Ghani Mohammad R, Yousaf Muhammad Ismail Khalid, Van Bussum Kelly, Shi Ping, Cordoves Feria Rolando M, Brown Martin
Neurology, University of Louisville School of Medicine, Louisville, USA.
Neurology, Jewish Hospital, UofL Health, Louisville, USA.
Cureus. 2022 Mar 21;14(3):e23371. doi: 10.7759/cureus.23371. eCollection 2022 Mar.
Miller Fisher syndrome (MFS) is a rare variant of Guillain-Barré syndrome (GBS) with a prevalence of one to two people per million each year. Viral and/or bacterial infection often precedes the classic triad of areflexia, ophthalmoplegia, and ataxia. Bulbar involvement is uncommon but can lead to extensive workup to rule out stroke, myasthenia gravis (MG), and other neuromuscular disorders. We present a case of a 32-year-old healthy male with a past medical history of Lyme disease as a teenager and sore throat two weeks prior. He presented to the hospital with rapidly ascending paresthesias in bilateral upper and lower extremities, urinary incontinence, and mild slurred speech. Exam on presentation revealed mild dysmetria in bilateral upper and lower limbs. The remainder of the exam was negative. Neuroradiological imaging, including magnetic resonance imaging (MRI) with and without contrast of the brain and the cervical and lumbar spine, did not show any acute process or abnormal enhancement. Lumbar puncture revealed cerebrospinal fluid (CSF) with normal protein and cell count, and hence no albuminocytological dissociation (ACD). Immunoserology was positive for Epstein-Barr virus (EBV) immunoglobulin G (IgG) but negative for immunoglobulin M (IgM). Despite the absent ACD, areflexia, and no third, fourth, and sixth cranial nerve deficits, there was high suspicion for GBS due to acutely rapid ascending paresthesia, mild dysarthria, and mild ataxia. The patient was started on intravenous immunoglobulin (IVIG) 2 mg/kg divided into five days within 24 hours of admission. The patient developed areflexia in all limbs on the second day of admission and complained of double vision. On the third day of admission, the patient's negative respiratory force (NIF) declined to -23, and he was intubated for airway protection. Our patient completed five days of IVIG. Positive anti-GQ1b antibodies further supported the diagnosis of MFS. After a seven-day ICU stay and 20 days of aggressive inpatient rehabilitation, the patient could do most of the activities of daily living independently. After six weeks, he was back to his normal baseline and restarted his job.
米勒-费希尔综合征（MFS）是吉兰-巴雷综合征（GBS）的一种罕见变异型，每年的发病率为百万分之一至二。病毒和/或细菌感染常先于无反射、眼肌麻痹和共济失调这一经典三联征出现。延髓受累不常见，但可能需要进行全面检查以排除中风、重症肌无力（MG）和其他神经肌肉疾病。我们报告一例32岁健康男性病例，该患者青少年时期有莱姆病病史，两周前出现咽痛。他因双侧上下肢迅速进展的感觉异常、尿失禁和轻度言语含糊不清入院。入院检查发现双侧上下肢轻度辨距不良。其余检查结果均为阴性。神经放射学成像，包括头颅及颈椎和腰椎的磁共振成像（MRI）平扫及增强扫描，未显示任何急性病变或异常强化。腰椎穿刺显示脑脊液（CSF）蛋白和细胞计数正常，因此无蛋白细胞分离（ACD）。免疫血清学检查显示爱泼斯坦-巴尔病毒（EBV）免疫球蛋白G（IgG）阳性，但免疫球蛋白M（IgM）阴性。尽管没有ACD、无反射，且无第三、第四和第六颅神经功能缺损，但由于急性快速进展的感觉异常、轻度构音障碍和轻度共济失调，高度怀疑为GBS。患者在入院24小时内开始静脉注射免疫球蛋白（IVIG），剂量为2 mg/kg，分五天给药。患者入院第二天出现四肢无反射，并主诉复视。入院第三天，患者的负吸气力（NIF）降至-23，遂行气管插管以保护气道。我们的患者完成了五天的IVIG治疗。抗GQ1b抗体阳性进一步支持了MFS的诊断。在重症监护病房（ICU）住院七天并积极进行20天的住院康复治疗后，患者能够独立完成大部分日常生活活动。六周后，他恢复到正常基线水平并重新开始工作。
