Agbo Sedine Marie Desiree Nina, Duan Xiaohui, Wang Li, Dong Mingrui, Wang Qian, Cai Xiaojing, Liu Fang
Department of Neurology, The First Hospital of Tsinghua University, Beijing, China.
Department of Neurology, China-Japan Friendship Hospital, Beijing, China.
Front Immunol. 2025 Apr 28;16:1567541. doi: 10.3389/fimmu.2025.1567541. eCollection 2025.
The aim of this study was to compare the clinical presentations, nerve conduction studies, neuroimaging findings of subacute combined degeneration (SCD) caused by NO abuse and primary vitamin B12 deficiency. The goal is to improve diagnostic accuracy, tailored therapeutic interventions, and ultimately enhancing patient outcomes in cases of SCD caused by NO abuse.
This study was a retrospective case-control study which enrolled 23 patients diagnosed with NO-induced subacute combined degeneration (NO-SCD) and 20 patients with vitamin B12 deficiency-induced subacute combined degeneration (Vit B12-SCD) between 2015 and 2023. Clinical manifestations, physical examinations, laboratory tests, nerve conduction studies, and spinal cord MRI imaging results were collected. Additionally, age-matched healthy control groups were also included for comparative electrophysiological analysis, consisting of 23 young individuals and 21 elderly individuals corresponding to the NO-SCD and Vit B12-SCD groups, respectively.
The study found that compared to Vit B12-SCD, NO-SCD patients exhibited more severe and extensive neurological damage. Both NO-SCD and Vit B12- SCD patients may present with numbness or abnormal sensations, limb weakness, difficulty walking and inability to walk, but these are more severe and widespread in NO-SCD patients. NO-SCD patients showed significant decreases in limb strength, with common walking difficulties and paralysis. Additionally, NO abuse patients more frequently exhibited psychiatric symptoms, especially memory loss, hallucinations and confusion. Both Vit B12-SCD and NO-SCD can cause peripheral nerve demyelination and axonal damage, but it is more severe in the NO-SCD group, with more damage in the lower limbs than in the upper limbs. The extensive nature of axonal damage also indicated a poor prognosis. The degree of spinal cord damage in the NO-SCD group was more severe and affected longer segments. These results suggest that in addition to affecting vitamin B12, NO also causes neurological damage through other mechanisms.
In summary, NO-SCD leads to more severe clinical symptoms, peripheral nerve damage, and spinal cord injury than Vit B12-SCD. These differences guide the clinical treatment of NO-SCD, requiring not only vitamin B12 supplementation but also an addition in neuroprotective treatments.
本研究旨在比较一氧化氮（NO）滥用所致亚急性联合变性（SCD）与原发性维生素B12缺乏所致亚急性联合变性的临床表现、神经传导研究及神经影像学表现。目标是提高NO滥用所致SCD病例的诊断准确性、制定针对性的治疗干预措施，并最终改善患者预后。
本研究为回顾性病例对照研究，纳入了2015年至2023年间诊断为NO诱导的亚急性联合变性（NO-SCD）的23例患者和维生素B12缺乏诱导的亚急性联合变性（Vit B12-SCD）的20例患者。收集了临床表现、体格检查、实验室检查、神经传导研究及脊髓MRI成像结果。此外，还纳入了年龄匹配的健康对照组进行比较电生理分析，分别由23名年轻人和21名老年人组成，对应于NO-SCD组和Vit B12-SCD组。
研究发现，与Vit B12-SCD相比，NO-SCD患者表现出更严重、更广泛的神经损伤。NO-SCD和Vit B12-SCD患者均可能出现麻木或异常感觉、肢体无力、行走困难及无法行走，但这些症状在NO-SCD患者中更严重、更广泛。NO-SCD患者肢体力量显著下降，常见行走困难及瘫痪。此外，NO滥用患者更常出现精神症状，尤其是记忆力减退、幻觉和意识模糊。Vit B12-SCD和NO-SCD均可导致周围神经脱髓鞘和轴突损伤，但在NO-SCD组更严重，下肢损伤比上肢更严重。轴突损伤的广泛性也表明预后不良。NO-SCD组脊髓损伤程度更严重，累及节段更长。这些结果表明，NO除了影响维生素B12外，还通过其他机制导致神经损伤。
总之，与Vit B12-SCD相比，NO-SCD导致更严重的临床症状、周围神经损伤和脊髓损伤。这些差异为NO-SCD的临床治疗提供了指导，不仅需要补充维生素B12，还需增加神经保护治疗。
