than in the N2O-unrelated SCD group (65.00%, 13/20, P=0.048). MRI examinations indicated the N2O-induced SCD cases presented a higher incidence of cord swelling [56.52% (13/23) vs. 20.00% (4/20), P=0.015]. The mRS scores for patients with N2O-induced SCD [3.0 (2.5, 4.0)] were lower than those with N2O-unrelated SCD [4.0 (3.5, 4.0), P=0.033] at admission. Moreover, patients with N2O-induced SCD presented significantly lower mRS [2.0 (1.0, 2.0)] scores than those with N2O-unrelated SCD [3.0 (3.0, 4.0), P < 0.001] at the last follow-up visit 3 months later. Conclusion These findings indicated that patients with N2O-induced SCD have less severe neurological function deficit, an increased incidence of cord swelling and better prognosis. -
表 1 2组SCD患者一般情况及临床症状比较
Table 1. Comparison of general conditions and clinical symptoms of SCD patients in 2 groups
组别 例数 年龄[M(P25, P75),岁] 性别(男/女,例) 肢体无力[例(%)] 四肢麻木[例(%)] 步态不稳[例(%)] 尿便功能障碍[例(%)] 认知障碍[例(%)] 精神症状[例(%)] N2O滥用组 23 21(19,25) 7/16 11(47.83) 20(86.96) 17(73.91) 8(34.78) 7(30.43) 5(21.73) 非N2O滥用组 20 69(62,74) 6/14 15(75.00) 18(90.00) 14(70.00) 13(65.00) 1(5.00) 0 统计量 -5.609a 0.001b 3.305b <0.001b 0.081b 3.909b 3.045b 3.032b P值 <0.001 0.975 0.069 0.999 0.775 0.048 0.081 0.082 注:a为Z值,b为χ2值。 表 2 2组SCD患者神经系统体征的比较[例(%)]
Table 2. Comparison of neurological signs between two groups of patients with SCD [Case (%)]
组别 例数 深感觉障碍 肌力下降 深反射消失或降低 深反射增高 Romberger征(+) Babinski征(+) 浅反射消失 Lhermitte征(+) N2O滥用组 23 10(43.48) 14(60.87) 15(65.22) 4(17.39) 13(56.52) 5(21.74) 2(8.69) 1(4.35) 非N2O滥用组 20 15(75.00) 17(85.00) 15(75.00) 3(15.00) 14(70.00) 7(35.00) 3(15.00) 0 χ2值 4.368 3.096 0.485 <0.001 0.832 0.935 0.028 P值 0.037 0.078 0.486 0.999 0.362 0.334 0.868 0.999a 注:a为采用Fisher精确检验。 表 3 2组SCD患者脊髓磁共振特点比较
Table 3. Comparison of spinal magnetic resonance characteristics between two groups of SCD patients
组别 例数 脊髓受累人数[例(%)] 矢状位 冠状位 病灶节段数[M(P25, P75),个] 颈髓[例(%)] 胸髓[例(%)] 颈胸均受累[例(%)] 病灶≥3个脊髓节段[例(%)] 脊髓肿胀[例(%)] 脊髓萎缩[例(%)] 侧索[例(%)] 后索[例(%)] 倒V征[例(%)] N2O滥用组 23 16(69.57) 2(0,4) 14(60.87) 3(13.04) 3(13.04) 12(52.17) 13(56.52) 4(17.39) 3(13.04) 7(30.43) 7(30.43) 非N2O滥用组 20 16(80.00) 3(0,5) 11(55.00) 8(40.00) 4(20.00) 8(40.00) 4(20.00) 5(25.00) 7(35.00) 5(25.00) 5(25.00) 统计量 0.621a -0.509b 0.151a 4.083a 0.041a 0.637a 5.969a 0.056a 1.790a 0.157a 0.157a P值 0.434 0.611 0.697 0.043 0.840 0.425 0.015 0.813 0.181 0.692 0.692 注:a为χ2值,b为Z值。 表 4 2组SCD患者实验室检查比较
Table 4. Comparison of laboratory examination between 2 groups of patients with SCD
