Yu Miaomiao, Miao Jing, Lv Yudan, Wang Xue, Zhang Wuqiong, Shao Na, Meng Hongmei
Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Changchun, China.
Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Front Neurol. 2021 Jan 28;11:549331. doi: 10.3389/fneur.2020.549331. eCollection 2020.
Glucose transporter type 1 deficiency syndrome (Glut1-DS) is a rare neurometabolic disorder caused by mutations of the SLC2A1 gene. Paroxysmal exercise-induced dyskinesia is regarded as a representative symptom of Glut1-DS. Paroxysmal non-kinesigenic dyskinesia is usually caused by aberrations of the MR1 and KCNMA1 genes, but it also appears in Glut1-DS. We herein document a patient with Glut1-DS who suffered first from paroxysmal exercise-induced dyskinesia and subsequently paroxysmal non-kinesigenic dyskinesia and experienced a recent worsening of symptoms accompanied with a low fever. The lumbar puncture result showed a decreased glucose concentration and increased white blood cell (WBC) count in cerebrospinal fluid (CSF). The exacerbated symptoms were initially suspected to be caused by intracranial infection due to a mild fever of <38.0°C, decreased CSF glucose, and increased CSF WBC count. However, the second lumbar puncture result indicated a decreased glucose concentration and normal WBC count in CSF with no anti-infective agents, and the patient's symptoms were not relieved apparently. The continuous low glucose concentration attracted our attention, and gene analysis was performed. According to the gene analysis result, the patient was diagnosed with Glut1-DS finally. This case indicates that the complex paroxysmal dyskinesia in Glut1-DS may be confusing and pose challenges for accurate diagnosis. Except intracranial infection, Glut1-DS should be considered as a differential diagnosis upon detection of a low CSF glucose concentration and dyskinesia. The case presented here may encourage clinicians to be mindful of this atypical manifestation of Glut1-DS in order to avoid misdiagnosis.
1型葡萄糖转运体缺乏综合征(Glut1-DS)是一种由SLC2A1基因突变引起的罕见神经代谢紊乱疾病。阵发性运动诱发性运动障碍被视为Glut1-DS的典型症状。阵发性非运动诱发性运动障碍通常由MR1和KCNMA1基因异常引起,但也会出现在Glut1-DS中。我们在此记录了一名Glut1-DS患者,该患者最初出现阵发性运动诱发性运动障碍,随后出现阵发性非运动诱发性运动障碍,且近期症状加重并伴有低热。腰椎穿刺结果显示脑脊液(CSF)中葡萄糖浓度降低,白细胞(WBC)计数增加。由于体温轻度升高<38.0°C、CSF葡萄糖降低以及CSF WBC计数增加,最初怀疑症状加重是由颅内感染引起。然而,第二次腰椎穿刺结果显示CSF中葡萄糖浓度降低,WBC计数正常,且未使用抗感染药物,患者症状未见明显缓解。持续的低葡萄糖浓度引起了我们的注意,并进行了基因分析。根据基因分析结果,该患者最终被诊断为Glut1-DS。该病例表明,Glut1-DS中复杂的阵发性运动障碍可能令人困惑,对准确诊断构成挑战。除颅内感染外,在检测到CSF葡萄糖浓度降低和运动障碍时,应考虑Glut1-DS作为鉴别诊断。本文介绍的病例可能会促使临床医生注意Glut1-DS的这种非典型表现,以避免误诊。