脊髓亚急性联合变性临床新特点
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摘要
目的了解当前人们生活方式及膳食结构改变引起的脊髓亚急性联合变性(SCD)临床新特点。方法对50例SCD患者的临床资料进行回顾性分析,连续数据采用均值±标准差,分类数据用数目和百分比表示;相关分析采用Logistic回归相关分析,P<0.05为显著水平。结果 (1)发病年龄19～83岁,平均(53.2±10.8),<45岁5例(10%),45～65岁18例(36%),≥65岁27例(54%)。(2)贫血15例(30%),消化道疾病8例(16%),酗酒5例(10%),长期素食5例(10%),糖尿病饮食7例(14%),长期厌食(神经症)2例(4%),吸食N_2O 2例(4%),甲状腺疾病1例(2%)。(3)年龄>65岁、血清血红蛋白(Hb)、血清维生素B_(12)水平与本病神经系统病变的严重程度与无显著相关性(P>0.05)。平均红细胞体积(MCV)与神经功能障碍的严重程度关系密切,外周血MCV越高时神经病变越严重(P<0.05)。(4)50例(100%)神经电生理检查示不同程度的损伤,其中运动神经传导速度减慢25例(50%),感觉神经传导速度减慢40例(80%),脑干听觉诱发电位(BAEP)异常3例(6%),视觉诱发电位(VEP)2例(4%)。(5)磁共振成像发现病灶14例(28%),累及颈髓6例,累及胸髓6例,同时累及颈髓和胸髓2例,病灶累及脊髓侧索或后索,位于下颈段及胸段。结论 65岁以后可能为SCD另一发病高峰期。青少年患者无明确危险因素出现SCD表现需警惕吸食N_2O病史。血清维生素B_(12)正常或升高并不能排除SCD诊断,新的生化指标MCV、Hcy及脑脊液碱性髓鞘蛋白(MBP)的测定有助于SCD的早期诊断。神经电生理检查可以客观反映SCD病变部位,其检出率高于MRI检出率,在SCD疾病的早期诊断中具有重要价值。
Objective To understand the new clinical features of subacute combined degeneration(SCD) caused by lifestyle and dietary changes.Methods The clinical data of 50 patients with SCD were retrospectively analyzed.The continuous data were average±standard deviation.The categorical data were expressed by the number and percentage.The correlation analysis was performed by Logistic regression correlation analysis,P<0.05 was significant.Results(1) The age of onset was 19-83 years old,with an average of(53.2±10.8),5 cases(10%) at 45 years old,18 cases(36%) at 45-65 years old,and 27 cases(54%) ≥65 years old.(2) 15 cases of anemia(30%),8 cases of digestive tract disease(16%),5 cases of alcohol abuse(10%),5 cases of long-term vegetarian diet(10%),7 cases of diabetic diet(14%),long-term anorexia(Neurosis) 2 cases(4%),2 cases of N_2O(4%),1 case of thyroid disease(2%).(3) Age>65 years old,serum hemoglobin(Hb),serum vitamin B12 level and the severity of the neurological lesions of the disease and wireless correlation(P>0.05).The mean red blood cell volume(MCV) was closely related to the severity of neurological dysfunction.The higher the peripheral blood MCV,the more severe the neuropathy(P<0.05).(4) 50 cases(100%) of neurophysiological examination showed different degrees of injury,in which motor nerve conduction velocity was slowed by 25 cases(50%),sensory nerve conduction velocity was slowed by 40 cases(80%),brainstem auditory induction The potential(BAEP) was abnormal in 3 cases(6%) and visual evoked potential(VEP) in 2 cases(4%).(5) Magnetic resonance imaging found 14 cases(28%) of lesions,involving 6 cases of cervical pulp,involving 6 cases of thoracic marrow,involving 2 cases of cervical and thoracic spinal cord,involving the lateral or posterior cord of the spinal cord,located in the lower cervical segment And the chest.Conclusion 65 years of age may be another peak incidence of SCD.Adolescent patients with no clear risk factors for SCD should be alert to the history of N2 O.The normal or elevated serum vitamin B12 does not rule out the diagnosis of SCD.The new biochemical indicators MCV,Hcy and cerebrospinal fluid basic myelin protein(MBP) determination contribute to the early diagnosis of SCD.Neurophysiological examination can objectively reflect the SCD lesions,and its detection rate is higher than the MRI detection rate,which is of great value in the early diagnosis of SCD diseases.