组别 例数 血清VB12浓度[M(P25, P75), g/mL] Hcy [M(P25, P75), μmol/L] 红细胞计数[M(P25, P75), ×109/L] 平均红细胞体积[M(P25, P75), fL] 血红蛋白[M(P25, P75), g/L] 大细胞性贫血[例(%)] N2O滥用组 23 160.00(150.24,218.00) 27.00(12.90,39.8) 3.84(3.57,4.21) 95.60(92.20,101.10) 126.00(117.00,139.00) 10(43.48) 非N2O滥用组 20 84.00(63.43,94.75) 28.00(10.90,60.25) 3.07(2.34,3.50) 110.00(100.90,118.85) 111.00(93.00,117.50) 16(80.00) 统计量 -4.288a -0.280a -3.959a -3.508a -3.364a 5.969b P值 <0.001 0.779 <0.001 <0.001 0.001 0.015 注:a为Z值,b为χ2值。 表 5 2组SCD患者mRS评分比较[M(P25, P75),分]
Table 5. Comparison of mRS scores between two groups of patients with SCD [M(P25, P75), points]
组别 例数 mRS评分 入院时 治疗3个月后 N2O滥用组 23 3.0(2.5,4.0) 2.0(1.0,2.0) 非N2O滥用组 20 4.0(3.5,4.0) 3.0(3.0,4.0) Z值 -2.133 -4.133 P值 0.033 <0.001 -
[1] 中华医学会神经病学分会, 中华医学会神经病学分会周围神经病协作组, 中华医学会神经病学分会肌电图与临床神经电生理学组, 等. 中国亚急性联合变性诊治共识[J]. 中华神经科杂志, 2020, 53(4): 269-273. doi: 10.3760/cma.j.cn113694-20191101-00677Chinese Society of Neurology, Peripheral Neuropathy Cooperative Group, Electromyography and Clinical Neurophysiology Group, Chinese Society of Neurology, et al. Chinese expert consensus on diagnosis and treatment of subacute combined degeneration[J]. Chinese Journal of Neurology, 2020, 53(4): 269-273. doi: 10.3760/cma.j.cn113694-20191101-00677 [2] CAO J, SU Z Y, XU S B, et al. Subacute combined degeneration: a retrospective study of 68 cases with short-term follow-up[J]. Eur Neurol, 2018, 79(5-6): 247-255. doi: 10.1159/000488913 [3] GREEN R, ALLEN L H, BJORKE-MONSEN A L, et al. Vitamin B (12) deficiency[J]. Nat Rev Dis Primers, 2017, 3(1): 17040. doi: 10.1038/nrdp.2017.40 [4] CHEN R, LIAO M, OU J. Laughing gas inhalation in Chinese youth: a public health issue[J]. Lancet Public Health, 2018, 3(10): e465. DOI: 10.1016/S2468-2667(18)30134-8. [5] KEDDIE S, ADAMS A, KELSO A R C, et al. No laughing matter: subacute degeneration of the spinal cord due to nitrous oxide inhalation[J]. J Neurol, 2018, 265(5): 1089-1095. doi: 10.1007/s00415-018-8801-3 [6] ZHENG D M, BA F, BI G R, 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]. J Neurol, 2020, 267(2): 422-429. doi: 10.1007/s00415-019-09600-w [7] BUHRE W, DISMA N, HENDRICK J, et al. European Society of Anaesthesiology Task Force on Nitrous Oxide: a narrative review of its role in clinical practice[J]. Br J Anaesth, 2019, 122(5): 587-604. doi: 10.1016/j.bja.2019.01.023 [8] ALLEN L H, MILLER J W, DE GROOT L, et al. Biomarkers of Nutrition for Development (BOND): vitamin B-12 review[J]. J Nutr, 2018, 148(4): 1995S-2027S. DOI: 10.1093/jn/nxy201. [9] LEWIS B, NELSON G, VU T, et al. No laughing matter-Myeloneuropathy due to heavy chronic nitrous oxide abuse[J]. Am J Emerg Med, 2021, 46(8): 799e1-799e2. [10] ROBERT H D, MARTINEZ B, TABAAC B J. B12 deficiency and clinical presentation in the setting of nitric oxide use[J]. Case Rep Neurol Med, 2021, 2021(4): e5590948. DOI: 10.1155/2021/5590948. [11] ZHANG J J, XIE D D, ZOU Y F, et al. Key characteristics of nitrous oxide-induced neurological disorders and differences between populations[J]. Front Neurol, 2021, 12(4): e627183. DOI: 10.3389/fneur.2021.627183. [12] 王瑞, 梁娜娜, 孙亚丽, 等. 笑气滥用致神经系统损害的临床特征[J]. 徐州医科大学学报, 2019, 39(5): 350-353. doi: 10.3969/j.issn.2096-3882.2019.05.009WANG R, LIANG N N, SUN Y L, et al. Clinical features of nervous system damage caused by nitrous oxide abuse[J]. Journal of Xuzhou Medical University, 2019, 39(5): 350-353. doi: 10.3969/j.issn.2096-3882.2019.05.009 [13] FANG X, LI W, GAO H, et al. Skin hyperpigmentation: a rare presenting symptom of nitrous oxide abuse[J]. Clinical toxicology, 2020, 58(6): 476-481. doi: 10.1080/15563650.2019.1665181 [14] SWART G, BLAIR C, LU Z, et al. Nitrous oxide-induced myeloneuropathy[J]. Eur J Neurol, 2021, 28(12): 3938-3944. doi: 10.1111/ene.15077 [15] XIANG Y Y, LI L, MA X T, et al. Recreational nitrous oxide abuse: prevalence, neurotoxicity, and treatment[J]. Neurotox Res, 2021, 39(3): 975-985. doi: 10.1007/s12640-021-00352-y [16] YUAN J L, WANG S K, JIANG T, et al. Nitrous oxide induced subacute combined degeneration with longitudinally extensive myelopathy with inverted V-sign on spinal MRI: A case report and literature review[J]. BMC neurology, 2017, 17(1): 222-224. doi: 10.1186/s12883-017-0990-3 [17] NOH T, OSMAN G, CHEDID M, et al. Nitrous oxide-induced demyelination: Clinical presentation, diagnosis, and treatment recommendations[J]. J Neurol Sci, 2020, 414(7): e116817. DOI: 10.1016/j.jns.2020.116817. [18] EINSIEDLER M, VOULLEMINOT P, DEMUTH S, et al. A rise in cases of nitrous oxide abuse: neurological complications and biological findings[J]. J Neurol, 2021, 1-6. DOI: 10.1007/s00415-021-10702-7. [19] 林妮, 柯渠青, 蒋玲燕, 等. 同型半胱氨酸临床应用的研究进展[J]. 中华全科医学, 2021, 19(8): 1358-1361. doi: 10.16766/j.cnki.issn.1674-4152.002060LIN N, KE Q Q, JIANG L Y, et al. The clinical application value of homocysteine[J]. Chinese Journal of General Practice, 2021, 19(8): 1358-1361. doi: 10.16766/j.cnki.issn.1674-4152.002060 [20] VOLLHARDT R, MAZOYER J, BERNARDAUD L, et al. Neurological consequences of recreational nitrous oxide abuse during SARS-CoV-2 pandemic[J]. J Neurol, 2021, 1-6. DOI: 10.1007/s00415-021-10748-7. [21] WILLIAMSON J, HUDA S, DAMODARAN D. Nitrous oxide myelopathy with functional vitamin B12 deficiency[J]. BMJ Case Reports, 2019, 12(2): e227439. DOI: 10.1136/bcr-2018-227439. -