Effect of phosphatidic acid on antiganglioside antibody reactivity in the isolated facial diplegia variant of Guillain-Barr? syndrome: a case report
Effect of phosphatidic acid on antiganglioside antibody reactivity in the isolated facial diplegia variant of Guillain-Barr? syndrome: a case report
复制标题
磷脂酸对格林-巴尔分离性面部双瘫变体抗神经节苷脂抗体反应性的影响？
DOI：
10.1007/s13760-020-01592-z
复制
发表时间：
2023
期刊：
影响因子：
2.7
通讯作者：
Ando Y.
中科院分区：
文献类型：
--
作者：
Nakahara K;Nakane S;Terasaki T;Ando Y.
格林-巴利综合征（GBS）是急性弛缓性麻痹的最常见原因，其特征为无反射性麻痹伴白蛋白细胞分离[1]。在常见的情况下，它表现为四肢和躯干的运动感觉神经病，缺乏腱反射。然而，也已知GBS的不同变体。因此，在不常见的情况下诊断GBS是棘手的。双侧面瘫（FD）是GBS的一种罕见变异。虽然大多数FD患者存在感觉异常等感觉障碍，但少数患者无感觉异常[2]。因此，到目前为止，无感觉异常的FD报告少得多[3 - 5]，并且比有感觉异常的FD更难诊断。我们报告一例无感觉异常的FD患者，通过添加磷脂酸（PA）检测到血清抗神经节苷脂免疫球蛋白G（IgG）抗体升高。一名83岁男性于3月14日发现双侧面部无力进行性加重，并于3月16日入住我院。他被诊断为高血压并服用抗高血压药物，近期无急性呼吸道炎症、急性肠炎或头部创伤病史。而且，他这几年也没有去过那些山和灌木丛。入院时体温36.6 ℃，体格检查无皮疹。神经系统检查显示双侧面神经麻痹。所有其他颅神经均完好无损，其他部位无运动和感觉缺陷的证据。他的腱反射是正常的，屈足底反射观察整个。实验室数据显示无炎症反应，如白细胞增多，C反应蛋白和红细胞沉降率升高。血清血管紧张素转换酶水平和血管炎筛查结果均在正常范围内。血清蛋白电泳未检出副蛋白。基于病毒抗体的检测显示既往感染单纯疱疹病毒、水痘带状疱疹病毒和巨细胞病毒。抗核和抗核胞浆抗体不存在。腰椎穿刺显示白蛋白细胞分离[蛋白质，97 mg/dl;白色血细胞，7个细胞/mm3（100%单形细胞）]和脑脊液（CSF）葡萄糖水平为54 mg/dl。血糖水平为78 mg/dl。神经传导检查显示正中神经异常（正中神经和尺神经感觉神经动作电位缺失），腓肠神经感觉反应正常。呼吸功能检查、胸部X光片和脑部MRI显示正常。
Guillain–Barré syndrome (GBS) is the most frequent cause of acute flaccid paralysis and characterized by areflexic paralysis with albuminocytologic dissociation [1]. In common cases, it manifests as a motor sensory neuropathy in the limbs and trunk with absent tendon reflexes. However, different variants of GBS are also known. Therefore, it is tricky to diagnose GBS in uncommon cases. Facial diplegia (FD) is a rare variant of GBS. Although the majority of patients with FD have sensory disturbance such as paresthesia, the minority has no paresthesia [2]. Thus, FD without paresthesia has been reported much less so far [3–5], and more difficult to diagnose than that with paresthesia. Here we report a case of FD without paresthesia wherein elevated serum anti-ganglioside immunoglobulin G (IgG) antibodies were detected by the addition of phosphatidic acid (PA).An 83-year-old man noticed bilateral facial weakness that progressively worsened on March 14, and he was admitted to our hospital on March 16. He had been diagnosed with hypertension and took an antihypertensive agent, and he had no recent history of acute respiratory inflammation, acute enteritis, or head trauma. Moreover, he had not visited the mountains or thickets in the last few years. On admission, his body temperature was 36.6 C, and physical examination revealed no rash. Neurological examination revealed bilateral facial nerve paresis. All other cranial nerves were intact, and there was no evidence of motor and sensory deficits elsewhere. His tendon reflexes were normal, and flexor plantar reflexes were observed throughout. Laboratory data showed no inflammatory reaction such as leukocytosis and elevation of C-reactive protein and the erythrocyte sedimentation rate. Serum angiotensin-converting enzyme levels and the results of screening tests for vasculitis were within normal limits. No paraproteins were detected in serum protein electrophoresis. A viral antibodybased test revealed prior infection with herpes simplex virus, varicella-zoster virus, and cytomegalovirus. Antinuclear and antinuclear cytoplasmic antibodies were absent. Lumbar puncture revealed albuminocytologic dissociation [protein, 97 mg/dl; white blood cell, 7 cells/mm3 (100% monomorphonuclear cells)] and a cerebrospinal fluid (CSF) glucose level of 54 mg/dl. The plasma glucose level was 78 mg/dl. Nerve conduction studies showed abnormal median (absent sensory nerve action potential in the median and ulnar nerves) and normal sural sensory responses. Respiratory function tests, a chest radiograph, and brain MRI showed normal findings.