Objective To understand the new clinical features of subacute combined degeneration(SCD) caused by lifestyle and dietary changes.Methods The clinical data of 50 patients with SCD were retrospectively analyzed.The continuous data were average±standard deviation.The categorical data were expressed by the number and percentage.The correlation analysis was performed by Logistic regression correlation analysis,P<0.05 was significant.Results(1) The age of onset was 19-83 years old,with an average of(53.2±10.8),5 cases(10%) at 45 years old,18 cases(36%) at 45-65 years old,and 27 cases(54%) ≥65 years old.(2) 15 cases of anemia(30%),8 cases of digestive tract disease(16%),5 cases of alcohol abuse(10%),5 cases of long-term vegetarian diet(10%),7 cases of diabetic diet(14%),long-term anorexia(Neurosis) 2 cases(4%),2 cases of N_2O(4%),1 case of thyroid disease(2%).(3) Age>65 years old,serum hemoglobin(Hb),serum vitamin B12 level and the severity of the neurological lesions of the disease and wireless correlation(P>0.05).The mean red blood cell volume(MCV) was closely related to the severity of neurological dysfunction.The higher the peripheral blood MCV,the more severe the neuropathy(P<0.05).(4) 50 cases(100%) of neurophysiological examination showed different degrees of injury,in which motor nerve conduction velocity was slowed by 25 cases(50%),sensory nerve conduction velocity was slowed by 40 cases(80%),brainstem auditory induction The potential(BAEP) was abnormal in 3 cases(6%) and visual evoked potential(VEP) in 2 cases(4%).(5) Magnetic resonance imaging found 14 cases(28%) of lesions,involving 6 cases of cervical pulp,involving 6 cases of thoracic marrow,involving 2 cases of cervical and thoracic spinal cord,involving the lateral or posterior cord of the spinal cord,located in the lower cervical segment And the chest.Conclusion 65 years of age may be another peak incidence of SCD.Adolescent patients with no clear risk factors for SCD should be alert to the history of N2 O.The normal or elevated serum vitamin B12 does not rule out the diagnosis of SCD.The new biochemical indicators MCV,Hcy and cerebrospinal fluid basic myelin protein(MBP) determination contribute to the early diagnosis of SCD.Neurophysiological examination can objectively reflect the SCD lesions,and its detection rate is higher than the MRI detection rate,which is of great value in the early diagnosis of SCD diseases.
引文
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[2] 胡秀丽.脊髓亚急性联合变性19例误诊分析[J].陕西医学杂志,2003,32:1 138-1 139.
[3] LIN C Y,GUO W Y,CHEN S P,et al.Neurotoxicity of nitrous oxide:multimodal evoked potentials in an abuser[J].Clin Toxicol,2007,45(1):67-71.
[4] 李楠.血清维生素B_(12)水平正常的脊髓亚急性联合变性患者临床特点[J].山东医药,2018,58(4):74-76.
[5] 翟跃芬,王虎清,杜赟,等.脊髓亚急性联合变性患者血清维生素 B12水平与临床表现的分析[J].中国临床神经科学,2017,25(1):31-33;48.
[6] HEMMER B,GLOCKER F X,SCHUMACHER M,et al.Subacute combined degeneration:clinical,electrophysiological,and magnetic resonance imaging findings[J].J Neurol Neurosurg Psychiatry,1998,65(6):822-827.
[7] KATSAROS V K,GLOCKER F X,HEMMER B,et al.MRI of spinal cord and brain lesions in subacute combined degeneration[J].Neuroradiology,1998,40(11):716-719.
[8] 孙涛.38例脊髓亚急性联合变性的临床分析[D].沈阳:中国医科大学,2010.
[9] 崔红卫.脊髓亚急性联合变性研究进展[J].中华神经科杂志,2011,44(12):860-862.
[10] 王丽娟.脊髓亚急性联合变性103例临床分析[J].临床荟萃,2016,31(4):411-413.
[11] 杜娜,毛西京,于挺敏,等.脊髓亚急性联合变性的临床特点及早期联合诊断(附18例报告)[J].吉林大学学报(医学版),2018,44(4):806-809.
[12] PAUTAS E,CHéRIN P,JAEGER C D,et al.[Vitamin B 12 deficiency in the aged][J].Presse Médicale,1999,28(32):1 767.
[13] 冯晓婷.维生素B12缺乏与相关疾病的关系[J].中国实用神经疾病杂志,2014,17(1):96-99.
[14] 韩燕飞.脊髓亚急性联合变性19例分析及文献复习[J].临床和实验医学杂志,2014,13(5):363-365.
[15] 郝绍江.27例脊髓亚急性联合变性临床分析[J].贵州医科大学学报,2012,37(3):318-319.
[16] 李兴明.脊髓亚急性联合变性23例临床分析[J].中国现代药物应用,2011,5(7):10-12.
[17] SHOU Y,LI C,FAN D,et al.Diagnosis and clinical manifestations of subacute combined degeneration of the spinal cord:Analysis of 21 cases[J].Neural Regen Res,2007,2(2):112-116.
[18] GUIHONG S,YUN-BO S.Thyroid hormone regula-tion of adult intestinal stem cell development:mechanisms and evolutionary conservations[J].Int J Biol Sci,2012,8(8):1 217-1 224.
[19] GUIHONG S,YUN-BO S.Thyroid hormone regulation of adult intestinal stem cell development:mechanisms and evolutionary conservations[J].Int J Biol Sci,2012,8(8):1 217-1 224.
[20] ABDUL J,AASMA Y,SABIHA W,et al.Vitamin B12 deficiency common in primary hypothyroidism[J].Jpma the Journal of the Pakistan Medical Association,1986,58(5):258-261.
[21] GARAKANI A,JAFFE R J,SAVLA D,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.
[22] 侯月.滥用一氧化二氮致脊髓亚急性联合变性一例[J].脑与神经疾病杂志,2018(7):397-401.
[23] STOCKTON L,SIMONSEN C,SEAGO S.Nitrous oxide-induced vitamin B12 deficiency[J].Proc,2017,30(2):171-172.
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