Cáceres-Marzal Cristina, Vaquerizo Julián, Galán Enrique, Fernández Santiago
Unit of Child Neurology, Department of Pediatrics, Hospital Materno-Infantil, Badajoz, Spain.
Pediatr Neurol. 2006 Oct;35(4):293-6. doi: 10.1016/j.pediatrneurol.2006.03.010.
Alexander disease is a neurodegenerative disorder characterized by macrocephaly and progressive demyelination with frontal lobe preponderance. The infantile form, the most frequent variant, appears between birth and 2 years of age and involves a severe course with a rapid neurologic deterioration. Although magnetic resonance imaging is useful for diagnosis, currently diagnosis is confirmed by the finding of missense mutation in the glial fibrillary acidic protein (GFAP) gene. This case reports a female who presented at the age of 5 months with refractory epilepsy and hypotonia. Laboratory examinations, muscle biopsy examination, and energetic metabolic study in muscle indicated increased concentrations of lactate, mitochondria with structural abnormalities, and decreased cytochrome-c oxidase activity respectively. Later, both clinical course and magnetic resonance findings were compatible with Alexander disease, which was confirmed by the finding of a novel glial fibrillary acidic protein gene mutation.
亚历山大病是一种神经退行性疾病,其特征为巨头畸形和以额叶为主的进行性脱髓鞘。婴儿型是最常见的变异型,出现在出生至2岁之间,病情严重,神经功能迅速恶化。虽然磁共振成像对诊断有用,但目前通过在胶质纤维酸性蛋白(GFAP)基因中发现错义突变来确诊。本病例报告了一名5个月大的女性,表现为难治性癫痫和肌张力减退。实验室检查、肌肉活检检查以及肌肉能量代谢研究分别表明乳酸浓度升高、线粒体结构异常以及细胞色素c氧化酶活性降低。后来,临床病程和磁共振成像结果均与亚历山大病相符,通过发现一种新的胶质纤维酸性蛋白基因突变得以确诊。