Baddam Sujatha, Patel Siddharth, Kahlon Navkirat, Thiriveedi Mrudula
Internal Medicine, Huntsville Hospital, Huntsville, USA.
Internal Medicine, Decatur Morgan Hospital, Decatur, USA.
Eur J Case Rep Intern Med. 2025 May 29;12(6):005467. doi: 10.12890/2025_005467. eCollection 2025.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare but emerging central nervous system demyelinating disorder that can mimic other neurological conditions. The use of TNF-α inhibitors in patients with autoimmune diseases has been linked to central nervous system demyelinating events, but the relationship remains poorly understood.
We present a 64-year-old male with a history of ankylosing spondylitis previously treated with a TNF-α inhibitor who developed progressive dizziness, ataxia, visual disturbances and cognitive changes. Despite extensive workup, including imaging and cerebrospinal fluid analysis, initial evaluations were inconclusive. MRI was non-diagnostic, and cerebrospinal fluid lacked oligoclonal bands. Ultimately, a serum MOG antibody titre of 1:1,000 confirmed the diagnosis of MOGAD. The patient improved with intravenous corticosteroids and was discharged on a tapering dose of oral prednisone. This case highlights an MRI-negative presentation of MOGAD with strong serologic findings.
This case emphasises the diagnostic challenge of MOGAD in patients with autoimmune backgrounds and neurologic symptoms without clear imaging findings. Clinicians should consider MOGAD in the differential diagnosis when evaluating such patients, particularly those with prior TNF-α inhibitor exposure. Early recognition and treatment with immunotherapy can lead to significant clinical improvement.
Clinicians should maintain a high index of suspicion for MOGAD in patients with atypical neurological symptoms, even when MRI findings are negative.TNF-α inhibitors may act as potential immunologic triggers for central nervous system demyelination, especially in patients with autoimmune conditions.Strong MOG antibody positivity can guide diagnosis in diagnostically ambiguous presentations and warrants the timely initiation of immunotherapy.
髓鞘少突胶质细胞糖蛋白抗体相关疾病（MOGAD）是一种罕见但正在被认识的中枢神经系统脱髓鞘疾病，可模仿其他神经系统疾病。自身免疫性疾病患者使用肿瘤坏死因子-α（TNF-α）抑制剂与中枢神经系统脱髓鞘事件有关，但这种关系仍了解甚少。
我们报告一名64岁男性，有强直性脊柱炎病史，曾接受TNF-α抑制剂治疗，出现进行性头晕、共济失调、视觉障碍和认知改变。尽管进行了广泛检查，包括影像学检查和脑脊液分析，但初始评估尚无定论。磁共振成像（MRI）未得出诊断结果，脑脊液中缺乏寡克隆带。最终，血清MOG抗体滴度为1:1000确诊为MOGAD。患者接受静脉注射皮质类固醇后病情改善，出院时口服泼尼松逐渐减量。该病例突出了MOGAD的MRI阴性表现但血清学检查结果阳性。
本病例强调了MOGAD在有自身免疫背景且有神经症状但无明确影像学表现患者中的诊断挑战。临床医生在评估此类患者时，尤其是那些既往接触过TNF-α抑制剂的患者，应在鉴别诊断中考虑MOGAD。早期识别并进行免疫治疗可带来显著临床改善。
临床医生对有非典型神经症状的患者应高度怀疑MOGAD，即使MRI结果为阴性。TNF-α抑制剂可能是中枢神经系统脱髓鞘的潜在免疫触发因素，尤其是在自身免疫性疾病患者中。强烈的MOG抗体阳性可在诊断不明确的情况下指导诊断，并保证及时开始免疫治疗。
