Objective: To analyze the clinical and imaging characteristics of the neurological damage caused by nitrous oxide (N2O).
Methods: In the study, 10 patients in the Department of Neurology of China-Japan Friendship Hospital from October 2015 to February 2018 were retrospectively analyzed for the demographic data, the history of inhaled N2O, clinical features, blood examination, electrophysiological examination, spinal magnetic resonance imaging and therapeutic efficacy profiles.
Results: The male-to-female ratio was 4:6 and it presented with an age-of-onset 17-26 years [the average age: (20.80±3.12) years]. The time from inhaled N2O to onset was 1 month to 1 year [the average time: (6.95±4.19) months]. Paralysis in all the patients and numbness in 9 patients were the main clinical features, while positive Lhermitte's sign in 3 patients, urinary and defecation disturbance in 4 patients were also found. Blood examination indicated anemia in 2 patients, giant cell anemia in 1 case and small cell hypochromic anemia in 1 case. 3 cases had been treated with vitamin B12 in an external hospital, and the other 7 cases had abnormal increase in homocysteine levels. Electrophysiological examinations showed sensory and motor nerve involvement in 9 patients, and motor nerve involvement in 1 patient. The severity of lower extremity lesion was significantly heavier than that of upper extremity. Spinal magnetic resonance imagings showed that long segmental lesions were present in the cervical spinal cord of all the patients, 3 cases with long segmental lesions of the thoracic cord and 2 cases with spinal cord swelling. In 6 cases, the horizontal axis had an "inverted V-type" T2 high signal, 1 case was classified as "crescent", and 3 cases were "eight-shaped". The symptoms in these 10 cases were alleviated in varying degrees after stopping the inhalation of nitrous oxide, actively supplementing high doses of vitamin B12 and doing early rehabilitation exercises.
Conclusion: Myelopathy with nitrous oxide presents as paralysis and numbness in limb extremities. In imaging, cervical spinal cord damage is common, accompanied by thoracic spinal cord damage. The horizontal axis is more common in the "inverted V-type". Treatment with high doses of vitamin B12 is effective.
目的: 分析滥用一氧化二氮导致长节段脊髓病变的临床表现和影像学特点。
方法: 对2015年10月至2018年2月在中日友好医院神经科就诊的10例滥用一氧化二氮患者的人口学数据、一氧化二氮接触史、临床特点、实验室检查、神经电生理检查、脊髓磁共振成像及治疗效果等进行回顾性分析。
结果: 10例患者中男性4例,女性6例,年龄17~26岁[平均年龄(20.80±3.12)岁]。10例患者吸入N2O至起病时间为1个月至1年,平均时间(6.95±4.19)个月。10例均以肢体远端无力为主要症状,9例伴肢体远端麻木,3例伴Lhermitte’s征(+),4例伴尿便障碍。2例血常规提示贫血,1例为巨细胞性贫血,1例为小细胞低色素性贫血。3例曾于外院补充维生素B12治疗,其余7例血清同型半胱氨酸均异常增高。电生理检查示9例患者感觉和运动神经均受累,1例仅运动神经受累,下肢病变严重程度明显重于上肢。脊髓磁共振成像示10例均有颈髓纵行条状T2高信号,3例伴胸髓长节段病变,2例伴脊髓肿胀,6例横轴位呈“倒V”征,1例呈“类月牙”征,3例呈“八字”征。10例均在停止一氧化二氮吸入、积极补充大剂量维生素B12、早期康复锻炼治疗后,症状有不同程度缓解。
结论: 一氧化二氮中毒性脊髓病变临床多以肢体远端无力麻木为主,影像学上以颈段脊髓后索受累常见,可伴有胸髓受累,横轴位以“倒V”征多见。停止接触一氧化二氮和补充高剂量维生素B12有效。